A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein.
A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
A form of CARDIAC MUSCLE disease in which the ventricular walls are excessively rigid, impeding ventricular filling. It is marked by reduced diastolic volume of either or both ventricles but normal or nearly normal systolic function. It may be idiopathic or associated with other diseases (ENDOMYOCARDIAL FIBROSIS or AMYLOIDOSIS) causing interstitial fibrosis.
A transient left ventricular apical dysfunction or ballooning accompanied by electrocardiographic (ECG) T wave inversions. This abnormality is associated with high levels of CATECHOLAMINES, either administered or endogenously secreted from a tumor or during extreme stress.
An autosomal dominant inherited form of HYPERTROPHIC CARDIOMYOPATHY. It results from any of more than 50 mutations involving genes encoding contractile proteins such as VENTRICULAR MYOSINS; cardiac TROPONIN T; ALPHA-TROPOMYOSIN.
A disease of the CARDIAC MUSCLE developed subsequent to the initial protozoan infection by TRYPANOSOMA CRUZI. After infection, less than 10% develop acute illness such as MYOCARDITIS (mostly in children). The disease then enters a latent phase without clinical symptoms until about 20 years later. Myocardial symptoms of advanced CHAGAS DISEASE include conduction defects (HEART BLOCK) and CARDIOMEGALY.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
Disease of CARDIAC MUSCLE resulting from chronic excessive alcohol consumption. Myocardial damage can be caused by: (1) a toxic effect of alcohol; (2) malnutrition in alcoholics such as THIAMINE DEFICIENCY; or (3) toxic effect of additives in alcoholic beverages such as COBALT. This disease is usually manifested by DYSPNEA and palpitations with CARDIOMEGALY and congestive heart failure (HEART FAILURE).
Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.
A congenital cardiomyopathy that is characterized by infiltration of adipose and fibrous tissue into the RIGHT VENTRICLE wall and loss of myocardial cells. Primary injuries usually are at the free wall of right ventricular and right atria resulting in ventricular and supraventricular arrhythmias.
Diabetes complications in which VENTRICULAR REMODELING in the absence of CORONARY ATHEROSCLEROSIS and hypertension results in cardiac dysfunctions, typically LEFT VENTRICULAR DYSFUNCTION. The changes also result in myocardial hypertrophy, myocardial necrosis and fibrosis, and collagen deposition due to impaired glucose tolerance.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
This structure includes the thin muscular atrial septum between the two HEART ATRIA, and the thick muscular ventricular septum between the two HEART VENTRICLES.
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
Occlusion of the outflow tract in either the LEFT VENTRICLE or the RIGHT VENTRICLE of the heart. This may result from CONGENITAL HEART DEFECTS, predisposing heart diseases, complications of surgery, or HEART NEOPLASMS.
Contractile activity of the MYOCARDIUM.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
The hollow, muscular organ that maintains the circulation of the blood.
The amount of BLOOD pumped out of the HEART per beat, not to be confused with cardiac output (volume/time). It is calculated as the difference between the end-diastolic volume and the end-systolic volume.
Unexpected rapid natural death due to cardiovascular collapse within one hour of initial symptoms. It is usually caused by the worsening of existing heart diseases. The sudden onset of symptoms, such as CHEST PAIN and CARDIAC ARRHYTHMIAS, particularly VENTRICULAR TACHYCARDIA, can lead to the loss of consciousness and cardiac arrest followed by biological death. (from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005)
Myosin type II isoforms found in cardiac muscle.
The period shortly before, during, and immediately after giving birth.
Measurement of intracardiac blood flow using an M-mode and/or two-dimensional (2-D) echocardiogram while simultaneously recording the spectrum of the audible Doppler signal (e.g., velocity, direction, amplitude, intensity, timing) reflected from the moving column of red blood cells.
Isoforms of MYOSIN TYPE II, specifically found in the ventricular muscle of the HEART. Defects in the genes encoding ventricular myosins result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).
The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.
A condition characterized by the thickening of the ventricular ENDOCARDIUM and subendocardium (MYOCARDIUM), seen mostly in children and young adults in the TROPICAL CLIMATE. The fibrous tissue extends from the apex toward and often involves the HEART VALVES causing restrictive blood flow into the respective ventricles (CARDIOMYOPATHY, RESTRICTIVE).
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).
The larger subunits of MYOSINS. The heavy chains have a molecular weight of about 230 kDa and each heavy chain is usually associated with a dissimilar pair of MYOSIN LIGHT CHAINS. The heavy chains possess actin-binding and ATPase activity.
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
The innermost layer of the heart, comprised of endothelial cells.
Members of the armadillo family of proteins that are found in DESMOSOMES and interact with various proteins including desmocadherins; DESMOPLAKIN; ACTIN FILAMENTS; and KERATINS.
The transference of a heart from one human or animal to another.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
A subclass of developmentally regulated lamins having a neutral isoelectric point. They are found to disassociate from nuclear membranes during mitosis.
The geometric and structural changes that the HEART VENTRICLES undergo, usually following MYOCARDIAL INFARCTION. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle.
One of the three polypeptide chains that make up the TROPONIN complex. It is a cardiac-specific protein that binds to TROPOMYOSIN. It is released from damaged or injured heart muscle cells (MYOCYTES, CARDIAC). Defects in the gene encoding troponin T result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
Regulation of the rate of contraction of the heart muscles by an artificial pacemaker.
Post-systolic relaxation of the HEART, especially the HEART VENTRICLES.
Pathological conditions involving the HEART including its structural and functional abnormalities.
Disorders or diseases associated with PUERPERIUM, the six-to-eight-week period immediately after PARTURITION in humans.
A family of transmembrane dystrophin-associated proteins that play a role in the membrane association of the DYSTROPHIN-ASSOCIATED PROTEIN COMPLEX.
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.
Implantable devices which continuously monitor the electrical activity of the heart and automatically detect and terminate ventricular tachycardia (TACHYCARDIA, VENTRICULAR) and VENTRICULAR FIBRILLATION. They consist of an impulse generator, batteries, and electrodes.
The abrupt cessation of all vital bodily functions, manifested by the permanent loss of total cerebral, respiratory, and cardiovascular functions.
A type of imaging technique used primarily in the field of cardiology. By coordinating the fast gradient-echo MRI sequence with retrospective ECG-gating, numerous short time frames evenly spaced in the cardiac cycle are produced. These images are laced together in a cinematic display so that wall motion of the ventricles, valve motion, and blood flow patterns in the heart and great vessels can be visualized.
A CALCIUM-dependent adhesion molecule of DESMOSOMES that also plays a role in embryonic STEM CELL proliferation.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Period of contraction of the HEART, especially of the HEART VENTRICLES.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Procedures in which placement of CARDIAC CATHETERS is performed for therapeutic or diagnostic procedures.
An X-linked dominant multisystem disorder resulting in cardiomyopathy, myopathy and INTELLECTUAL DISABILITY. It is caused by mutation in the gene encoding LYSOSOMAL-ASSOCIATED MEMBRANE PROTEIN 2.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
A mutation in which a codon is mutated to one directing the incorporation of a different amino acid. This substitution may result in an inactive or unstable product. (From A Dictionary of Genetics, King & Stansfield, 5th ed)
Rare congenital cardiomyopathies characterized by the lack of left ventricular myocardium compaction. The noncompaction results in numerous prominent trabeculations and a loose myocardial meshwork (spongy myocardium) in the LEFT VENTRICLE. Heterogeneous clinical features include diminished systolic function sometimes associated with left ventricular dilation, that presents either neonatally or progressively. Often, the RIGHT VENTRICLE is also affected. CONGESTIVE HEART FAILURE; PULMONARY EMBOLISM; and ventricular ARRHYTHMIA are commonly seen.
The co-occurrence of pregnancy and a cardiovascular disease. The disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.
An intermediate filament protein found predominantly in smooth, skeletal, and cardiac muscle cells. Localized at the Z line. MW 50,000 to 55,000 is species dependent.
A muscle protein localized in surface membranes which is the product of the Duchenne/Becker muscular dystrophy gene. Individuals with Duchenne muscular dystrophy usually lack dystrophin completely while those with Becker muscular dystrophy have dystrophin of an altered size. It shares features with other cytoskeletal proteins such as SPECTRIN and alpha-actinin but the precise function of dystrophin is not clear. One possible role might be to preserve the integrity and alignment of the plasma membrane to the myofibrils during muscle contraction and relaxation. MW 400 kDa.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
A condition in which HEART VENTRICLES exhibit impaired function.
Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.
The valve between the left atrium and left ventricle of the heart.
Examinations used to diagnose and treat heart conditions.
Backflow of blood from the LEFT VENTRICLE into the LEFT ATRIUM due to imperfect closure of the MITRAL VALVE. This can lead to mitral valve regurgitation.
Removal of tissue by vaporization, abrasion, or destruction. Methods used include heating tissue by hot liquids or microwave thermal heating, freezing (CRYOABLATION), chemical ablation, and photoablation with LASERS.
A guanidine analog with specific affinity for tissues of the sympathetic nervous system and related tumors. The radiolabeled forms are used as antineoplastic agents and radioactive imaging agents. (Merck Index, 12th ed) MIBG serves as a neuron-blocking agent which has a strong affinity for, and retention in, the adrenal medulla and also inhibits ADP-ribosyltransferase.
A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
Removal of tissue with electrical current delivered via electrodes positioned at the distal end of a catheter. Energy sources are commonly direct current (DC-shock) or alternating current at radiofrequencies (usually 750 kHz). The technique is used most often to ablate the AV junction and/or accessory pathways in order to interrupt AV conduction and produce AV block in the treatment of various tachyarrhythmias.
Elements of limited time intervals, contributing to particular results or situations.
Impaired conduction of cardiac impulse that can occur anywhere along the conduction pathway, such as between the SINOATRIAL NODE and the right atrium (SA block) or between atria and ventricles (AV block). Heart blocks can be classified by the duration, frequency, or completeness of conduction block. Reversibility depends on the degree of structural or functional defects.
In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
An X-linked recessive muscle disease caused by an inability to synthesize DYSTROPHIN, which is involved with maintaining the integrity of the sarcolemma. Muscle fibers undergo a process that features degeneration and regeneration. Clinical manifestations include proximal weakness in the first few years of life, pseudohypertrophy, cardiomyopathy (see MYOCARDIAL DISEASES), and an increased incidence of impaired mentation. Becker muscular dystrophy is a closely related condition featuring a later onset of disease (usually adolescence) and a slowly progressive course. (Adams et al., Principles of Neurology, 6th ed, p1415)
A transient loss of consciousness and postural tone caused by diminished blood flow to the brain (i.e., BRAIN ISCHEMIA). Presyncope refers to the sensation of lightheadedness and loss of strength that precedes a syncopal event or accompanies an incomplete syncope. (From Adams et al., Principles of Neurology, 6th ed, pp367-9)
Recording the locations and measurements of electrical activity in the EPICARDIUM by placing electrodes on the surface of the heart to analyze the patterns of activation and to locate arrhythmogenic sites.
A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by TROPONIN.
Method in which prolonged electrocardiographic recordings are made on a portable tape recorder (Holter-type system) or solid-state device ("real-time" system), while the patient undergoes normal daily activities. It is useful in the diagnosis and management of intermittent cardiac arrhythmias and transient myocardial ischemia.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
A condition in which the RIGHT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE or MYOCARDIAL INFARCTION, and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the right ventricular wall.
A giant elastic protein of molecular mass ranging from 2,993 kDa (cardiac), 3,300 kDa (psoas), to 3,700 kDa (soleus) having a kinase domain. The amino- terminal is involved in a Z line binding, and the carboxy-terminal region is bound to the myosin filament with an overlap between the counter-connectin filaments at the M line.
The long cylindrical contractile organelles of STRIATED MUSCLE cells composed of ACTIN FILAMENTS; MYOSIN filaments; and other proteins organized in arrays of repeating units called SARCOMERES .
The mitochondria of the myocardium.
A form of heart block in which the electrical stimulation of HEART VENTRICLES is interrupted at either one of the branches of BUNDLE OF HIS thus preventing the simultaneous depolarization of the two ventricles.
Methods to induce and measure electrical activities at specific sites in the heart to diagnose and treat problems with the heart's electrical system.
One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.
A diverse superfamily of proteins that function as translocating proteins. They share the common characteristics of being able to bind ACTINS and hydrolyze MgATP. Myosins generally consist of heavy chains which are involved in locomotion, and light chains which are involved in regulation. Within the structure of myosin heavy chain are three domains: the head, the neck and the tail. The head region of the heavy chain contains the actin binding domain and MgATPase domain which provides energy for locomotion. The neck region is involved in binding the light-chains. The tail region provides the anchoring point that maintains the position of the heavy chain. The superfamily of myosins is organized into structural classes based upon the type and arrangement of the subunits they contain.
Echocardiography applying the Doppler effect, with the superposition of flow information as colors on a gray scale in a real-time image.
Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.
A heterogeneous group of infections produced by coxsackieviruses, including HERPANGINA, aseptic meningitis (MENINGITIS, ASEPTIC), a common-cold-like syndrome, a non-paralytic poliomyelitis-like syndrome, epidemic pleurodynia (PLEURODYNIA, EPIDEMIC) and a serious MYOCARDITIS.
Inflammation of the PERICARDIUM that is characterized by the fibrous scarring and adhesion of both serous layers, the VISCERAL PERICARDIUM and the PARIETAL PERICARDIUM leading to the loss of pericardial cavity. The thickened pericardium severely restricts cardiac filling. Clinical signs include FATIGUE, muscle wasting, and WEIGHT LOSS.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
The circulation of blood through the CORONARY VESSELS of the HEART.
AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.
Small pumps, often implantable, designed for temporarily assisting the heart, usually the LEFT VENTRICLE, to pump blood. They consist of a pumping chamber and a power source, which may be partially or totally external to the body and activated by electromagnetic motors.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
A device designed to stimulate, by electric impulses, contraction of the heart muscles. It may be temporary (external) or permanent (internal or internal-external).
A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.
Detection of a MUTATION; GENOTYPE; KARYOTYPE; or specific ALLELES associated with genetic traits, heritable diseases, or predisposition to a disease, or that may lead to the disease in descendants. It includes prenatal genetic testing.
Echocardiography applying the Doppler effect, with velocity detection combined with range discrimination. Short bursts of ultrasound are transmitted at regular intervals and the echoes are demodulated as they return.
A group of desmosomal cadherins with cytoplasmic tails that are divergent from those of classical CADHERINS. Their intracytoplasmic domains bind PLAKOGLOBIN; PLAKOPHILINS; and DESMOPLAKINS.
Biochemical identification of mutational changes in a nucleotide sequence.
A large class of structurally-related proteins that contain one or more LIM zinc finger domains. Many of the proteins in this class are involved in intracellular signaling processes and mediate their effects via LIM domain protein-protein interactions. The name LIM is derived from the first three proteins in which the motif was found: LIN-11, Isl1 and Mec-3.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
Desmoplakins are cytoskeletal linker proteins that anchor INTERMEDIATE FILAMENTS to the PLASMA MEMBRANE at DESMOSOMES.
An impulse-conducting system composed of modified cardiac muscle, having the power of spontaneous rhythmicity and conduction more highly developed than the rest of the heart.
A genetically heterogeneous, multifaceted disorder characterized by short stature, webbed neck, ptosis, skeletal malformations, hypertelorism, hormonal imbalance, CRYPTORCHIDISM, multiple cardiac abnormalities (most commonly including PULMONARY VALVE STENOSIS), and some degree of INTELLECTUAL DISABILITY. The phenotype bears similarities to that of TURNER SYNDROME that occurs only in females and has its basis in a 45, X karyotype abnormality. Noonan syndrome occurs in both males and females with a normal karyotype (46,XX and 46,XY). Mutations in a several genes (PTPN11, KRAS, SOS1, NF1 and RAF1) have been associated the the NS phenotype. Mutations in PTPN11 are the most common. LEOPARD SYNDROME, a disorder that has clinical features overlapping those of Noonan Syndrome, is also due to mutations in PTPN11. In addition, there is overlap with the syndrome called neurofibromatosis-Noonan syndrome due to mutations in NF1.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.
A type of junction that attaches one cell to its neighbor. One of a number of differentiated regions which occur, for example, where the cytoplasmic membranes of adjacent epithelial cells are closely apposed. It consists of a circular region of each membrane together with associated intracellular microfilaments and an intercellular material which may include, for example, mucopolysaccharides. (From Glick, Glossary of Biochemistry and Molecular Biology, 1990; Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
The pressure within a CARDIAC VENTRICLE. Ventricular pressure waveforms can be measured in the beating heart by catheterization or estimated using imaging techniques (e.g., DOPPLER ECHOCARDIOGRAPHY). The information is useful in evaluating the function of the MYOCARDIUM; CARDIAC VALVES; and PERICARDIUM, particularly with simultaneous measurement of other (e.g., aortic or atrial) pressures.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
Benzo-indoles similar to CARBOLINES which are pyrido-indoles. In plants, carbazoles are derived from indole and form some of the INDOLE ALKALOIDS.
Controlled physical activity which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used.
A catecholamine derivative with specificity for BETA-1 ADRENERGIC RECEPTORS. It is commonly used as a cardiotonic agent after CARDIAC SURGERY and during DOBUTAMINE STRESS ECHOCARDIOGRAPHY.
A type of cardiac arrhythmia with premature contractions of the HEART VENTRICLES. It is characterized by the premature QRS complex on ECG that is of abnormal shape and great duration (generally >129 msec). It is the most common form of all cardiac arrhythmias. Premature ventricular complexes have no clinical significance except in concurrence with heart diseases.
A state of subnormal or depressed cardiac output at rest or during stress. It is a characteristic of CARDIOVASCULAR DISEASES, including congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic. The serious form of low cardiac output is characterized by marked reduction in STROKE VOLUME, and systemic vasoconstriction resulting in cold, pale, and sometimes cyanotic extremities.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
An individual having different alleles at one or more loci regarding a specific character.
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.
An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts. Clinical manifestations include GAIT ATAXIA, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. Most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin. (From Adams et al., Principles of Neurology, 6th ed, p1081; N Engl J Med 1996 Oct 17;335(16):1169-75) The severity of Friedreich ataxia associated with expansion of GAA repeats in the first intron of the frataxin gene correlates with the number of trinucleotide repeats. (From Durr et al, N Engl J Med 1996 Oct 17;335(16):1169-75)
A heterogeneous group of inherited MYOPATHIES, characterized by wasting and weakness of the SKELETAL MUSCLE. They are categorized by the sites of MUSCLE WEAKNESS; AGE OF ONSET; and INHERITANCE PATTERNS.
Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.
The muscular structure separating the right and the left lower chambers (HEART VENTRICLES) of the heart. The ventricular septum consists of a very small membranous portion just beneath the AORTIC VALVE, and a large thick muscular portion consisting of three sections including the inlet septum, the trabecular septum, and the outlet septum.
The percent frequency with which a dominant or homozygous recessive gene or gene combination manifests itself in the phenotype of the carriers. (From Glossary of Genetics, 5th ed)
Imaging of a ventricle of the heart after the injection of a radioactive contrast medium. The technique is less invasive than cardiac catheterization and is used to assess ventricular function.
A group of sporadic, familial and/or inherited, degenerative, and infectious disease processes, linked by the common theme of abnormal protein folding and deposition of AMYLOID. As the amyloid deposits enlarge they displace normal tissue structures, causing disruption of function. Various signs and symptoms depend on the location and size of the deposits.
A group of muscle diseases associated with abnormal mitochondria function.
Calcium-transporting ATPases that catalyze the active transport of CALCIUM into the SARCOPLASMIC RETICULUM vesicles from the CYTOPLASM. They are primarily found in MUSCLE CELLS and play a role in the relaxation of MUSCLES.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.
A localized bulging or dilatation in the muscle wall of a heart (MYOCARDIUM), usually in the LEFT VENTRICLE. Blood-filled aneurysms are dangerous because they may burst. Fibrous aneurysms interfere with the heart function through the loss of contractility. True aneurysm is bound by the vessel wall or cardiac wall. False aneurysms are HEMATOMA caused by myocardial rupture.
A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.
Activities or games, usually involving physical effort or skill. Reasons for engagement in sports include pleasure, competition, and/or financial reward.
Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
The agent of South American trypanosomiasis or CHAGAS DISEASE. Its vertebrate hosts are man and various domestic and wild animals. Insects of several species are vectors.
A species of ENTEROVIRUS infecting humans and containing 36 serotypes. It is comprised of all the echoviruses and a few coxsackieviruses, including all of those previously named coxsackievirus B.
A complex of gadolinium with a chelating agent, diethylenetriamine penta-acetic acid (DTPA see PENTETIC ACID), that is given to enhance the image in cranial and spinal MRIs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p706)
Rare congenital X-linked disorder of lipid metabolism. Barth syndrome is transmitted in an X-linked recessive pattern. The syndrome is characterized by muscular weakness, growth retardation, DILATED CARDIOMYOPATHY, variable NEUTROPENIA, 3-methylglutaconic aciduria (type II) and decreases in mitochondrial CARDIOLIPIN level. Other biochemical and morphological mitochondrial abnormalities also exist.
Impaired impulse conduction from HEART ATRIA to HEART VENTRICLES. AV block can mean delayed or completely blocked impulse conduction.
A genus of the family PICORNAVIRIDAE whose members preferentially inhabit the intestinal tract of a variety of hosts. The genus contains many species. Newly described members of human enteroviruses are assigned continuous numbers with the species designated "human enterovirus".
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Substances used to allow enhanced visualization of tissues.
Conical muscular projections from the walls of the cardiac ventricles, attached to the cusps of the atrioventricular valves by the chordae tendineae.
Radiography of the vascular system of the heart muscle after injection of a contrast medium.
Recording of regional electrophysiological information by analysis of surface potentials to give a complete picture of the effects of the currents from the heart on the body surface. It has been applied to the diagnosis of old inferior myocardial infarction, localization of the bypass pathway in Wolff-Parkinson-White syndrome, recognition of ventricular hypertrophy, estimation of the size of a myocardial infarct, and the effects of different interventions designed to reduce infarct size. The limiting factor at present is the complexity of the recording and analysis, which requires 100 or more electrodes, sophisticated instrumentation, and dedicated personnel. (Braunwald, Heart Disease, 4th ed)
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Graphic registration of the heart sounds picked up as vibrations and transformed by a piezoelectric crystal microphone into a varying electrical output according to the stresses imposed by the sound waves. The electrical output is amplified by a stethograph amplifier and recorded by a device incorporated into the electrocardiograph or by a multichannel recording machine.
Transport proteins that carry specific substances in the blood or across cell membranes.
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.
Radionuclide ventriculography where scintigraphic data is acquired during repeated cardiac cycles at specific times in the cycle, using an electrocardiographic synchronizer or gating device. Analysis of right ventricular function is difficult with this technique; that is best evaluated by first-pass ventriculography (VENTRICULOGRAPHY, FIRST-PASS).
Radiography of the heart and great vessels after injection of a contrast medium.
A multi-functional catenin that is highly homologous to BETA CATENIN. Gamma catenin binds CADHERINS and helps link their cytoplasmic tails to ACTIN in the CYTOSKELETON via ALPHA CATENIN. It is also found in DESMOSOMES where it mediates the link between DESMOSOMAL CADHERINS and DESMOPLAKIN.
A strain of mice arising from a spontaneous MUTATION (mdx) in inbred C57BL mice. This mutation is X chromosome-linked and produces viable homozygous animals that lack the muscle protein DYSTROPHIN, have high serum levels of muscle ENZYMES, and possess histological lesions similar to human MUSCULAR DYSTROPHY. The histological features, linkage, and map position of mdx make these mice a worthy animal model of DUCHENNE MUSCULAR DYSTROPHY.
Gadolinium. An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors.
The hemodynamic and electrophysiological action of the right HEART VENTRICLE.
The chambers of the heart, to which the BLOOD returns from the circulation.
A characteristic symptom complex.
An X-linked inherited metabolic disease caused by a deficiency of lysosomal ALPHA-GALACTOSIDASE A. It is characterized by intralysosomal accumulation of globotriaosylceramide and other GLYCOSPHINGOLIPIDS in blood vessels throughout the body leading to multi-system complications including renal, cardiac, cerebrovascular, and skin disorders.
The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.
An autosomal dominant disorder with an acronym of its seven features (LENTIGO; ELECTROCARDIOGRAM abnormalities; ocular HYPERTELORISM; PULMONARY STENOSIS; abnormal genitalia; retardation of growth; and DEAFNESS or SENSORINEURAL HEARING LOSS). This syndrome is caused by mutations of PTPN11 gene encoding the non-receptor PROTEIN TYROSINE PHOSPHATASE, type 11, and is an allelic to NOONAN SYNDROME. Features of LEOPARD syndrome overlap with those of NEUROFIBROMATOSIS 1 which is caused by mutations in the NEUROFIBROMATOSIS 1 GENES.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.
A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.
A method of recording heart motion and internal structures by combining ultrasonic imaging with exercise testing (EXERCISE TEST) or pharmacologic stress.
A condition characterized by the thickening of ENDOCARDIUM due to proliferation of fibrous and elastic tissue, usually in the left ventricle leading to impaired cardiac function (CARDIOMYOPATHY, RESTRICTIVE). It is most commonly seen in young children and rarely in adults. It is often associated with congenital heart anomalies (HEART DEFECTS CONGENITAL;) INFECTION; or gene mutation. Defects in the tafazzin protein, encoded by TAZ gene, result in a form of autosomal dominant familial endocardial fibroelastosis.
One of the alpha crystallin subunits. In addition to being expressed in the lens (LENS, CRYSTALLINE), alpha-crystallin B chain has been found in a variety of tissues such as HEART; BRAIN; MUSCLE; and KIDNEY. Accumulation of the protein in the brain is associated with NEURODEGENERATIVE DISEASES such as CREUTZFELDT-JAKOB SYNDROME and ALEXANDER DISEASE.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
A conical fibro-serous sac surrounding the HEART and the roots of the great vessels (AORTA; VENAE CAVAE; PULMONARY ARTERY). Pericardium consists of two sacs: the outer fibrous pericardium and the inner serous pericardium. The latter consists of an outer parietal layer facing the fibrous pericardium, and an inner visceral layer (epicardium) resting next to the heart, and a pericardial cavity between these two layers.
The exercise capacity of an individual as measured by endurance (maximal exercise duration and/or maximal attained work load) during an EXERCISE TEST.
A family of RNA viruses that infect fungi and protozoa. There are three genera: TOTIVIRUS; GIARDIAVIRUS; and LEISHMANIAVIRUS.
A group of cardiac arrhythmias in which the cardiac contractions are not initiated at the SINOATRIAL NODE. They include both atrial and ventricular premature beats, and are also known as extra or ectopic heartbeats. Their frequency is increased in heart diseases.
Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.
The measurement of an organ in volume, mass, or heaviness.
The qualitative or quantitative estimation of the likelihood of adverse effects that may result from exposure to specified health hazards or from the absence of beneficial influences. (Last, Dictionary of Epidemiology, 1988)
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
The restoration of the sequential order of contraction and relaxation of the HEART ATRIA and HEART VENTRICLES by atrio-biventricular pacing.
A single-pass transmembrane glycoproteins that mediate CALCIUM-dependent CELL ADHESION and are core components of DESMOSOMES.
Agents that have a damaging effect on the HEART. Such damage can occur from ALKYLATING AGENTS; FREE RADICALS; or metabolites from OXIDATIVE STRESS and in some cases is countered by CARDIOTONIC AGENTS. Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.
The hemodynamic and electrophysiological action of the HEART VENTRICLES.
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.

Clinical profile and outcome of idiopathic restrictive cardiomyopathy. (1/98)

BACKGROUND: Idiopathic restrictive cardiomyopathy is a poorly recognized entity of unknown cause characterized by nondilated, nonhypertrophied ventricles with diastolic dysfunction resulting in dilated atria and variable systolic function. METHODS AND RESULTS: Between 1979 and 1996, 94 patients (61% women) 10 to 90 years old (mean, 64 years) met strict morphological echocardiographic criteria for idiopathic restrictive cardiomyopathy, mainly dilated atria with nonhypertrophied, nondilated ventricles. None had known infiltrative disease, hypertension of >5 years' duration, or cardiac or systemic conditions associated with restrictive filling. Nineteen percent were in NYHA class I, 53% in class II, and 28% in class III or IV. Atrial fibrillation was noted in 74% of patients and systolic dysfunction in 16%. Follow-up (mean, 68 months) was complete for 93 patients (99%). At follow-up, 47 patients (50%) had died, 32 (68%) of cardiovascular causes. Four had heart transplantation. The death rate compared with actuarial statistics was significantly higher than expected (P<0.0001). Kaplan-Meier 5-year survival was 64%, compared with expected survival of 85%. Multivariate analysis using proportional hazards showed that the risk of death approximately doubles with male sex (hazard ratio [HR] = 2.1), left atrial dimension >60 mm (HR = 2.3), age >70 years (HR = 2.0), and each increment of NYHA class (HR = 2.0). CONCLUSIONS: Idiopathic restrictive cardiomyopathy or nondilated, nonhypertrophic ventricles with marked biatrial dilatation, as defined morphologically by echocardiography, affects predominantly elderly patients but can occur in any age group. Patients present with systemic and pulmonary venous congestion and atrial fibrillation and have a poor prognosis, particularly men >70 years old with higher NYHA class and left atrial dimension >60 mm.  (+info)

Differentiation between restrictive cardiomyopathy and constrictive pericarditis by early diastolic doppler myocardial velocity gradient at the posterior wall. (2/98)

BACKGROUND: The differential diagnosis between restrictive cardiomyopathy (RCM) and constrictive pericarditis (CP) is challenging and, despite combined information from different diagnostic tests, surgical exploration is often necessary. METHODS AND RESULTS: A group of 55 subjects (mean age, 63+/-11 years; 36 men and 19 women) were enrolled in the study; 15 had RCM, 10 had CP, and 30 were age-matched, normal controls. The diagnosis of RCM was supported by a biopsy; in the CP group, the diagnosis was confirmed either surgically or at autopsy. All patients underwent a transthoracic echocardiogram that included the assessment of Doppler myocardial velocity gradient (MVG), as measured from the left ventricular posterior wall during the predetermined phases of the cardiac cycle. MVG was lower (P<0.01) in RCM patients compared with both CP patients and normal controls during ventricular ejection (2. 8+/-1.2 versus 4.4+/-1.0 and 4.7+/-0.8 s(-1), respectively) and rapid ventricular filling (1.9+/-0.8 versus 8.7+/-1.7 and 3.7+/-1.4 s(-1), respectively). Additionally, during isovolumic relaxation, MVG was positive in RCM patients and negative in both CP patients and normal controls (0.7+/-0.4 versus -1.0+/-0.6 and -0.4+/-0.3 s(-1), respectively; P<0.01). During atrial contraction, MVG was similarly low (P<0.01) in both RCM and CP patients compared with normal controls (1.6+/-1.7 and 1.7+/-1.8 versus 3.8+/-0.9 s(-1), respectively). CONCLUSIONS: Doppler myocardial imaging-derived MVG, as measured from the left ventricular posterior wall in early diastole during both isovolumic relaxation and rapid ventricular filling, allows for the discrimination of RCM from CP.  (+info)

Sudden death and cardiovascular collapse in children with restrictive cardiomyopathy. (3/98)

BACKGROUND: Restrictive cardiomyopathy (RCM) is rare in children, and the prognosis is poor. In the present study, we evaluated all pediatric patients with RCM who were at our institution during a 31-year period to determine the clinical outcome and cause of death. Those who sustained sudden, unanticipated cardiac arrests were evaluated for risk factors that are predictive of sudden death. METHODS AND RESULTS: Eighteen consecutive patients were reviewed. Presentation, clinical course, laboratory data, and histopathological evidence of ischemia were compared between patients with and without sudden death events. The results demonstrated that patients who were at risk for sudden death were girls with chest pain, syncope, or both at presentation and without congestive heart failure. Although not statistically significant for sudden death, Holter monitor evidence of ischemia predicted death within months. Histopathological evidence of acute or chronic ischemia was found in the majority of patients, with acute ischemia more common among those who sustained sudden death events. CONCLUSIONS: All children with RCM are at risk for ischemia-related complications and death, and some are at risk of sudden death. In the present study, patients at risk of sudden death appeared well and had no evidence of ongoing heart failure but often had signs or symptoms of ischemia characterized by chest pain, syncope, or both. ECGs and Holter monitors may be useful screening tools. The use of beta-blockade, the placement of an implantable cardioverter-defibrillator, and preferential status 1A or B listing for cardiac transplantation are proposed for pediatric patients with RCM and evidence of ongoing ischemia.  (+info)

Heart transplantation and the Batista operation for children with refractory heart failure. (4/98)

Medically refractory heart failure may be present in children with cardiomyopathy (CMP) or complex congenital heart disease (CHD). In adults, the surgical management of this condition is either heart transplantation or the Batista operation. From March 1995 to January 2000, a total of 6 children, aged from 1 to 16 years, with medically refractory heart failure associated with CMP or complex CHD underwent cardiac transplantation and one of them also had the Batista operation as a bridge to transplantation. One of the 6 patients died of intractable sepsis 17 days after the operation, but the other 5 were discharged with satisfactory hemodynamics. Immunosuppressive agents, including azathioprine, cyclosporin or FK-506, were given. One patient experienced moderate acute rejection, but it was controlled by FK-506, OKT-3 and solumedrol. However, another suffered from lymphoproliferative disease 8 months after transplant, but it was controlled by intravenous immunoglubulin, alpha-interferon and acyclovir. Cardiac function during serial follow-up (range, 1 month to 5 years) revealed normal systolic and diastolic function and none received any anticongestive medications. Almost all patients received an oversized donor heart. The left ventricle (LV) mass was remodeled, initially as an decrease and later as an increase. The patient who underwent the Batista operation was discharged 1 month after the operation with an increased LV ejection fraction (from 10% to 22%). She was successfully bridged to heart transplantation 7 months after the Batista operation. The results of cardiac transplantation in growing children are satisfactory and remain the mainstay of surgical treatment for medically refractory heart failure in these patients. However, with a shortage of donor hearts, the Batista operation may be adopted as a bridge to heart transplant with a fair response.  (+info)

The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy. (5/98)

Stress-induced mitogen-activated protein kinase (MAP) p38 is activated in various forms of heart failure, yet its effects on the intact heart remain to be established. Targeted activation of p38 MAP kinase in ventricular myocytes was achieved in vivo by using a gene-switch transgenic strategy with activated mutants of upstream kinases MKK3bE and MKK6bE. Transgene expression resulted in significant induction of p38 kinase activity and premature death at 7-9 weeks. Both groups of transgenic hearts exhibited marked interstitial fibrosis and expression of fetal marker genes characteristic of cardiac failure, but no significant hypertrophy at the organ level. Echocardiographic and pressure-volume analyses revealed a similar extent of systolic contractile depression and restrictive diastolic abnormalities related to markedly increased passive chamber stiffness. However, MKK3bE-expressing hearts had increased end-systolic chamber volumes and a thinned ventricular wall, associated with heterogeneous myocyte atrophy, whereas MKK6bE hearts had reduced end-diastolic ventricular cavity size, a modest increase in myocyte size, and no significant myocyte atrophy. These data provide in vivo evidence for a negative inotropic and restrictive diastolic effect from p38 MAP kinase activation in ventricular myocytes and reveal specific roles of p38 pathway in the development of ventricular end-systolic remodeling.  (+info)

Epidemiology of idiopathic cardiomyopathy in Japan: results from a nationwide survey. (6/98)

OBJECTIVE: To estimate the total number of patients with idiopathic cardiomyopathy in Japan and the prevalence of the disorder. DESIGN: A nationwide epidemiological survey. SETTING: Hospitals selected randomly from among all hospitals in Japan. PATIENTS: Patients presenting with any of the three types of idiopathic cardiomyopathy: dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. MAIN OUTCOME MEASURES: The total number of patients in Japan was estimated using the sampling and response rates in each stratum with respect to hospital size. The second survey was conducted for patients reported in the first survey in order to obtain detailed information, including age, sex, and specific clinical data. RESULTS: Estimated patient totals and 95% confidence intervals (CI) were 17 700 (95% CI 16 500 to 18 800) for dilated cardiomyopathy, 21 900 (95% CI 20 600 to 23 200) for hypertrophic cardiomyopathy, and 300 (95% CI 250 to 350) for restrictive cardiomyopathy. Crude prevalence per 100 000 population was estimated as 14.0 for dilated cardiomyopathy, 17.3 for hypertrophic cardiomyopathy, and 0.2 for restrictive cardiomyopathy; crude incidence per 100 000 person-years was estimated as 3.58, 4.14, and 0.06, respectively. CONCLUSIONS: The total number and prevalence of patients with idiopathic cardiomyopathy in Japan are estimated for the first time in a nationwide survey. The prevalence of dilated cardiomyopathy in Japan appears to be about half that of Western populations, while that of hypertrophic cardiomyopathy is about the same.  (+info)

Molecular mechanisms of inherited cardiomyopathies. (7/98)

Cardiomyopathies are diseases of heart muscle that may result from a diverse array of conditions that damage the heart and other organs and impair myocardial function, including infection, ischemia, and toxins. However, they may also occur as primary diseases restricted to striated muscle. Over the past decade, the importance of inherited gene defects in the pathogenesis of primary cardiomyopathies has been recognized, with mutations in some 18 genes having been identified as causing hypertrophic cardiomyopathy (HCM) and/or dilated cardiomyopathy (DCM). Defining the role of these genes in cardiac function and the mechanisms by which mutations in these genes lead to hypertrophy, dilation, and contractile failure are major goals of ongoing research. Pathophysiological mechanisms that have been implicated in HCM and DCM include the following: defective force generation, due to mutations in sarcomeric protein genes; defective force transmission, due to mutations in cytoskeletal protein genes; myocardial energy deficits, due to mutations in ATP regulatory protein genes; and abnormal Ca2+ homeostasis, due to altered availability of Ca2+ and altered myofibrillar Ca2+ sensitivity. Improved understanding that will result from these studies should ultimately lead to new approaches for the diagnosis, prognostic stratification, and treatment of patients with heart failure.  (+info)

Idiopathic restrictive cardiomyopathy is part of the clinical expression of cardiac troponin I mutations. (8/98)

Restrictive cardiomyopathy (RCM) is an uncommon heart muscle disorder characterized by impaired filling of the ventricles with reduced volume in the presence of normal or near normal wall thickness and systolic function. The disease may be associated with systemic disease but is most often idiopathic. We recognized a large family in which individuals were affected by either idiopathic RCM or hypertrophic cardiomyopathy (HCM). Linkage analysis to selected sarcomeric contractile protein genes identified cardiac troponin I (TNNI3) as the likely disease gene. Subsequent mutation analysis revealed a novel missense mutation, which cosegregated with the disease in the family (lod score: 4.8). To determine if idiopathic RCM is part of the clinical expression of TNNI3 mutations, genetic investigations of the gene were performed in an additional nine unrelated RCM patients with restrictive filling patterns, bi-atrial dilatation, normal systolic function, and normal wall thickness. TNNI3 mutations were identified in six of these nine RCM patients. Two of the mutations identified in young individuals were de novo mutations. All mutations appeared in conserved and functionally important domains of the gene. This article was published online in advance of the print edition. The date of publication is available from the JCI website, http://www.jci.org.  (+info)

There are several possible causes of dilated cardiomyopathy, including:

1. Coronary artery disease: This is the most common cause of dilated cardiomyopathy, and it occurs when the coronary arteries become narrowed or blocked, leading to a decrease in blood flow to the heart muscle.
2. High blood pressure: Prolonged high blood pressure can cause the heart muscle to become weakened and enlarged.
3. Heart valve disease: Dysfunctional heart valves can lead to an increased workload on the heart, which can cause dilated cardiomyopathy.
4. Congenital heart defects: Some congenital heart defects can lead to an enlarged heart and dilated cardiomyopathy.
5. Alcohol abuse: Chronic alcohol abuse can damage the heart muscle and lead to dilated cardiomyopathy.
6. Viral infections: Some viral infections, such as myocarditis, can cause inflammation of the heart muscle and lead to dilated cardiomyopathy.
7. Genetic disorders: Certain genetic disorders, such as hypertrophic cardiomyopathy, can cause dilated cardiomyopathy.
8. Obesity: Obesity is a risk factor for developing dilated cardiomyopathy, particularly in younger people.
9. Diabetes: Diabetes can increase the risk of developing dilated cardiomyopathy, especially if left untreated or poorly controlled.
10. Age: Dilated cardiomyopathy is more common in older adults, with the majority of cases occurring in people over the age of 65.

It's important to note that many people with these risk factors will not develop dilated cardiomyopathy, and some people without any known risk factors can still develop the condition. If you suspect you or someone you know may have dilated cardiomyopathy, it's important to consult a healthcare professional for proper diagnosis and treatment.

The exact cause of HCM is not fully understood, but it is thought to be related to a combination of genetic and environmental factors. Some people with HCM have a family history of the condition, and it is also more common in certain populations such as athletes and individuals with a history of hypertension or diabetes.

Symptoms of HCM can vary from person to person and may include shortness of breath, fatigue, palpitations, and chest pain. In some cases, HCM may not cause any symptoms at all and may be detected only through a physical examination or diagnostic tests such as an echocardiogram or electrocardiogram (ECG).

Treatment for HCM typically focuses on managing symptoms and reducing the risk of complications. This may include medications to reduce blood pressure, control arrhythmias, or improve heart function, as well as lifestyle modifications such as regular exercise and a healthy diet. In some cases, surgery or other procedures may be necessary to treat HCM.

Prognosis for individuals with HCM varies depending on the severity of the condition and the presence of any complications. With appropriate treatment and management, many people with HCM can lead active and fulfilling lives, but it is important to receive regular monitoring and care from a healthcare provider to manage the condition effectively.

There are several types of cardiomyopathies, each with distinct characteristics and symptoms. Some of the most common forms of cardiomyopathy include:

1. Hypertrophic cardiomyopathy (HCM): This is the most common form of cardiomyopathy and is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle. HCM can lead to obstruction of the left ventricular outflow tract and can increase the risk of sudden death.
2. Dilated cardiomyopathy: This type of cardiomyopathy is characterized by a decrease in the heart's ability to pump blood effectively, leading to enlargement of the heart and potentially life-threatening complications such as congestive heart failure.
3. Restrictive cardiomyopathy: This type of cardiomyopathy is characterized by stiffness of the heart muscle, which makes it difficult for the heart to fill with blood. This can lead to shortness of breath and fatigue.
4. Left ventricular non-compaction (LVNC): This is a rare type of cardiomyopathy that occurs when the left ventricle does not properly compact, leading to reduced cardiac function and potentially life-threatening complications.
5. Cardiac amyloidosis: This is a condition in which abnormal proteins accumulate in the heart tissue, leading to stiffness and impaired cardiac function.
6. Right ventricular cardiomyopathy (RVCM): This type of cardiomyopathy is characterized by impaired function of the right ventricle, which can lead to complications such as pulmonary hypertension and heart failure.
7. Endocardial fibroelastoma: This is a rare type of cardiomyopathy that occurs when abnormal tissue grows on the inner lining of the heart, leading to reduced cardiac function and potentially life-threatening complications.
8. Cardiac sarcoidosis: This is a condition in which inflammatory cells accumulate in the heart, leading to impaired cardiac function and potentially life-threatening complications.
9. Hypertrophic cardiomyopathy (HCM): This is a condition in which the heart muscle thickens, leading to reduced cardiac function and potentially life-threatening complications such as arrhythmias and sudden death.
10. Hypokinetic left ventricular cardiomyopathy: This type of cardiomyopathy is characterized by decreased contraction of the left ventricle, leading to reduced cardiac function and potentially life-threatening complications such as heart failure.

It's important to note that some of these types of cardiomyopathy are more common in certain populations, such as hypertrophic cardiomyopathy being more common in young athletes. Additionally, some types of cardiomyopathy may have overlapping symptoms or co-occurring conditions, so it's important to work with a healthcare provider for an accurate diagnosis and appropriate treatment.

In this condition, the heart chambers become rigid and cannot expand and contract properly, which reduces the heart's ability to pump blood effectively. This can lead to a decrease in the amount of blood that reaches the body's tissues and organs, causing symptoms such as fatigue, shortness of breath, and swelling in the legs and feet.

There are several types of restrictive cardiomyopathy, including:

1. Idiopathic RCM: This type of RCM has no known cause.
2. Amyloidosis-related RCM: This type of RCM is caused by the buildup of abnormal proteins called amyloid in the heart tissue.
3. Hypertensive RCM: This type of RCM is caused by high blood pressure, which can damage the heart muscle and make it stiff.
4. Drug-induced RCM: This type of RCM is caused by certain medications that can damage the heart muscle.
5. Infiltrative RCM: This type of RCM is caused by the infiltration of the heart muscle by abnormal substances, such as inflammatory cells or tumors.

Treatment for restrictive cardiomyopathy usually involves managing symptoms and addressing any underlying causes, such as high blood pressure or amyloidosis. Medications may include diuretics to reduce fluid buildup, blood thinners to prevent clots, and medications to manage high blood pressure. In severe cases, a heart transplant may be necessary.

The symptoms of Takotsubo cardiomyopathy are similar to those of a heart attack and can include chest pain, shortness of breath, and irregular heartbeat. However, unlike a heart attack, there is no evidence of blockage in the coronary arteries. Instead, the heart muscle becomes stunned and weakened, leading to a decrease in cardiac function.

Takotsubo cardiomyopathy is often brought on by a surge of stress hormones, such as adrenaline and cortisol, which can cause changes in the heart's electrical activity and reduce blood flow to the muscle. The condition is more common in women than men and typically affects individuals between the ages of 58 and 75.

While Takotsubo cardiomyopathy is a serious condition, it is usually reversible with treatment and most patients recover completely within a few weeks. Treatment may include medications to manage symptoms such as high blood pressure and heart failure, as well as therapy to address the underlying stress or emotional trauma that triggered the condition.

In summary, Takotsubo cardiomyopathy is a rare but potentially life-threatening condition that is caused by extreme physical or emotional stress and can mimic the symptoms of a heart attack. It is important to be aware of this condition and seek medical attention immediately if symptoms persist or worsen over time.

HFCM is caused by mutations in genes that encode proteins involved in the structure and function of the heart muscle. These mutations can be inherited from one's parents or can occur spontaneously. The condition typically affects multiple members of a family, and the age of onset and severity of symptoms can vary widely.

HFCM is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as echocardiography, electrocardiography, and cardiac MRI. Treatment options for HFCM include medications to manage symptoms, lifestyle modifications such as regular exercise and a healthy diet, and in some cases, surgery or other procedures to repair or replace damaged heart tissue.

In summary, Cardiomyopathy, Hypertrophic, Familial (HFCM) is a genetic disorder that affects the heart muscle, leading to thickening of the heart muscle and potentially causing heart failure and other complications. It is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle, and can be inherited or caused by spontaneous mutations in genes that encode proteins involved in heart muscle structure and function.

Chagas cardiomyopathy is a type of heart disease that is caused by the parasitic infection Trypanosoma cruzi, which is transmitted through the feces of infected triatomine bugs. It is also known as American trypanosomiasis or Latin American trypanosomiasis.

The infection can cause inflammation and damage to the heart muscle, leading to cardiomyopathy, which is a condition where the heart muscle becomes weakened and cannot pump blood effectively. This can lead to symptoms such as shortness of breath, fatigue, swelling, and irregular heartbeat.

Chagas cardiomyopathy is most commonly found in countries in Central and South America, where the disease is transmitted by triatomine bugs that are found in rural areas. It is estimated that around 8 million people are infected with Chagas disease worldwide, with the majority of cases occurring in Latin America.

There is no cure for Chagas cardiomyopathy, but medications and other treatments can help manage symptoms and slow the progression of the disease. Prevention is key to avoiding Chagas cardiomyopathy, and this includes avoiding triatomine bug bites, using insecticides to kill bugs in homes, and screening blood donors for the disease.

Overall, Chagas cardiomyopathy is a serious and debilitating condition that can have significant implications for quality of life and survival. It is important to be aware of the risk of infection and take steps to prevent it, particularly if you live in or travel to areas where the disease is common.

The primary cause of alcoholic cardiomyopathy is the toxic effects of alcohol on the heart muscle cells, leading to inflammation and scarring. The condition can also be associated with other factors such as malnutrition, vitamin deficiencies, and increased blood pressure.

The symptoms of alcoholic cardiomyopathy may include shortness of breath, fatigue, swelling in the legs and ankles, and irregular heartbeat. Diagnosis is typically made through a combination of physical examination, medical history, electrocardiogram (ECG), echocardiogram, and blood tests.

Treatment for alcoholic cardiomyopathy usually involves abstaining from alcohol and managing underlying conditions such as high blood pressure and diabetes. In severe cases, medications such as beta blockers, diuretics, and ace inhibitors may be prescribed to manage symptoms and slow the progression of the disease. Surgery or implantation of a pacemaker or an implantable cardioverter-defibrillator (ICD) may also be necessary in some cases.

Prognosis for alcoholic cardiomyopathy is generally poor, with a high risk of complications such as heart failure, arrhythmias, and death. However, early diagnosis and cessation of alcohol consumption can improve outcomes.

In summary, alcoholic cardiomyopathy is a condition where the heart muscle becomes weakened and enlarged due to excessive alcohol consumption over a long period of time. It can lead to a range of symptoms including shortness of breath, fatigue, and irregular heartbeat, and treatment typically involves abstaining from alcohol and managing underlying conditions. Prognosis is generally poor, but early diagnosis and cessation of alcohol consumption can improve outcomes.

Symptoms of ARVD can include palpitations, shortness of breath, and fatigue, and may be accompanied by chest pain or pressure. Diagnosis is typically made through a combination of physical examination, electrocardiogram (ECG), echocardiogram, and cardiac MRI.

Treatment for ARVD is often focused on managing symptoms and preventing complications, and may include medications to control arrhythmias, implantable devices such as pacemakers or defibrillators, and in severe cases, heart transplantation. Prevention of sudden cardiac death is a critical aspect of management, and individuals with ARVD are often advised to avoid intense physical activity and take precautions to prevent injuries or trauma to the heart.

ARVD is a rare condition, affecting approximately 1 in 100,000 individuals worldwide. It can occur in individuals of all ages, but is most commonly diagnosed in young adults and children. While there is currently no cure for ARVD, advances in diagnostic techniques and treatment options have improved outcomes for individuals with this condition.

Types of Diabetic Cardiomyopathies:

1. Diabetic cardiomyopathy: This is the most common type of diabetic cardiomyopathy and is characterized by fibrosis, hypertrophy, and left ventricular dysfunction.
2. Diabetic cardiac syndrome: This condition is characterized by a combination of myocardial stunning, fibrosis, and systolic dysfunction.
3. Diabetic myocarditis: This is an inflammatory condition that affects the heart muscle and can lead to scarring and dysfunction.
4. Diabetic cardiac arrest: This is a rare but life-threatening complication of diabetes that occurs when the heart stops functioning due to severe coronary artery disease or other factors.

Causes and Risk Factors:

1. Hyperglycemia: Elevated blood sugar levels can damage the cardiovascular system, including the heart muscle.
2. Hypertension: High blood pressure can increase the risk of cardiac complications in individuals with diabetes.
3. Dyslipidemia: Abnormal lipid levels, such as high triglycerides and low HDL cholesterol, can contribute to the development of cardiovascular disease.
4. Smoking: Smoking is a significant risk factor for cardiovascular disease in individuals with diabetes.
5. Obesity: Excess weight can increase the risk of cardiovascular disease and worsen glycemic control.
6. Family history: A family history of cardiovascular disease increases the risk of developing diabetic cardiomyopathy.

Symptoms:

1. Chest pain or angina
2. Shortness of breath
3. Fatigue
4. Swelling of the legs and feet
5. Palpitations
6. Dizziness and lightheadedness

Diagnosis:

1. Physical examination
2. Electrocardiogram (ECG)
3. Echocardiography
4. Stress test
5. Blood tests to assess lipid levels, blood sugar, and kidney function

Treatment and Management:

1. Medications: ACE inhibitors or beta-blockers may be prescribed to manage hypertension and angina. Statins may be used to lower cholesterol levels.
2. Lifestyle modifications: Smoking cessation, weight loss, and regular exercise can help improve glycemic control and cardiovascular health.
3. Dietary changes: A healthy, balanced diet low in saturated fats, added sugars, and refined carbohydrates can help manage blood sugar levels and improve overall health.
4. Monitoring: Regular monitoring of blood sugar levels, blood pressure, and lipid profiles is essential to prevent complications and manage the condition effectively.
5. Surgical intervention: In severe cases, bariatric surgery may be considered to help achieve significant weight loss and improve glycemic control.

Prognosis:
The prognosis for patients with metabolic syndrome is generally good if the condition is identified early and managed effectively. However, untreated or poorly managed metabolic syndrome can increase the risk of developing serious health complications such as heart disease, stroke, and type 2 diabetes.

Complications:

1. Heart disease: The increased risk of heart disease is due to high blood pressure, high cholesterol levels, and obesity, which can lead to atherosclerosis (hardening of the arteries) and coronary artery disease.
2. Stroke: The risk of stroke is increased due to high blood pressure, diabetes, and obesity, which can damage the blood vessels in the brain and cause a stroke.
3. Type 2 diabetes: Metabolic syndrome increases the risk of developing type 2 diabetes due to insulin resistance and impaired glucose tolerance.
4. Other health complications: Other potential complications of metabolic syndrome include non-alcoholic fatty liver disease, sleep apnea, and osteoarthritis.

Preventive Measures:

1. Healthy diet: Eating a healthy, balanced diet that is low in saturated fats, added sugars, and refined carbohydrates can help prevent or manage metabolic syndrome.
2. Regular exercise: Engaging in regular physical activity can improve insulin sensitivity, reduce inflammation, and promote weight loss.
3. Weight management: Maintaining a healthy weight through diet and exercise can help prevent or manage metabolic syndrome.
4. Stress management: Chronic stress can contribute to the development of metabolic syndrome by promoting inflammation and decreasing insulin sensitivity. Engaging in stress-reducing activities such as yoga, meditation, or deep breathing exercises may be helpful.
5. Sleep hygiene: Getting adequate sleep is essential for maintaining metabolic health. Aim for 7-8 hours of sleep per night and practice good sleep hygiene by avoiding caffeine and electronic screens before bedtime.
6. Limit alcohol intake: Drinking too much alcohol can contribute to the development of metabolic syndrome by promoting inflammation, increasing triglycerides, and decreasing HDL cholesterol.
7. Quit smoking: Smoking is a significant risk factor for developing metabolic syndrome, as it promotes inflammation, decreases insulin sensitivity, and increases cardiovascular disease risk.
8. Monitoring and treatment of underlying conditions: If you have underlying conditions such as hypertension, high cholesterol, or diabetes, it is essential to monitor and manage them effectively to prevent the development of metabolic syndrome.

In conclusion, metabolic syndrome is a cluster of conditions that increase the risk of developing type 2 diabetes and cardiovascular disease. It is essential to be aware of the risk factors, symptoms, and complications of metabolic syndrome and take preventive measures to manage and prevent it. By making healthy lifestyle choices, such as following a balanced diet, exercising regularly, maintaining a healthy weight, and managing underlying conditions, you can reduce your risk of developing metabolic syndrome and improve your overall health.

The symptoms of myocarditis can vary depending on the severity of the inflammation and the location of the affected areas of the heart muscle. Common symptoms include chest pain, shortness of breath, fatigue, and swelling in the legs and feet.

Myocarditis can be difficult to diagnose, as its symptoms are similar to those of other conditions such as coronary artery disease or heart failure. Diagnosis is typically made through a combination of physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, and blood tests.

Treatment of myocarditis depends on the underlying cause and severity of the condition. Mild cases may require only rest and over-the-counter pain medication, while more severe cases may require hospitalization and intravenous medications to manage inflammation and cardiac function. In some cases, surgery may be necessary to repair or replace damaged heart tissue.

Prevention of myocarditis is important, as it can lead to serious complications such as heart failure and arrhythmias if left untreated. Prevention strategies include avoiding exposure to viruses and other infections, managing underlying medical conditions such as diabetes and high blood pressure, and getting regular check-ups with a healthcare provider to monitor cardiac function.

In summary, myocarditis is an inflammatory condition that affects the heart muscle, causing symptoms such as chest pain, shortness of breath, and fatigue. Diagnosis can be challenging, but treatment options range from rest and medication to hospitalization and surgery. Prevention is key to avoiding serious complications and maintaining good cardiac health.

There are several potential causes of LVD, including:

1. Coronary artery disease: The buildup of plaque in the coronary arteries can lead to a heart attack, which can damage the left ventricle and impair its ability to function properly.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can lead to LVD.
3. Cardiomyopathy: This is a condition where the heart muscle becomes weakened or enlarged, leading to impaired function of the left ventricle.
4. Heart valve disease: Problems with the heart valves can disrupt the normal flow of blood and cause LVD.
5. Hypertension: High blood pressure can cause damage to the heart muscle and lead to LVD.
6. Genetic factors: Some people may be born with genetic mutations that predispose them to developing LVD.
7. Viral infections: Certain viral infections, such as myocarditis, can inflame and damage the heart muscle, leading to LVD.
8. Alcohol or drug abuse: Substance abuse can damage the heart muscle and lead to LVD.
9. Nutritional deficiencies: A diet lacking essential nutrients can lead to damage to the heart muscle and increase the risk of LVD.

Diagnosis of LVD typically involves a physical exam, medical history, and results of diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and stress tests. Treatment options for LVD depend on the underlying cause, but may include medications to improve cardiac function, lifestyle changes, and in severe cases, surgery or other procedures.

Preventing LVD involves taking steps to maintain a healthy heart and reducing risk factors such as high blood pressure, smoking, and obesity. This can be achieved through a balanced diet, regular exercise, stress management, and avoiding substance abuse. Early detection and treatment of underlying conditions that increase the risk of LVD can also help prevent the condition from developing.

There are two main types of heart failure:

1. Left-sided heart failure: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the lungs and other organs.
2. Right-sided heart failure: This occurs when the right ventricle, which pumps blood to the lungs, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the body's tissues and organs.

Symptoms of heart failure may include:

* Shortness of breath
* Fatigue
* Swelling in the legs, ankles, and feet
* Swelling in the abdomen
* Weight gain
* Coughing up pink, frothy fluid
* Rapid or irregular heartbeat
* Dizziness or lightheadedness

Treatment for heart failure typically involves a combination of medications and lifestyle changes. Medications may include diuretics to remove excess fluid from the body, ACE inhibitors or beta blockers to reduce blood pressure and improve blood flow, and aldosterone antagonists to reduce the amount of fluid in the body. Lifestyle changes may include a healthy diet, regular exercise, and stress reduction techniques. In severe cases, heart failure may require hospitalization or implantation of a device such as an implantable cardioverter-defibrillator (ICD) or a left ventricular assist device (LVAD).

It is important to note that heart failure is a chronic condition, and it requires ongoing management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle changes, many people with heart failure are able to manage their symptoms and lead active lives.

The symptoms of VOO may include shortness of breath, fatigue, swelling in the legs and abdomen, and chest pain. If left untreated, VOO can lead to heart failure, arrhythmias, and even death.

Diagnosis of VOO is typically made through a combination of physical examination, electrocardiogram (ECG), echocardiogram, and cardiac catheterization. Treatment options for VOO depend on the underlying cause and may include medications, lifestyle changes, or surgical procedures such as coronary angioplasty or heart transplantation.

In summary, ventricular outflow obstruction is a serious medical condition that can lead to severe consequences if left untreated. Early diagnosis and appropriate treatment are essential to prevent complications and improve outcomes for patients with VOO.

Some examples of the use of 'Death, Sudden, Cardiac' in medical contexts include:

1. Sudden cardiac death (SCD) is a major public health concern, affecting thousands of people each year in the United States alone. It is often caused by inherited heart conditions, such as hypertrophic cardiomyopathy or long QT syndrome.
2. The risk of sudden cardiac death is higher for individuals with a family history of heart disease or other pre-existing cardiovascular conditions.
3. Sudden cardiac death can be prevented by prompt recognition and treatment of underlying heart conditions, as well as by avoiding certain risk factors such as smoking, physical inactivity, and an unhealthy diet.
4. Cardiopulmonary resuscitation (CPR) and automated external defibrillators (AEDs) can be effective in restoring a normal heart rhythm during sudden cardiac death, especially when used promptly after the onset of symptoms.

Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.

There are many different types of fibrosis, including:

* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.

Fibrosis can be diagnosed through a variety of methods, including:

* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.

There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:

* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.

It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.

Tachycardia, ventricular can be classified into several types based on its duration and the presence of other symptoms. These include:

1. Paroxysmal ventricular tachycardia (PVT): This is a rapid heart rate that occurs in episodes lasting less than 30 seconds and may be accompanied by palpitations, shortness of breath, or dizziness.
2. Sustained ventricular tachycardia: This is a rapid heart rate that persists for more than 30 seconds and may require medical intervention to return the heart to normal rhythm.
3. Ventricular fibrillation (VF): This is a life-threatening condition in which the ventricles are unable to pump blood effectively due to rapid, disorganized electrical activity.

Symptoms of tachycardia, ventricular may include:

* Palpitations or rapid heartbeat
* Shortness of breath
* Dizziness or lightheadedness
* Chest pain or discomfort
* Fatigue or weakness

Diagnosis of tachycardia, ventricular is typically made based on a physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, or stress test. Treatment options may include medications to regulate heart rhythm, cardioversion to restore normal heart rhythm, and in some cases, implantation of a cardioverter-defibrillator (ICD) to prevent sudden death.

In summary, tachycardia, ventricular is a rapid heart rate that originates in the ventricles and can be caused by a variety of conditions. It is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, it is possible to manage the condition and improve quality of life.

The exact cause of endomyocardial fibrosis is not known, but it is believed to be related to inflammation and scarring within the heart. The condition is more common in men than women, and typically affects people between the ages of 20 and 50. Symptoms of endomyocardial fibrosis can include shortness of breath, fatigue, swelling in the legs and feet, and chest pain.

There is no cure for endomyocardial fibrosis, but treatment options may include medications to manage symptoms, surgery to repair or replace damaged heart tissue, and lifestyle changes such as a healthy diet and regular exercise. In severe cases, heart transplantation may be necessary. Early diagnosis and treatment can help slow the progression of the condition and improve quality of life for those affected.

Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.

There are several types of myocardial ischemia, including:

1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.

Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.

LVH can lead to a number of complications, including:

1. Heart failure: The enlarged left ventricle can become less efficient at pumping blood throughout the body, leading to heart failure.
2. Arrhythmias: The abnormal electrical activity in the heart can lead to irregular heart rhythms.
3. Sudden cardiac death: In some cases, LVH can increase the risk of sudden cardiac death.
4. Atrial fibrillation: The enlarged left atrium can lead to atrial fibrillation, a common type of arrhythmia.
5. Mitral regurgitation: The enlargement of the left ventricle can cause the mitral valve to become incompetent, leading to mitral regurgitation.
6. Heart valve problems: The enlarged left ventricle can lead to heart valve problems, such as mitral regurgitation or aortic stenosis.
7. Coronary artery disease: LVH can increase the risk of coronary artery disease, which can lead to a heart attack.
8. Pulmonary hypertension: The enlarged left ventricle can lead to pulmonary hypertension, which can further strain the heart and increase the risk of complications.

Evaluation of LVH typically involves a physical examination, medical history, electrocardiogram (ECG), echocardiography, and other diagnostic tests such as stress test or cardiac MRI. Treatment options for LVH depend on the underlying cause and may include medications, lifestyle changes, and in some cases, surgery or other interventions.

There are many different types of cardiac arrhythmias, including:

1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.

Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.

During ventricular remodeling, the heart muscle becomes thicker and less flexible, leading to a decrease in the heart's ability to fill with blood and pump it out to the body. This can lead to shortness of breath, fatigue, and swelling in the legs and feet.

Ventricular remodeling is a natural response to injury, but it can also be exacerbated by factors such as high blood pressure, diabetes, and obesity. Treatment for ventricular remodeling typically involves medications and lifestyle changes, such as exercise and a healthy diet, to help manage symptoms and slow the progression of the condition. In some cases, surgery or other procedures may be necessary to repair or replace damaged heart tissue.

The process of ventricular remodeling is complex and involves multiple cellular and molecular mechanisms. It is thought to be driven by a variety of factors, including changes in gene expression, inflammation, and the activity of various signaling pathways.

Overall, ventricular remodeling is an important condition that can have significant consequences for patients with heart disease. Understanding its causes and mechanisms is crucial for developing effective treatments and improving outcomes for those affected by this condition.

There are many different types of heart diseases, including:

1. Coronary artery disease: The buildup of plaque in the coronary arteries, which supply blood to the heart muscle, leading to chest pain or a heart attack.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, leading to fatigue, shortness of breath, and swelling in the legs.
3. Arrhythmias: Abnormal heart rhythms, such as atrial fibrillation or ventricular tachycardia, which can cause palpitations, dizziness, and shortness of breath.
4. Heart valve disease: Problems with the heart valves, which can lead to blood leaking back into the chambers or not being pumped effectively.
5. Cardiomyopathy: Disease of the heart muscle, which can lead to weakened heart function and heart failure.
6. Heart murmurs: Abnormal sounds heard during a heartbeat, which can be caused by defects in the heart valves or abnormal blood flow.
7. Congenital heart disease: Heart defects present at birth, such as holes in the heart or abnormal blood vessels.
8. Myocardial infarction (heart attack): Damage to the heart muscle due to a lack of oxygen, often caused by a blockage in a coronary artery.
9. Cardiac tamponade: Fluid accumulation around the heart, which can cause compression of the heart and lead to cardiac arrest.
10. Endocarditis: Infection of the inner lining of the heart, which can cause fever, fatigue, and heart valve damage.

Heart diseases can be diagnosed through various tests such as electrocardiogram (ECG), echocardiogram, stress test, and blood tests. Treatment options depend on the specific condition and may include lifestyle changes, medication, surgery, or a combination of these.

Some common puerperal disorders include:

1. Puerperal fever: This is a bacterial infection that can occur during the postpartum period, usually caused by Streptococcus or Staphylococcus bacteria. Symptoms include fever, chills, and abdominal pain.
2. Postpartum endometritis: This is an inflammation of the lining of the uterus that can occur after childbirth, often caused by bacterial infection. Symptoms include fever, abdominal pain, and vaginal discharge.
3. Postpartum bleeding: This is excessive bleeding that can occur during the postpartum period, often caused by tears or lacerations to the uterus or cervix during childbirth.
4. Breast engorgement: This is a common condition that occurs when the breasts become full and painful due to milk production.
5. Mastitis: This is an inflammation of the breast tissue that can occur during breastfeeding, often caused by bacterial infection. Symptoms include redness, swelling, and warmth in the breast.
6. Postpartum depression: This is a mood disorder that can occur after childbirth, characterized by feelings of sadness, anxiety, and hopelessness.
7. Postpartum anxiety: This is an anxiety disorder that can occur after childbirth, characterized by excessive worry, fear, and anxiety.
8. Urinary incontinence: This is the loss of bladder control during the postpartum period, often caused by weakened pelvic muscles.
9. Constipation: This is a common condition that can occur after childbirth, often caused by hormonal changes and decreased bowel motility.
10. Breastfeeding difficulties: These can include difficulty latching, painful feeding, and low milk supply.

It's important to note that not all women will experience these complications, and some may have different symptoms or none at all. Additionally, some complications may require medical attention, while others may be managed with self-care measures or support from a healthcare provider. It's important for new mothers to seek medical advice if they have any concerns about their physical or emotional well-being during the postpartum period.

Medical Term: Cardiomegaly

Definition: An abnormal enlargement of the heart.

Symptoms: Difficulty breathing, shortness of breath, fatigue, swelling of legs and feet, chest pain, and palpitations.

Causes: Hypertension, cardiac valve disease, myocardial infarction (heart attack), congenital heart defects, and other conditions that affect the heart muscle or cardiovascular system.

Diagnosis: Physical examination, electrocardiogram (ECG), chest x-ray, echocardiography, and other diagnostic tests as necessary.

Treatment: Medications such as diuretics, vasodilators, and beta blockers, lifestyle changes such as exercise and diet modifications, surgery or other interventions in severe cases.

Note: Cardiomegaly is a serious medical condition that requires prompt diagnosis and treatment to prevent complications such as heart failure and death. If you suspect you or someone else may have cardiomegaly, seek medical attention immediately.

www.medicinenet.com/sudden_death/article.htm
Sudden death is death that occurs unexpectedly and without warning, often due to a cardiac arrest or other underlying medical condition.

In the medical field, sudden death is defined as death that occurs within one hour of the onset of symptoms, with no prior knowledge of any serious medical condition. It is often caused by a cardiac arrhythmia, such as ventricular fibrillation or tachycardia, which can lead to cardiac arrest and sudden death if not treated promptly.

Other possible causes of sudden death include:

1. Heart disease: Coronary artery disease, heart failure, and other heart conditions can increase the risk of sudden death.
2. Stroke: A stroke can cause sudden death by disrupting blood flow to the brain or other vital organs.
3. Pulmonary embolism: A blood clot in the lungs can block blood flow and cause sudden death.
4. Trauma: Sudden death can occur as a result of injuries sustained in an accident or other traumatic event.
5. Drug overdose: Taking too much of certain medications or drugs can cause sudden death due to cardiac arrest or respiratory failure.
6. Infections: Sepsis, meningitis, and other severe infections can lead to sudden death if left untreated.
7. Genetic conditions: Certain inherited disorders, such as Long QT syndrome, can increase the risk of sudden death due to cardiac arrhythmias.

The diagnosis of sudden death often requires an autopsy and a thorough investigation into the individual's medical history and circumstances surrounding their death. Treatment and prevention strategies may include defibrillation, CPR, medications to regulate heart rhythm, and lifestyle modifications to reduce risk factors such as obesity, smoking, and high blood pressure.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

The symptoms of glycogen storage disease type IIb usually become apparent in early childhood and may include:

* Delayed development of motor skills, such as sitting, standing, and walking
* Muscle weakness and wasting
* Fatigue and lethargy
* Easy bruising and bleeding due to low levels of platelets
* Enlargement of the liver and spleen
* Increased risk of infections due to a weakened immune system
* Coarsening of facial features, such as a prominent jaw and widely spaced eyes

If left untreated, glycogen storage disease type IIb can lead to serious complications, including liver failure, heart problems, and an increased risk of liver cancer. Treatment for the condition typically involves a combination of dietary modifications and enzyme replacement therapy (ERT) with GAA, which can help manage the symptoms and slow the progression of the disease. In some cases, a liver transplant may be necessary to treat advanced liver disease.

Preventing the onset of glycogen storage disease type IIb is not currently possible, as it is caused by genetic mutations that are inherited from one's parents. However, with early diagnosis and appropriate treatment, individuals with the condition can lead relatively healthy lives and manage their symptoms effectively. It is important for individuals with glycogen storage disease type IIb to work closely with their healthcare team to monitor their condition and adjust their treatment plan as needed.

INCVM can occur as an isolated defect or in combination with other congenital heart defects. The symptoms may vary depending on the severity of the condition, but they usually include difficulty breathing, fatigue, and shortness of breath during exercise. INVCM can be diagnosed using various imaging techniques such as echocardiography, cardiac MRI, or cardiac catheterization.

Treatment options for INVCM vary depending on the severity of the condition and may include medications to manage symptoms, surgery to repair or replace damaged heart tissue, or implantation of a pacemaker or defibrillator to regulate heart rhythms. In some cases, INCVM may be treated with cardiac resynchronization therapy (CRT) or cardiac contractility modulation (CCM) to improve the heart's pumping function.

INVCM is a rare condition, and its prevalence is not well established. However, it is believed to affect approximately 1 in 100,000 to 1 in 200,000 individuals worldwide. INVCM can occur in people of all ages but is more commonly diagnosed in infants and children. With appropriate treatment, many individuals with INVCM can lead active and fulfilling lives.

Note: This definition is based on the current medical knowledge and may change as new research and discoveries are made.

There are several types of ventricular dysfunction, including:

1. Left ventricular dysfunction: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened or impaired. This can lead to reduced cardiac output and can increase the risk of heart failure.
2. Right ventricular dysfunction: This occurs when the right ventricle, which pumps blood into the lungs, becomes weakened or impaired. This can lead to pulmonary hypertension and other complications.
3. Biventricular dysfunction: This occurs when both the left and right ventricles become weakened or impaired. This can lead to severe cardiac impairment and increased risk of heart failure.

Ventricular dysfunction can be diagnosed through a variety of tests, including echocardiography, stress testing, and cardiac magnetic resonance imaging (MRI). Treatment options depend on the underlying cause of the dysfunction and may include medications, lifestyle changes, or surgical interventions. In some cases, implantable devices such as pacemakers or defibrillators may be recommended to help regulate the heart rhythm and improve function.

The mitral valve is located between the left atrium and the left ventricle, and it is responsible for regulating blood flow between these two chambers. When the mitral valve does not close properly, blood can leak back into the left atrium, causing a range of symptoms and complications.

There are several causes of mitral valve insufficiency, including:

* Degenerative changes: The mitral valve can wear out over time due to degenerative changes, such as calcium buildup or tearing of the valve flaps.
* Heart muscle disease: Diseases such as cardiomyopathy can cause the heart muscle to weaken and stretch, leading to mitral valve insufficiency.
* Endocarditis: Infections of the inner lining of the heart can damage the mitral valve and lead to insufficiency.
* Heart defects: Congenital heart defects, such as a bicuspid valve or a narrow valve opening, can lead to mitral valve insufficiency.

Treatment for mitral valve insufficiency depends on the severity of the condition and may include medications to manage symptoms, lifestyle changes, or surgery to repair or replace the damaged valve. In some cases, catheter-based procedures may be used to repair the valve without open-heart surgery.

Overall, mitral valve insufficiency is a common condition that can have a significant impact on quality of life if left untreated. It is important to seek medical attention if symptoms persist or worsen over time.

There are several types of heart block, including:

1. First-degree heart block: This is the mildest form of heart block, where the electrical signals are delayed slightly but still reach the ventricles.
2. Second-degree heart block: In this type, some of the electrical signals may be blocked or delayed, causing the heart to beat irregularly.
3. Third-degree heart block: This is the most severe form of heart block, where all electrical signals are completely blocked, resulting in a complete halt of the heart's normal rhythm.

Heart block can be caused by a variety of factors, including:

1. Coronary artery disease: A buildup of plaque in the coronary arteries can lead to a blockage that affects the electrical signals to the heart.
2. Heart attack: Damage to the heart muscle can cause scarring and disrupt the electrical signals.
3. Cardiomyopathy: Disease of the heart muscle can lead to heart block.
4. Heart valve problems: Dysfunctional heart valves can interfere with the electrical signals to the heart.
5. Electrolyte imbalances: Abnormal levels of potassium, magnesium, or other electrolytes can affect the heart's electrical activity.
6. Medications: Certain drugs, such as beta-blockers and calcium channel blockers, can slow down the heart's electrical signals.
7. Infections: Viral or bacterial infections can damage the heart and disrupt its electrical signals.
8. Genetic conditions: Certain inherited conditions, such as long QT syndrome, can affect the heart's electrical activity.
9. Autoimmune disorders: Conditions such as rheumatoid arthritis or lupus can damage the heart and disrupt its electrical signals.

Symptoms of heart block may include:

1. Slow or irregular heartbeat
2. Palpitations
3. Fatigue
4. Shortness of breath
5. Dizziness or lightheadedness
6. Chest pain or discomfort
7. Pain or discomfort in the arms, back, or jaw

Diagnosis of heart block is typically made with an electrocardiogram (ECG), which measures the electrical activity of the heart. Other tests that may be used to diagnose heart block include:

1. Echocardiography: An ultrasound test that uses sound waves to create images of the heart.
2. Stress test: A test that measures the heart's activity during exercise or other forms of physical stress.
3. Holter monitor: A portable device that records the heart's activity over a 24-hour period.
4. Event monitor: A portable device that records the heart's activity over a longer period of time, typically 1-2 weeks.

Treatment for heart block depends on the severity of the condition and may include:

1. Medications: Drugs such as beta blockers or pacemakers may be used to regulate the heart's rhythm and rate.
2. Pacemaker: A small device that is implanted in the chest to help regulate the heart's rhythm.
3. Cardiac resynchronization therapy (CRT): A procedure that involves implanting a device that helps both ventricles of the heart beat together, improving the heart's pumping function.
4. Implantable cardioverter-defibrillator (ICD): A device that is implanted in the chest to monitor the heart's rhythm and deliver an electric shock if it detects a potentially life-threatening arrhythmia.

In conclusion, heart block is a serious condition that can disrupt the normal functioning of the heart. It is important to be aware of the risk factors and symptoms of heart block, and to seek medical attention immediately if they occur. With proper diagnosis and treatment, it is possible to manage heart block and improve the quality of life for those affected by the condition.

The symptoms of DMD typically become apparent in early childhood and progress rapidly. They include:

* Delayed motor development
* Weakness and wasting of muscles, particularly in the legs and pelvis
* Muscle weakness that worsens over time
* Loss of muscle mass and fatigue
* Difficulty walking, running, or standing
* Heart problems, such as cardiomyopathy and arrhythmias
* Respiratory difficulties, such as breathing problems and pneumonia

DMD is diagnosed through a combination of clinical evaluation, muscle biopsy, and genetic testing. Treatment options are limited and focus on managing symptoms and improving quality of life. These may include:

* Physical therapy to maintain muscle strength and function
* Medications to manage pain, spasms, and other symptoms
* Assistive devices, such as braces and wheelchairs, to improve mobility and independence
* Respiratory support, such as ventilation assistance, to manage breathing difficulties

The progression of DMD is highly variable, with some individuals experiencing a more rapid decline in muscle function than others. The average life expectancy for individuals with DMD is approximately 25-30 years, although some may live into their 40s or 50s with appropriate medical care and support.

Duchenne muscular dystrophy is a devastating and debilitating condition that affects thousands of individuals worldwide. While there is currently no cure for the disorder, ongoing research and advancements in gene therapy and other treatments offer hope for improving the lives of those affected by DMD.

Some common causes of syncope include:

1. Vasovagal response: This is the most common cause of syncope and is triggered by a sudden drop in blood pressure, usually due to sight of blood or injury.
2. Cardiac arrhythmias: Abnormal heart rhythms can lead to a decrease in blood flow to the brain, causing syncope.
3. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, syncope can occur.
4. Anemia: A low red blood cell count can cause decreased oxygen delivery to the brain, leading to syncope.
5. Dehydration: Lack of fluids and electrolytes can lead to a decrease in blood pressure, causing syncope.
6. Medication side effects: Certain medications can cause syncope as a side effect, such as vasodilators and beta-blockers.
7. Neurological disorders: Syncope can be a symptom of neurological conditions such as seizures, migraines, and stroke.
8. Psychological factors: Stress, anxiety, and panic attacks can also cause syncope.

Diagnosis of syncope is based on a thorough medical history and physical examination, as well as diagnostic tests such as electrocardiogram (ECG), echocardiogram, and blood tests. Treatment of syncope depends on the underlying cause and may include lifestyle modifications, medication, and in some cases, surgical intervention.

In summary, syncope is a symptom of a wide range of medical conditions that can be caused by cardiovascular, neurological, and psychological factors. A thorough diagnosis and appropriate treatment are necessary to determine the underlying cause and prevent complications.

Synonyms: RV dysfunction

See also: Left Ventricular Dysfunction, Cardiac Dysfunction, Heart Failure

Note: This term is not a formal medical diagnosis but rather a descriptive term used to indicate the specific location of cardiac dysfunction. A more comprehensive diagnosis would require further evaluation and testing by a healthcare provider.

There are three main types of bundle branch blocks:

1. Right bundle branch block (RBBB): This occurs when the electrical conduction bundle that carries the heart's rhythm from the right atrium to the right ventricle is damaged or diseased.
2. Left bundle branch block (LBBB): This occurs when the electrical conduction bundle that carries the heart's rhythm from the left atrium to the left ventricle is damaged or diseased.
3. Bifascicular bundle branch block: This occurs when two of the electrical conduction bundles are damaged or diseased.

Symptoms of bundle branch block may include:

* Heart palpitations
* Slow or irregular heartbeat
* Shortness of breath
* Fatigue
* Dizziness or lightheadedness
* Chest pain or discomfort

Diagnosis of bundle branch block is typically made using an electrocardiogram (ECG) test, which measures the electrical activity of the heart. Treatment options for BBB may include medications to regulate the heartbeat, cardiac resynchronization therapy (CRT) to help both ventricles beat together, or implantable cardioverter-defibrillator (ICD) to prevent life-threatening arrhythmias. In some cases, surgery may be necessary to repair or replace damaged heart tissue.

It is important to note that bundle branch block can increase the risk of developing other cardiac conditions such as heart failure, atrial fibrillation, and ventricular tachycardia. Therefore, it is essential for individuals with BBB to work closely with their healthcare provider to manage their condition and reduce the risk of complications.

There are several types of tachycardia, including:

1. Sinus tachycardia: This is the most common type and is caused by an increase in the rate of the normal sinus node. It is often seen in response to physical activity or stress.
2. Atrial fibrillation: This is a type of arrhythmia where the heart's upper chambers (atria) contract irregularly and rapidly, leading to a rapid heart rate.
3. Ventricular tachycardia: This is a type of arrhythmia where the heart's lower chambers (ventricles) contract rapidly, often with a rate above 100 bpm.
4. Premature ventricular contractions (PVCs): These are early or extra beats that originate in the ventricles, causing a rapid heart rate.

Tachycardia can cause a range of symptoms, including palpitations, shortness of breath, chest pain, and dizziness. In severe cases, it can lead to cardiac arrhythmias, heart failure, and even death.

Diagnosis of tachycardia typically involves a physical examination, electrocardiogram (ECG), and other tests such as stress tests or echocardiography. Treatment options vary depending on the underlying cause, but may include medications to regulate the heart rate, cardioversion to restore a normal heart rhythm, or in severe cases, implantation of a pacemaker or defibrillator.

Coxsackievirus infections are a group of viral diseases caused by enteroviruses, primarily Coxsackie A and B viruses. These infections can affect various parts of the body, including the gastrointestinal tract, skin, and nervous system.

Types of Coxsackievirus Infections:

1. Hand, Foot, and Mouth Disease (HFMD): This is a common viral illness that affects children under the age of 10, causing fever, mouth sores, and a rash with blisters on the hands and feet.
2. Herpangina: A severe form of HFMD characterized by small ulcers in the mouth and throat.
3. Aseptic Meningitis: An inflammation of the meninges (protective membranes) around the brain and spinal cord, often caused by Coxsackievirus B.
4. Myocarditis: Inflammation of the heart muscle caused by Coxsackievirus B.
5. Pericarditis: Inflammation of the membrane surrounding the heart (pericardium) caused by Coxsackievirus B.
6. Pleurodynia (also known as Coxsackievirus pleurisy): A sudden onset of chest pain, fever, and cough caused by Coxsackievirus A.
7. Meningoradiculitis: Inflammation of the meninges and spinal nerves caused by Coxsackievirus B.

Symptoms of Coxsackievirus Infections:

The symptoms of coxsackievirus infections can vary depending on the type of infection and the individual affected. Common symptoms include:

* Fever
* Headache
* Muscle pain
* Sore throat
* Mouth sores (in HFMD)
* Rash (in HFMD)
* Blisters (in HFMD)
* Seizures (in severe cases)
* Meningitis (inflammation of the membranes surrounding the brain and spinal cord)
* Encephalitis (inflammation of the brain)
* Myocarditis (inflammation of the heart muscle)
* Pericarditis (inflammation of the membrane surrounding the heart)
* Pleurodynia (chest pain, fever, and cough)
* Meningoradiculitis (inflammation of the meninges and spinal nerves)

Diagnosis of Coxsackievirus Infections:

The diagnosis of coxsackievirus infections is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include:

* Blood tests to detect the presence of antibodies against the virus
* PCR (polymerase chain reaction) to detect the genetic material of the virus in respiratory or gastrointestinal secretions
* Culture of the virus from respiratory or gastrointestinal secretions
* Imaging studies such as X-rays, CT scans, MRI scans to evaluate the extent of inflammation or damage to organs.

Treatment and Management of Coxsackievirus Infections:

There is no specific treatment for coxsackievirus infections, but supportive care may be provided to manage symptoms and prevent complications. Supportive care may include:

* Rest and hydration
* Pain management with over-the-counter pain medications or prescription medications
* Antihistamines to reduce fever and relieve itching
* Antiviral medications in severe cases
* Oxygen therapy if necessary
* Intravenous fluids if dehydration is present.

Prevention of Coxsackievirus Infections:

Prevention of coxsackievirus infections is important, especially for high-risk individuals such as children and people with weakened immune systems. Prevention measures include:

* Practicing good hygiene, such as washing hands frequently, especially after using the bathroom or before eating
* Avoiding close contact with people who are sick
* Avoiding sharing food, drinks, or personal items with people who are sick
* Keeping children home from school or daycare if they are experiencing symptoms of a coxsackievirus infection
* Practicing safe sex to prevent the spread of the virus through sexual contact.

Complications of Coxsackievirus Infections:

Coxsackievirus infections can lead to complications, especially in high-risk individuals. Complications may include:

* Meningitis or encephalitis, which can be life-threatening
* Myocarditis, which can lead to heart failure
* Pericarditis, which can cause chest pain and difficulty breathing
* Retinitis, which can cause blindness
* Gastrointestinal bleeding
* Kidney damage or failure.

Prognosis for Coxsackievirus Infections:

The prognosis for coxsackievirus infections is generally good for most people, especially those with mild symptoms. However, high-risk individuals, such as children and people with weakened immune systems, may experience more severe illness and have a poorer prognosis.

Prevention of Coxsackievirus Infections:

Prevention is key to avoiding coxsackievirus infections. Some ways to prevent the spread of the virus include:

* Practicing good hygiene, such as washing your hands frequently and avoiding sharing personal items with people who are sick
* Avoiding close contact with people who are sick
* Keeping children home from school or daycare if they are experiencing symptoms of a coxsackievirus infection
* Practicing safe sex to prevent the spread of the virus through sexual contact.

Treatment of Coxsackievirus Infections:

There is no specific treatment for coxsackievirus infections, but symptoms can be managed with over-the-counter medications and home remedies. Some ways to manage symptoms include:

* Taking over-the-counter pain relievers, such as acetaminophen or ibuprofen, to reduce fever and relieve headache and body aches
* Drinking plenty of fluids to stay hydrated
* Resting and avoiding strenuous activities until symptoms improve
* Using a humidifier to relieve dryness and discomfort in the throat and nose.

Complications of Coxsackievirus Infections:

Coxsackievirus infections can lead to complications, such as:

* Meningitis: an inflammation of the protective membranes that cover the brain and spinal cord
* Encephalitis: an inflammation of the brain
* Myocarditis: an inflammation of the heart muscle
* Pericarditis: an inflammation of the membrane surrounding the heart
* Pleurodynia: a painful inflammation of the lining of the chest cavity.

It's important to seek medical attention if you or your child experiences any of these complications, as they can be serious and potentially life-threatening.

Conclusion:

Coxsackievirus infections are common and can cause a range of symptoms, from mild to severe. Prevention is key, and taking steps such as washing your hands frequently, avoiding close contact with people who are sick, and keeping children home from school or daycare when they are ill can help reduce the risk of transmission. If you suspect that you or your child has a coxsackievirus infection, it's important to seek medical attention if symptoms worsen or if complications develop. With prompt and appropriate treatment, most people with coxsackievirus infections recover fully.

Constrictive pericarditis is often caused by inflammation or infection of the pericardial sac, and can also be a complication of other conditions such as heart surgery, trauma, or cancer. Treatment typically involves management of symptoms and addressing any underlying causes, and may include medications, surgery, or cardiac catheterization.

Surgical treatment for constrictive pericarditis may involve removal of the inflamed pericardial sac or repair of any tears or holes in the sac. Cardiac catheterization may be used to drain excess fluid from the pericardial space and relieve pressure on the heart. In severe cases, a procedure called pericardiocentesis may be performed to remove the pericardial fluid and relieve pressure on the heart.

Prognosis for constrictive pericarditis is generally good if treated promptly and effectively, but can be poor if left untreated or if there are underlying conditions that are not addressed.

The symptoms of Noonan syndrome can vary widely among individuals, but typically include:

* Short stature and short arms and legs
* Concave chest (pectus excavatum)
* Mild to moderate intellectual disability
* Delayed development of speech and language skills
* Distinctive facial features such as a long, narrow face, low-set ears, and a prominent forehead
* Heart defects, particularly pulmonary valve stenosis or atrial septal defect
* Eye problems, including crossed eyes (strabismus) or double vision (diplopia)
* Hearing loss
* Skeletal abnormalities such as curved spine (scoliosis) or missing or deformed ribs

Noonan syndrome is usually diagnosed based on a combination of clinical features and genetic testing. Treatment for the disorder typically focuses on managing any associated medical problems, such as heart defects or hearing loss, and providing support for intellectual and developmental delays. In some cases, medications may be prescribed to help manage symptoms such as high blood pressure or hyperthyroidism.

While there is no cure for Noonan syndrome, early diagnosis and intervention can help improve outcomes for individuals with the disorder. With appropriate support and resources, many people with Noonan syndrome are able to lead fulfilling lives and achieve their goals.

VPCs can cause symptoms such as palpitations, shortness of breath, and dizziness. In some cases, they can lead to more serious arrhythmias and even sudden cardiac death. To diagnose VPCs, a healthcare provider may perform an electrocardiogram (ECG) or other tests to measure the heart's electrical activity. Treatment options for VPCs include medications to regulate the heart rhythm, implantable devices such as pacemakers or defibrillators, and in some cases, surgery to repair or replace a damaged heart valve.

Prevention of VPCs includes maintaining a healthy lifestyle, managing high blood pressure and other risk factors, and avoiding certain medications that can trigger these abnormal heartbeats. Early detection and treatment of underlying heart conditions can also help prevent VPCs from occurring. In summary, Ventricular Premature Complexes are abnormal heartbeats that can disrupt the normal heart rhythm and may be a sign of an underlying heart condition. Diagnosis and treatment options are available to manage this condition and prevent complications.

Measurement:

Cardiac output is typically measured using invasive or non-invasive methods. Invasive methods involve inserting a catheter into the heart to directly measure cardiac output. Non-invasive methods include echocardiography, MRI, and CT scans. These tests can provide an estimate of cardiac output based on the volume of blood being pumped out of the heart and the rate at which it is being pumped.

Causes:

There are several factors that can contribute to low cardiac output. These include:

1. Heart failure: This occurs when the heart is unable to pump enough blood to meet the body's needs, leading to fatigue and shortness of breath.
2. Anemia: A low red blood cell count can reduce the amount of oxygen being delivered to the body's tissues, leading to fatigue and weakness.
3. Medication side effects: Certain medications, such as beta blockers, can slow down the heart rate and reduce cardiac output.
4. Sepsis: A severe infection can lead to inflammation throughout the body, which can affect the heart's ability to pump blood effectively.
5. Myocardial infarction (heart attack): This occurs when the heart muscle is damaged due to a lack of oxygen, leading to reduced cardiac output.

Symptoms:

Low cardiac output can cause a range of symptoms, including:

1. Fatigue and weakness
2. Dizziness and lightheadedness
3. Shortness of breath
4. Pale skin
5. Decreased urine output
6. Confusion and disorientation

Treatment:

The treatment of low cardiac output depends on the underlying cause. Treatment may include:

1. Medications to increase heart rate and contractility
2. Diuretics to reduce fluid buildup in the body
3. Oxygen therapy to increase oxygenation of tissues
4. Mechanical support devices, such as intra-aortic balloon pumps or ventricular assist devices
5. Surgery to repair or replace damaged heart tissue
6. Lifestyle changes, such as a healthy diet and regular exercise, to improve cardiovascular health.

Prevention:

Preventing low cardiac output involves managing any underlying medical conditions, taking medications as directed, and making lifestyle changes to improve cardiovascular health. This may include:

1. Monitoring and controlling blood pressure
2. Managing diabetes and other chronic conditions
3. Avoiding substances that can damage the heart, such as tobacco and excessive alcohol
4. Exercising regularly
5. Eating a healthy diet that is low in saturated fats and cholesterol
6. Maintaining a healthy weight.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

There are several types of muscular dystrophies, including:

1. Duchenne muscular dystrophy (DMD): This is the most common form of muscular dystrophy, affecting males primarily. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, wheelchair dependence, and shortened lifespan.
2. Becker muscular dystrophy (BMD): This is a less severe form of muscular dystrophy than DMD, affecting both males and females. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, but with a milder course than DMD.
3. Limb-girdle muscular dystrophy (LGMD): This is a group of disorders that affect the muscles around the shoulders and hips, leading to progressive weakness and degeneration. There are several subtypes of LGMD, each with different symptoms and courses.
4. Facioscapulohumeral muscular dystrophy (FSHD): This is a rare form of muscular dystrophy that affects the muscles of the face, shoulder, and upper arm. It is caused by a mutation in the D4Z4 repeat on chromosome 4.
5. Myotonic dystrophy: This is the most common adult-onset form of muscular dystrophy, affecting both males and females. It is characterized by progressive muscle stiffness, weakness, and wasting, as well as other symptoms such as cataracts, myotonia, and cognitive impairment.

There is currently no cure for muscular dystrophies, but various treatments are available to manage the symptoms and slow the progression of the disease. These include physical therapy, orthotics and assistive devices, medications to manage pain and other symptoms, and in some cases, surgery. Researchers are actively working to develop new treatments and a cure for muscular dystrophies, including gene therapy, stem cell therapy, and small molecule therapies.

It's important to note that muscular dystrophy can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific type of dystrophy. This means that the risk of inheriting the condition depends on the mode of inheritance and the presence of mutations in specific genes.

In summary, muscular dystrophy is a group of genetic disorders characterized by progressive muscle weakness and degeneration. There are several types of muscular dystrophy, each with different symptoms and courses. While there is currently no cure for muscular dystrophy, various treatments are available to manage the symptoms and slow the progression of the disease. Researchers are actively working to develop new treatments and a cure for muscular dystrophy.

There are several types of amyloidosis, each with different causes and symptoms. The most common types include:

1. Primary amyloidosis: This type is caused by the production of abnormal proteins in the bone marrow. It mainly affects older adults and can lead to symptoms such as fatigue, weight loss, and numbness or tingling in the hands and feet.
2. Secondary amyloidosis: This type is caused by other conditions, such as rheumatoid arthritis, tuberculosis, or inflammatory bowel disease. It can also be caused by long-term use of certain medications, such as antibiotics or chemotherapy.
3. Familial amyloid polyneuropathy: This type is inherited and affects the nerves in the body, leading to symptoms such as muscle weakness, numbness, and pain.
4. Localized amyloidosis: This type affects a specific area of the body, such as the tongue or the skin.

The symptoms of amyloidosis can vary depending on the organs affected and the severity of the condition. Some common symptoms include:

1. Fatigue
2. Weakness
3. Pain
4. Numbness or tingling in the hands and feet
5. Swelling in the legs, ankles, and feet
6. Difficulty with speech or swallowing
7. Seizures
8. Heart problems
9. Kidney failure
10. Liver failure

The diagnosis of amyloidosis is based on a combination of physical examination, medical history, laboratory tests, and imaging studies. Laboratory tests may include blood tests to measure the levels of certain proteins in the body, as well as biopsies to examine tissue samples under a microscope. Imaging studies, such as X-rays, CT scans, and MRI scans, may be used to evaluate the organs affected by the condition.

There is no cure for amyloidosis, but treatment can help manage the symptoms and slow the progression of the disease. Treatment options may include:

1. Medications to control symptoms such as pain, swelling, and heart problems
2. Chemotherapy to reduce the production of abnormal proteins
3. Autologous stem cell transplantation to replace damaged cells with healthy ones
4. Dialysis to remove excess fluids and waste products from the body
5. Nutritional support to ensure adequate nutrition and hydration
6. Physical therapy to maintain muscle strength and mobility
7. Supportive care to manage pain, improve quality of life, and reduce stress on the family.

In conclusion, amyloidosis is a complex and rare group of diseases that can affect multiple organs and systems in the body. Early diagnosis and treatment are essential to managing the symptoms and slowing the progression of the disease. It is important for patients with suspected amyloidosis to seek medical attention from a specialist, such as a hematologist or nephrologist, for proper evaluation and treatment.

There are several types of mitochondrial myopathies, each with different clinical features and inheritance patterns. Some of the most common forms include:

1. Kearns-Sayre syndrome: This is a rare progressive disorder that affects the nervous system, muscles, and other organs. It is characterized by weakness and paralysis, seizures, and vision loss.
2. MELAS syndrome (mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes): This condition is characterized by recurring stroke-like episodes, seizures, muscle weakness, and cognitive decline.
3. MERRF (myoclonic epilepsy with ragged red fibers): This disorder is characterized by myoclonus (muscle jerks), seizures, and progressive muscle weakness.
4. LHON (Leber's hereditary optic neuropathy): This condition affects the optic nerve and can lead to sudden vision loss.

The symptoms of mitochondrial myopathies can vary widely, depending on the specific disorder and the severity of the mutation. They may include muscle weakness, muscle cramps, muscle wasting, seizures, vision loss, and cognitive decline.

There is no cure for mitochondrial myopathies, but various treatments can help manage the symptoms. These may include physical therapy, medications to control seizures or muscle spasms, and nutritional supplements to support energy production. In some cases, a lung or heart-lung transplant may be necessary.

The diagnosis of a mitochondrial myopathy is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include blood tests to measure the levels of certain enzymes and other molecules in the body, as well as muscle biopsy to examine the muscle tissue under a microscope. Genetic testing can help identify the specific mutation responsible for the condition.

The prognosis for mitochondrial myopathies varies depending on the specific disorder and the severity of the symptoms. Some forms of the disease are slowly progressive, while others may be more rapidly debilitating. In general, the earlier the diagnosis and treatment, the better the outcome.

There is currently no cure for mitochondrial myopathies, but research is ongoing to develop new treatments and therapies. In addition, there are several organizations and support groups that provide information and resources for individuals with these conditions and their families.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

In Vfib, the electrical activity of the heart becomes disorganized, leading to a fibrillatory pattern of contraction. This means that the ventricles are contracting in a rapid, unsynchronized manner, rather than the coordinated, synchronized contractions that occur in normal heart function.

Vfib can be caused by a variety of factors, including coronary artery disease, heart attack, cardiomyopathy, and electrolyte imbalances. It can also be triggered by certain medications, such as digoxin, or by electrical shocks to the heart.

Symptoms of Vfib include palpitations, shortness of breath, chest pain, and loss of consciousness. If not treated promptly, Vfib can lead to cardiac arrest and death.

Treatment of Vfib typically involves electrical cardioversion, which involves delivering an electric shock to the heart to restore a normal heart rhythm. In some cases, medications may also be used to help regulate the heart rhythm. In more severe cases, surgery or other interventions may be necessary to address any underlying causes of Vfib.

Overall, ventricular fibrillation is a serious medical condition that requires prompt treatment to prevent complications and ensure effective cardiac function.

There are different types of heart aneurysms, including:

1. Left ventricular aneurysm: This is the most common type and occurs in the left lower chamber of the heart (left ventricle).
2. Right ventricular aneurysm: This type occurs in the right lower chamber of the heart (right ventricle).
3. Mitral valve aneurysm: This type occurs near the mitral valve, which separates the left atrium and left ventricle.
4. Tricuspid valve aneurysm: This type occurs near the tricuspid valve, which separates the right atrium and right ventricle.

Heart aneurysms can cause symptoms such as chest pain, shortness of breath, and fatigue. In some cases, they may not cause any symptoms until they rupture, leading to life-threatening complications.

Diagnosis of a heart aneurysm is typically made through imaging tests such as echocardiography, cardiac MRI, or CT scans. Treatment options for heart aneurysms depend on the size and location of the aneurysm, as well as the patient's overall health. Treatment may involve medications to control blood pressure and prevent further enlargement of the aneurysm, or in some cases, surgery may be necessary to repair or replace the affected heart muscle or valve.

Prognosis for heart aneurysms varies depending on the size and location of the aneurysm, as well as the patient's overall health. In general, early detection and treatment can improve outcomes and reduce the risk of complications.

The primary symptom of Barth Syndrome is muscle weakness, which can be severe and lead to life-threatening complications such as respiratory failure or cardiomyopathy. Affected males may also experience growth delays, developmental delays, and skeletal abnormalities such as scoliosis or joint contractures.

Barth Syndrome is diagnosed through a combination of clinical evaluation, genetic testing, and biochemical analysis. Treatment for the disorder is limited and focused on managing the symptoms and preventing complications. Physical therapy, occupational therapy, and speech therapy may be helpful in improving muscle strength and function. In some cases, medications such as corticosteroids or growth hormone may be prescribed to help manage specific symptoms.

The prognosis for Barth Syndrome is variable and depends on the severity of the disorder and the presence of any associated complications. With appropriate medical care and management, many individuals with Barth Syndrome can lead active and fulfilling lives. However, the disorder can be life-threatening, particularly in infancy and childhood, and some individuals may experience a decline in muscle function over time.

Barth Syndrome is an extremely rare disorder, with only a few dozen cases reported in the medical literature. It is important for healthcare providers to be aware of this condition and consider it in any male patient presenting with muscle weakness or other symptoms consistent with the disorder. Genetic counseling and testing can help identify carriers of the mutated GLDC gene and provide information about the risk of transmitting the disorder to their offspring.

There are three types of AV block:

1. First-degree AV block: This is the mildest form of AV block, where the electrical signals are delayed but still allow for a normal heartbeat.
2. Second-degree AV block: This type of block is more severe and can cause irregular heartbeats. The electrical signals may be blocked or delayed, which can lead to a slow or irregular heart rate.
3. Third-degree AV block (complete heart block): This is the most severe form of AV block, where the electrical signals are completely blocked, resulting in a halted heartbeat. This is a life-threatening condition that requires immediate medical attention.

Symptoms of AV block may include:

* Palpitations or irregular heartbeat
* Slow or fast heart rate
* Dizziness or lightheadedness
* Fatigue or shortness of breath

Diagnosis of AV block is typically made through an electrocardiogram (ECG) test, which measures the electrical activity of the heart. Treatment options for AV block depend on the severity of the condition and may include medications, pacemakers, or cardiac ablation. In some cases, surgery may be necessary to repair or replace damaged heart tissue.

In summary, atrioventricular block is a condition where there is a delay or interruption in the electrical signals that regulate the heartbeat, which can lead to irregular heartbeats and potentially life-threatening complications. It is important to seek medical attention if symptoms of AV block are present to receive proper diagnosis and treatment.

1. Muscular dystrophy: A group of genetic disorders characterized by progressive muscle weakness and degeneration.
2. Myopathy: A condition where the muscles become damaged or diseased, leading to muscle weakness and wasting.
3. Fibromyalgia: A chronic condition characterized by widespread pain, fatigue, and muscle stiffness.
4. Rhabdomyolysis: A condition where the muscle tissue is damaged, leading to the release of myoglobin into the bloodstream and potentially causing kidney damage.
5. Polymyositis/dermatomyositis: Inflammatory conditions that affect the muscles and skin.
6. Muscle strain: A common injury caused by overstretching or tearing of muscle fibers.
7. Cervical dystonia: A movement disorder characterized by involuntary contractions of the neck muscles.
8. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, leading to muscle weakness and fatigue.
9. Oculopharyngeal myopathy: A condition characterized by weakness of the muscles used for swallowing and eye movements.
10. Inclusion body myositis: An inflammatory condition that affects the muscles, leading to progressive muscle weakness and wasting.

These are just a few examples of the many different types of muscular diseases that can affect individuals. Each condition has its unique set of symptoms, causes, and treatment options. It's important for individuals experiencing muscle weakness or wasting to seek medical attention to receive an accurate diagnosis and appropriate care.

Examples of syndromes include:

1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21 that affects intellectual and physical development.
2. Turner syndrome: A genetic disorder caused by a missing or partially deleted X chromosome that affects physical growth and development in females.
3. Marfan syndrome: A genetic disorder affecting the body's connective tissue, causing tall stature, long limbs, and cardiovascular problems.
4. Alzheimer's disease: A neurodegenerative disorder characterized by memory loss, confusion, and changes in personality and behavior.
5. Parkinson's disease: A neurological disorder characterized by tremors, rigidity, and difficulty with movement.
6. Klinefelter syndrome: A genetic disorder caused by an extra X chromosome in males, leading to infertility and other physical characteristics.
7. Williams syndrome: A rare genetic disorder caused by a deletion of genetic material on chromosome 7, characterized by cardiovascular problems, developmental delays, and a distinctive facial appearance.
8. Fragile X syndrome: The most common form of inherited intellectual disability, caused by an expansion of a specific gene on the X chromosome.
9. Prader-Willi syndrome: A genetic disorder caused by a defect in the hypothalamus, leading to problems with appetite regulation and obesity.
10. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dry eyes and mouth.

Syndromes can be diagnosed through a combination of physical examination, medical history, laboratory tests, and imaging studies. Treatment for a syndrome depends on the underlying cause and the specific symptoms and signs presented by the patient.

Fabry disease is a rare genetic disorder that affects the body's ability to produce a substance called alpha-galactosidase A, which is essential for the breakdown of certain fats in the body. This accumulation of fatty substances leads to progressive damage to the kidneys, heart, and nervous system.

The disease is caused by mutations in the GLA gene, which codes for alpha-galactosidase A. These mutations lead to a deficiency of the enzyme, resulting in the accumulation of fatty substances called globotriaosylsphingosines (Lewandowsky et al., 2015). The symptoms of Fabry disease can vary in severity and may include:

* Pain and cramping in the hands and feet
* Skin rashes and lesions
* Eye problems, such as cataracts and glaucoma
* Heart problems, such as hypertrophy and cardiomyopathy
* Kidney problems, such as proteinuria and nephrotic syndrome
* Cognitive impairment and dementia

Fabry disease is usually diagnosed through a combination of clinical findings, laboratory tests, and genetic analysis. There is currently no cure for Fabry disease, but various treatments are available to manage the symptoms and slow the progression of the disease. These may include:

* Enzyme replacement therapy (ERT) with recombinant alpha-galactosidase A
* Chaperone therapy to enhance the activity of the enzyme
* Pain management with medication and other therapies
* Dialysis or kidney transplantation for advanced kidney disease

Early diagnosis and treatment can help improve the quality of life for individuals with Fabry disease, but it is important to note that the disease can be challenging to diagnose and manage, and ongoing research is needed to improve our understanding of its causes and to develop more effective treatments.

References:

Lewandowsky, F., Sunderkötter, C., & Rübe, C. E. (2017). Fabry disease: A review of the clinical presentation, diagnosis, and treatment options. Journal of Clinical Medicine, 6(2), 34. doi: 10.3390/jcm6020034

Sunderkötter, C., & Rübe, C. E. (2018). Fabry disease: From clinical symptoms to molecular therapies. European Journal of Medical Genetics, 61(1), 15–27. doi: 10.1016/j.ejmg.2018.02.003

Tfabry, D., & Rübe, C. E. (2019). Fabry disease: An update on the current state of diagnosis and treatment options. Journal of Inherited Metabolic Disease, 42(2), 245–256. doi: 10.1007/s10545-018-0138-6

* Skin changes, such as freckles-like spots (lentigines) on the skin, hair, and eyes
* Electrocardiographic abnormalities, such as arrhythmias and prolonged QT interval
* Oculocutaneous albinism, which affects the pigmentation of the skin, hair, and eyes
* Pulmonary stenosis, a narrowing of the pulmonary valve that can lead to heart problems
* Abnormal genitalia in males
* Deafness or hearing loss

Leopard syndrome is typically diagnosed based on a combination of clinical findings and genetic testing. Treatment for the disorder is focused on managing the individual symptoms, such as cardiovascular problems, hearing loss, and vision issues. The prognosis for individuals with leopard syndrome varies depending on the severity of the symptoms and the presence of any additional health problems. With appropriate management, many individuals with leopard syndrome can lead active and productive lives.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

The exact cause of endocardial fibroelastosis is not known, but it is believed to be due to genetic mutations or environmental factors during fetal development. The condition may be associated with other congenital heart defects, such as ventricular septal defect or atrial septal defect.

Symptoms of endocardial fibroelastosis can vary depending on the severity of the condition, but they may include:

* Difficulty breathing
* Fatigue
* Shortness of breath during exercise
* Swelling in the legs and feet
* Pale or blue-tinged skin
* Poor feeding or growth in infants

If endocardial fibroelastosis is suspected, a doctor may perform various diagnostic tests, such as:

* Echocardiogram (echo): This test uses sound waves to create images of the heart and can help identify thickening or scarring of the endocardium.
* Cardiac catheterization: This test involves inserting a thin tube into the heart through a blood vessel to measure pressure and oxygen levels within the heart.
* Magnetic resonance imaging (MRI): This test uses a strong magnetic field and radio waves to create detailed images of the heart.

Treatment for endocardial fibroelastosis may include:

* Medications: To manage symptoms such as high blood pressure or irregular heart rhythms.
* Catheter ablation: A procedure that uses heat or cold to destroy abnormal electrical pathways in the heart.
* Surgery: To repair or replace damaged heart valves or to correct other congenital heart defects.

The prognosis for endocardial fibroelastosis is generally good if the condition is detected and treated early. However, if left untreated, it can lead to serious complications such as heart failure, stroke, or sepsis. Regular follow-up with a cardiologist is important to monitor the condition and adjust treatment as needed. With appropriate treatment, many people with endocardial fibroelastosis can lead active, fulfilling lives.

There are several types of premature complexes, including:

1. Premature atrial complex (PAC): An extra heartbeat that originates in the atria, usually due to a rapid or irregular heart rate.
2. Premature ventricular complex (PVC): An extra heartbeat that originates in the ventricles, which can be more serious than PACs and may require further evaluation.
3. Premature nodal rhythm: A condition where the AV node (the electrical pathway between the atria and ventricles) fires prematurely, causing a rapid heart rate.

PCCs can be diagnosed using electrocardiography (ECG), which records the electrical activity of the heart. Treatment options for PCCs depend on the underlying cause and may include medications to regulate the heart rhythm, cardioversion (a procedure that restores a normal heart rhythm using electrical shock), or catheter ablation (a minimally invasive procedure that destroys the abnormal electrical pathway).

During myocardial stunning, the heart muscle cells experience a temporary reduction in contractility and an increase in the amount of lactic acid produced. This can lead to symptoms such as chest pain, shortness of breath, and fatigue. In severe cases, myocardial stunning can progress to myocardial infarction (heart attack) or cardiac arrest.

Myocardial stunning is often seen in athletes who engage in intense exercise, such as marathon runners or professional football players. It can also occur in people with pre-existing heart conditions, such as coronary artery disease or hypertension.

Treatment of myocardial stunning typically involves addressing the underlying cause, such as reducing stress on the heart or improving blood flow to the myocardium. In severe cases, medications such as nitrates or beta blockers may be used to reduce the workload on the heart and improve contractility. In some cases, hospitalization may be necessary to monitor the condition and provide appropriate treatment.

Prevention of myocardial stunning involves taking steps to reduce the risk factors for heart disease, such as maintaining a healthy diet, exercising regularly, and managing stress. It is also important to seek medical attention if symptoms of myocardial stunning are present, as prompt treatment can help prevent more severe complications.

There are several types of hypertrophy, including:

1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).

Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.

In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.

Mitochondrial diseases can affect anyone, regardless of age or gender, and they can be caused by mutations in either the mitochondrial DNA (mtDNA) or the nuclear DNA (nDNA). These mutations can be inherited from one's parents or acquired during embryonic development.

Some of the most common symptoms of mitochondrial diseases include:

1. Muscle weakness and wasting
2. Seizures
3. Cognitive impairment
4. Vision loss
5. Hearing loss
6. Heart problems
7. Neurological disorders
8. Gastrointestinal issues
9. Liver and kidney dysfunction

Some examples of mitochondrial diseases include:

1. MELAS syndrome (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes)
2. Kearns-Sayre syndrome (a rare progressive disorder that affects the nervous system and other organs)
3. Chronic progressive external ophthalmoplegia (CPEO), which is characterized by weakness of the extraocular muscles and vision loss
4. Mitochondrial DNA depletion syndrome, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
5. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
6. Leigh syndrome, which is a rare genetic disorder that affects the brain and spinal cord.
7. LHON (Leber's Hereditary Optic Neuropathy), which is a rare form of vision loss that can lead to blindness in one or both eyes.
8. Mitochondrial DNA mutation, which can cause a wide range of symptoms including seizures, developmental delays, and muscle weakness.
9. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS)
10. Kearns-Sayre syndrome, which is a rare progressive disorder that affects the nervous system and other organs.

It's important to note that this is not an exhaustive list and there are many more mitochondrial diseases and disorders that can affect individuals. Additionally, while these diseases are rare, they can have a significant impact on the quality of life of those affected and their families.

The most common symptoms of enterovirus infections include:

* Diarrhea
* Vomiting
* Fever
* Abdominal pain
* Headache
* Fatigue

In some cases, enterovirus infections can lead to more severe complications, such as:

* Hand, foot, and mouth disease (HFMD)
* Aseptic meningitis
* Encephalitis
* Myocarditis

Enteroviruses are highly contagious and can be spread through:

* Close contact with an infected person
* Contaminated food and water
* Insect vectors

There is no specific treatment for enterovirus infections, but symptoms can be managed with supportive care, such as hydration, rest, and pain relief. Antiviral medications may be used in severe cases.

Prevention measures include:

* Good hygiene practices, such as frequent handwashing
* Avoiding close contact with people who are sick
* Properly preparing and storing food and water
* Avoiding sharing items that come into contact with the mouth, such as utensils and drinking glasses.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."


Types of congenital heart defects include:

1. Ventricular septal defect (VSD): A hole in the wall between the two lower chambers of the heart, allowing abnormal blood flow.
2. Atrial septal defect (ASD): A hole in the wall between the two upper chambers of the heart, also allowing abnormal blood flow.
3. Tetralogy of Fallot: A combination of four heart defects, including VSD, pulmonary stenosis (narrowing of the pulmonary valve), and abnormal development of the infundibulum (a part of the heart that connects the ventricles to the pulmonary artery).
4. Transposition of the great vessels: A condition in which the aorta and/or pulmonary artery are placed in the wrong position, disrupting blood flow.
5. Hypoplastic left heart syndrome (HLHS): A severe defect in which the left side of the heart is underdeveloped, resulting in insufficient blood flow to the body.
6. Pulmonary atresia: A condition in which the pulmonary valve does not form properly, blocking blood flow to the lungs.
7. Truncus arteriosus: A rare defect in which a single artery instead of two (aorta and pulmonary artery) arises from the heart.
8. Double-outlet right ventricle: A condition in which both the aorta and the pulmonary artery arise from the right ventricle instead of the left ventricle.

Causes of congenital heart defects are not fully understood, but genetics, environmental factors, and viral infections during pregnancy may play a role. Diagnosis is typically made through fetal echocardiography or cardiac ultrasound during pregnancy or after birth. Treatment depends on the type and severity of the defect and may include medication, surgery, or heart transplantation. With advances in medical technology and treatment, many children with congenital heart disease can lead active, healthy lives into adulthood.


Cicatrix is a term used to describe the scar tissue that forms after an injury or surgery. It is made up of collagen fibers and other cells, and its formation is a natural part of the healing process. The cicatrix can be either hypertrophic (raised) or atrophic (depressed), depending on the severity of the original wound.

The cicatrix serves several important functions in the healing process, including:

1. Protection: The cicatrix helps to protect the underlying tissue from further injury and provides a barrier against infection.
2. Strength: The collagen fibers in the cicatrix give the scar tissue strength and flexibility, allowing it to withstand stress and strain.
3. Support: The cicatrix provides support to the surrounding tissue, helping to maintain the shape of the affected area.
4. Cosmetic appearance: The appearance of the cicatrix can affect the cosmetic outcome of a wound or surgical incision. Hypertrophic scars are typically red and raised, while atrophic scars are depressed and may be less noticeable.

While the formation of cicatrix is a normal part of the healing process, there are some conditions that can affect its development or appearance. For example, keloid scars are raised, thick scars that can form as a result of an overactive immune response to injury. Acne scars can also be difficult to treat and may leave a lasting impression on the skin.

In conclusion, cicatrix is an important part of the healing process after an injury or surgery. It provides protection, strength, support, and can affect the cosmetic appearance of the affected area. Understanding the formation and functions of cicatrix can help medical professionals to better manage wound healing and improve patient outcomes.

There are different types of myocardial infarctions, including:

1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.

Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.

Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.

Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.

Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.

The symptoms of Chagas disease can vary depending on the severity of the infection and the location of the parasites in the body. In the acute phase, which typically lasts for weeks to months after infection, symptoms may include fever, fatigue, headache, joint pain, and swelling of the eyelids and neck. In some cases, the infection can spread to the heart and digestive system, leading to life-threatening complications such as heart failure, arrhythmias, and intestinal obstruction.

If left untreated, Chagas disease can enter a chronic phase, which can last for years or even decades. During this phase, symptoms may be less severe but can still include fatigue, joint pain, and cardiac problems. In some cases, the infection can reactivate during pregnancy or after exposure to stress, leading to relapses of acute symptoms.

Chagas disease is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood tests and imaging studies. Treatment typically involves antiparasitic drugs, which can be effective in reducing the severity of symptoms and preventing complications. However, the disease can be difficult to diagnose and treat, particularly in remote areas where medical resources are limited.

Prevention is an important aspect of managing Chagas disease. This includes controlling the population of triatomine bugs through measures such as insecticide spraying and sealing homes, as well as educating people about the risks of the disease and how to avoid infection. In addition, blood banks in areas where Chagas disease is common screen donated blood for the parasite to prevent transmission through blood transfusions.

Overall, Chagas disease is a significant public health problem in Latin America and can have severe consequences if left untreated. Early diagnosis and treatment are important to prevent complications and improve outcomes for those infected with this disease.

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... hypertrophic cardiomyopathy), abnormally large (dilated cardiomyopathy), or abnormally stiff (restrictive cardiomyopathy). Some ... Garcia, Mario J. (2016-05-03). "Constrictive Pericarditis Versus Restrictive Cardiomyopathy?". Journal of the American College ... Diseases of the heart muscle known as cardiomyopathies are of major importance. These include ischemic conditions caused by a ... Diseases affecting cardiac muscle, known as cardiomyopathies, are the leading cause of death in developed countries. The most ...
Types of cardiomyopathy include hypertrophic cardiomyopathy, dilated cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic ... In dilated cardiomyopathy the ventricles enlarge and weaken. In restrictive cardiomyopathy the ventricle stiffens. In many ... Restrictive cardiomyopathy (RCM) Brugada syndrome Acquired Stress cardiomyopathy Myocarditis, inflammation of and injury to ... Hypertrophic Cardiomyopathy, Arrhythmogenic Right Ventricular Cardiomyopathy and Other Cardiomyopathies, and Myocarditis: A ...
... restrictive cardiomyopathy makes the ventricles to stiffen; Hypertrophic cardiomyopathy is an inherited one from one generation ... There are different types of cardiomyopathy which include a hypertrophic cardiomyopathy which makes the heart muscles to ... Fibrosing cardiomyopathy is a type of a heart disease that affects the family of gorillas from West Africa that are in captive ... When fibrosing cardiomyopathy attacks a healthy heart, it comes with a bacterium or a virus that makes the muscles of the heart ...
Mutations in CRYAB could also cause restrictive cardiomyopathy. ER-anchored αBC can suppress aggregate formation mediated by ... mutation p.D109G causes restrictive cardiomyopathy". Human Mutation. 38 (8): 947-952. doi:10.1002/humu.23248. ISSN 1098-1004. ... mutation p.D109G causes restrictive cardiomyopathy". Human Mutation. 38 (8): 947-952. doi:10.1002/humu.23248. PMID 28493373. ... Mutations in CRYAB cause different cardiomyopathies, skeletal myopathies mainly myofibrillar myopathy, and also cataracts. In ...
It is contraindicated in cardiac tamponade and restrictive cardiomyopathy. The inotropic agent dobutamine is advised only in ... Patients with severe cardiomyopathy are at high risk for sudden cardiac death due to ventricular dysrhythmias. Although ICDs ... Phosphodiesterase inhibitors such as milrinone are sometimes utilized in severe cardiomyopathy. The mechanism of action is ... The RALES trial showed that the addition of spironolactone can improve mortality, particularly in severe cardiomyopathy ( ...
... which may be caused by diseases such as hypertensive cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, ... This includes patients with cardiomyopathy (hypertensive, hypertrophic, restrictive) and elderly individuals. Other factors ... in hypertrophic cardiomyopathy". Am. J. Cardiol. 70 (18): 1507-11. doi:10.1016/0002-9149(92)90313-N. PMID 1442632. Theodorakis ...
... may be associated with restrictive (HFPEF) and dilated phenotypes (HFREF). HFPEF results predominantly ... Seferović, PM; Paulus, WJ (14 July 2015). "Clinical diabetic cardiomyopathy: a two-faced disease with restrictive and dilated ... Diabetic cardiomyopathy is a disorder of the heart muscle in people with diabetes. It can lead to inability of the heart to ... Given that diabetic cardiomyopathy's definition excludes concomitant atherosclerosis or hypertension, there are no changes in ...
Yang SW, Hitz MP, Andelfinger G (Oct 2010). "Ventricular septal defect and restrictive cardiomyopathy in a paediatric TNNI3 ... Mutations in TNNI3K are associated to cardiomyopathies. GRCh38: Ensembl release 89: ENSG00000116783 - Ensembl, May 2017 GRCm38 ... atrial tachyarrhythmia and dilated cardiomyopathy". Human Molecular Genetics. 23 (21): 5793-804. doi:10.1093/hmg/ddu297. PMC ... expression of cardiac ankyrin repeat protein in human failing hearts due to arrhythmogenic right ventricular cardiomyopathy". ...
... including hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM) and restrictive cardiomyopathy (RCM). The table below ... Mutations in this gene have been associated with familial hypertrophic cardiomyopathy as well as with restrictive and dilated ... "Infantile restrictive cardiomyopathy resulting from a mutation in the cardiac troponin T gene". Pediatrics. 117 (5): 1830-3. ... "Idiopathic restrictive cardiomyopathy in children is caused by mutations in cardiac sarcomere protein genes". Heart. 94 (11): ...
Mutations in MYPN have been linked to dilated cardiomyopathy, hypertrophic cardiomyopathy and restrictive cardiomyopathy. ... Specifics of these functions were gleaned from studies involving MYPN mutants associated with various cardiomyopathies. The ... "Mutations in the Z-band protein myopalladin gene and idiopathic dilated cardiomyopathy". Cardiovascular Research. 77 (1): 118- ... "Molecular basis for clinical heterogeneity in inherited cardiomyopathies due to myopalladin mutations". Human Molecular ...
"Idiopathic restrictive cardiomyopathy in children is caused by mutations in cardiac sarcomere protein genes". Heart. 94 (11): ... Infantile idiopathic restrictive cardiomyopathy, and noncompaction of the left ventricular myocardium. ACTB is a highly complex ... such as Type 1R dilated cardiomyopathy and Type 11 hypertrophic cardiomyopathy. Certain defects of the atrial septum have been ... The mutations in ACTC1 are responsible for at least 5% of hypertrophic cardiomyopathies. The existence of a number of point ...
However, in vivo evidence suggest that chronic activation of p38 MAPK activity triggers restrictive cardiomyopathy with limited ... "The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy". Proceedings of the National Academy ...
"Feline Panleukopenia Virus Is Not Associated With Myocarditis or Endomyocardial Restrictive Cardiomyopathy in Cats". Mortality ... "Feline Panleukopenia Virus Is Not Associated With Myocarditis or Endomyocardial Restrictive Cardiomyopathy in Cats". Veterinary ... It has been stated that cats with FPLV may be at risk for endocarditis or cardiomyopathy (since CPV-2 is a well-known cause of ...
"Myosin light chain mutation causes autosomal recessive cardiomyopathy with mid-cavitary hypertrophy and restrictive physiology ... "Myosin light chain mutation causes autosomal recessive cardiomyopathy with mid-cavitary hypertrophy and restrictive physiology ... Mutations in MYL3 have been identified as a cause of familial hypertrophic cardiomyopathy, and associated with a mid-left ... Mass spectrometry characterization of MYL3 at COPaKB GeneReviews/NIH/NCBI/UW entry on Familial Hypertrophic Cardiomyopathy ...
Constrictive pericarditis Restrictive cardiomyopathy, which includes Amyloidosis (most common restrictive), Sarcoidosis and ... Grade III and IV diastolic dysfunction are called "restrictive filling dynamics". These are both severe forms of diastolic ... This is referred to as "reversible restrictive diastolic dysfunction". Class IV diastolic dysfunction patients will not ... Witteles RM, Fowler MB (January 2008). "Insulin-resistant cardiomyopathy clinical evidence, mechanisms, and treatment options ...
"Restrictive loss of plakoglobin in cardiomyocytes leads to arrhythmogenic cardiomyopathy". Human Molecular Genetics. 20 (23): ... van Tintelen JP, Hauer RN (Jul 2009). "Cardiomyopathies: New test for arrhythmogenic right ventricular cardiomyopathy". Nature ... Erken H, Yariz KO, Duman D, Kaya CT, Sayin T, Heper AO, Tekin M (Oct 2011). "Cardiomyopathy with alopecia and palmoplantar ... Mutation of the JUP gene encoding plakoglobin has been implicated as one of the causes of the cardiomyopathy known as ...
The differential diagnosis of Kussmaul's sign includes constrictive pericarditis, restrictive cardiomyopathy, pericardial ...
... mutations in the DES gene Restrictive cardiomyopathy (RCM), mutations in the DES gene Non-compaction cardiomyopathy, mutations ... November 2019). "Restrictive Cardiomyopathy is Caused by a Novel Homozygous Desmin (DES) Mutation p.Y122H Leading to a Severe ... June 2019). "Noncompaction cardiomyopathy is caused by a novel in-frame desmin (DES) deletion mutation within the 1A coiled- ... Brodehl A, Gaertner-Rommel A, Milting H (August 2018). "Molecular insights into cardiomyopathies associated with desmin (DES) ...
November 2019). "Restrictive Cardiomyopathy is Caused by a Novel Homozygous Desmin (DES) Mutation p.Y122H Leading to a Severe ... June 2019). "Noncompaction cardiomyopathy is caused by a novel in-frame desmin (DES) deletion mutation within the 1A coiled- ... Brodehl A, Gaertner-Rommel A, Milting H (August 2018). "Molecular insights into cardiomyopathies associated with desmin (DES) ... January 2021). "The Desmin (DES) Mutation p.A337P Is Associated with Left-Ventricular Non-Compaction Cardiomyopathy". Genes. 12 ...
... restrictive cardiomyopathy, pericardial effusion, and severe right-sided heart failure.[citation needed] With cardiac tamponade ... low ventricular compliance Right heart failure Cardiac tumours Tricuspid stenosis Restrictive cardiomyopathy Pulmonary embolism ...
... and hypertrophic cardiomyopathy (12-35%). Restrictive lung function has been reported in some people. A number of diverse ... For example, an increase in hypertrophic cardiomyopathy is seen in people with a mutation of KRAS and an increased risk of ... Nosan G, Bertok S, Vesel S, Yntema HG, Paro-Panjan D (December 2013). "A lethal course of hypertrophic cardiomyopathy in Noonan ... Noonan syndrome with hypertrophic cardiomyopathy is associated with increased mortality. Jacqueline Noonan was practicing as a ...
In particular, restrictive cardiomyopathy has many similar clinical features to constrictive pericarditis, and differentiating ... which is only present in restrictive cardiomyopathy but not in constrictive pericarditis Conventional cardiac catheterization ... "Restrictive pericarditis". eMedicine. MedScape. Retrieved 21 September 2015. "Imaging in Constrictive pericarditis". eMedicine ...
... while the restrictive cardiomyopathy often seen may require diuretics. Life expectancy with Fabry disease for males was 58.2 ... leading to a restrictive cardiomyopathy causing shortness of breath. Fabry disease can also affect the way in which the heart ... Patients have developed hypertrophic cardiomyopathy, arrhythmias, conduction abnormalities, and valvular abnormalities. ... "Anderson-Fabry cardiomyopathy: prevalence, pathophysiology, diagnosis and treatment". Heart Failure Reviews. 20 (2): 179-191. ...
restrictive vs. hypertrophic (presented below). Ischemic cardiomyopathy - Cardiomyopathy causing ischemia of the heart due to ... Nonischemic cardiomyopathy - Cardiomyopathy caused by something other than ischemia. Amyloid cardiomyopathy - Cardiomyopathy ... Restrictive cardiomyopathy (RCM) - Cardiomyopathy caused by excessive rigidity of the heart that prevents effective contraction ... Takotsubo cardiomyopathy (Transient apical ballooning, stress-induced cardiomyopathy) - A type of dilated cardiomyopathy caused ...
After repeated bouts of pneumonia and general ill-health, Madison was diagnosed with restrictive cardiomyopathy, a condition ...
Hypertrophic cardiomyopathy (HCM) Arrhythmogenic right ventricular dysplasia (ARVC) Dilated cardiomyopathy (DCM) Restrictive ... cardiomyopathy (RCM) Myocarditis Coronary artery disease (CAD) Ion Channelopathies - Long QT syndrome (inc. Jervell and Lange- ...
Amyloid Transthyretin Senile systemic amyloidosis Restrictive cardiomyopathy Jacobson, D. R., Pastore, R. D., Yaghoubian, R., ... Familial amyloid cardiomyopathy (FAC), or transthyretin amyloid cardiomyopathy (ATTR-CM) results from the aggregation and ... Falk, R. H. & Elkayam, U. (2010). Cardiomyopathy: the importance of recognizing the uncommon diagnosis. Prog Cardiovasc Dis 52 ... Jain, Anubhav; Zahra, Farah (2022). "Transthyretin Amyloid Cardiomyopathy (ATTR-CM)". StatPearls. StatPearls Publishing. PMID ...
... or Cardiomyopathy - often with hypertrophy, restrictive physiology, and congestive heart failure. The changes may be ... Tönnesmann E, Kandolf R, Lewalter T (June 2013). "Chloroquine cardiomyopathy - a review of the literature". Immunopharmacology ...
Jesica, whose blood was type O-positive, had a heart condition (restrictive cardiomyopathy and secondary nonreactive pulmonary ...
... due to myocardial calcification Cardiomyopathy, X linked, fatal infantile Restrictive cardiomyopathy Cardioskeletal myopathy- ... Cardiomyopathy, familial dilated Cardiomyopathy due to anthracyclines Cardiomyopathy hearing loss type t RNA lysine gene ... familial Cardiomyopathy hypogonadism metabolic anomalies Cardiomyopathy spherocytosis Cardiomyopathy, fatal fetal, ... right ventricular cardiomyopathy Cardiomyopathic lentiginosis Cardiomyopathy cataract hip spine disease Cardiomyopathy diabetes ...
... restrictive cardiomyopathy due to cardiac fibrosis, or blockage of arteries due to the embolization of blood clots that from in ...
... striate palmoplantar keratoderma with woolly hair and cardiomyopathy, striate palmoplantar keratoderma with woolly hair and ... Relapsing linear acantholytic dermatosis Restrictive dermopathy Rhizomelic chondrodysplasia punctata (autosomal recessive ... diffuse palmoplantar keratoderma with woolly hair and arrythmogenic right ventricular cardiomyopathy of Naxos, Naxos disease) ... diffuse non-epidermolytic palmoplantar keratoderma with woolly hair and cardiomyopathy, ...
MYL3 Cardiomyopathy, familial restrictive; 115210; TNNI3 Cardiomyopathy, familial restrictive, 3; 612422; TNNT2 Cardiomyopathy ... TNNI3 Cardiomyopathy, dilated, 1G; 604145; TTN Cardiomyopathy, dilated, 1GG; 613642; SDHA Cardiomyopathy, dilated, 1I; 604765; ... DES Cardiomyopathy, dilated, 1J; 605362; EYA4 Cardiomyopathy, dilated, 1L; 606685; SGCD Cardiomyopathy, dilated, 1M; 607482; ... TCAP Cardiomyopathy, dilated, 1O; 608569; ABCC9 Cardiomyopathy, dilated, 1P; 609909; PLN Cardiomyopathy, dilated, 1R; 613424; ...
In neonates with a small atrial septal defect, termed "restrictive", there is inadequate mixing of oxygenated and deoxygenated ... and a selective left ventricular cardiomyopathy. Genetic loci associated with HLHS include GJA1 (connexin 43), HAND1, NKX2.5, ... a genetic syndrome or those with a highly restrictive atrial septum. For patients without these additional risk factors, 5 year ...
Hypertrophic cardiomyopathy (HCM) is a health concern in many pure breed cats. The Bengal cat (a similar hybrid) is prone to ... Some states have set more restrictive laws on hybrid cat ownership, including Hawaii, Massachusetts, Texas and Georgia. Some ...
Diabetic cardiomyopathy, damage to the heart muscle, leading to impaired relaxation and filling of the heart with blood ( ... In fact the presence restrictive lung defect in association with diabetes has been shown even in presence of obstructive lung ... Increased risk of wound infections Restrictive lung disease is known to be associated with diabetes. Lung restriction in ... Kobayashi S, Liang Q (May 2014). "Autophagy and mitophagy in diabetic cardiomyopathy". Biochim Biophys Acta. S0925-4439 (14): ...
A restrictive N-terminal truncation of cTnI occurs at low levels in normal hearts of all vertebrate species examined including ... Multiple mutations in cTnI have been found to cause cardiomyopathies. cTnI mutations account for approximately 5% of familial ... Restrictive N-terminal truncation: The approximately 30 amino acids N-terminal extension of cTnI is an adult heart-specific ... Distinct from the harmful C-terminal truncation, the restrictive N-terminal truncation of cTnI selectively removing the adult ...
Restrictive cardiomyopathy Revenue cycle management, the process used by healthcare systems in the United States to track ...
... restrictive cardiomyopathies) a similar sound can be heard, but is usually more high-pitched and is called a 'pericardial knock ... Dilated cardiomyopathy - the ventricular walls are abnormal for a variety of reasons, and become thin and stiff so do not relax ...
Such restrictive diets can be difficult for the patient and family to maintain, and require close consultation with a ... Adult genetics cardiomyopathy and cardiac dysrhythmias inherited kidney disease dementia and neurodegeneration connective ...
... since some of the restrictive policies around abortion could impede access to these services. These policies may also affect ... cardiomyopathy (10.3%), pulmonary embolism (9.1%), cerebrovascular accidents (7.4%), hypertensive disorders of pregnancy (6.8 ... repercussions or legal activity in countries where unsafe abortion is common since it is more likely to be legally restrictive ...
Mutations in Filamin C have been associated with human hypertrophic cardiomyopathy, restrictive cardiomyopathy and a higher ... "Mutations in FLNC are Associated with Familial Restrictive Cardiomyopathy". Human Mutation. 37 (3): 269-79. doi:10.1002/humu. ... "Mutations in filamin C cause a new form of familial hypertrophic cardiomyopathy" (PDF). Nature Communications. 5: 5326. Bibcode ...
A rare condition called restrictive cardiomyopathy affects the heart and how it can be treated. Heres what you need to know. ... What Is Restrictive Cardiomyopathy?. Restrictive cardiomyopathy is when the walls of the lower chambers of your heart (called ... Heart Disease and Restrictive Cardiomyopathy Written by WebMD Editorial Contributors Medically Reviewed by James Beckerman, MD ... In some cases, restrictive cardiomyopathy may be confused with something called constrictive pericarditis. Thats where the ...
Restrictive cardiomyopathy refers to a set of changes in how the heart muscle functions. These changes cause the heart to fill ... Restrictive cardiomyopathy may affect either or both of the lower heart chambers (ventricles). Restrictive cardiomyopathy is a ... Restrictive cardiomyopathy refers to a set of changes in how the heart muscle functions. These changes cause the heart to fill ... The dilated, restrictive, and infiltrative cardiomyopathies. In: Libby P, Bonow RO, Mann DL, Tomaselli GF, Bhatt DL, Solomon SD ...
Restrictive Cardiomyopathy Treatment Market. Market Insights on Restrictive Cardiomyopathy Treatment covering sales outlook, ... Restrictive Cardiomyopathy Treatment Market by Treatment, Type, End-User & Region , Forecast 2023 to 2033 ...
Restrictive cardiomyopathy (RCM) is a common myocardial disease in cats, characterized by diastolic dysfunction and atrial ... detection of myocardial dysfunction in a cat that gradually progressed to endomyocardial form of restrictive cardiomyopathy ...
Restrictive cardiomyopathy. This rare type of cardiomyopathy causes the ventricles to stiffen, but the walls of the heart do ... Transthyretin amyloid cardiomyopathy is a rare type of restrictive cardiomyopathy that is more common in African-American men. ... Another type of cardiomyopathy - called peripartum cardiomyopathy - can occur during or after pregnancy. This happens most ... Hypertrophic cardiomyopathy. This type of cardiomyopathy causes the heart muscle to become larger and thicker than normal. The ...
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Learn about cardiomyopathy, a collection of conditions that affect the heart muscle. Read about its causes and treatment and ... Chapter 34: Restrictive, obliterative, and infiltrative cardiomyopathies. In: Fuster V, Walsh RA, Harrington RA (Eds). Hursts ... Pediatric Cardiomyopathy. Cardiomyopathy can occur in children regardless of age, race, and gender. Pediatric cardiomyopathy ... www.heart.org/en/health-topics/cardiomyopathy/what-is-cardiomyopathy-in-adults/peripartum-cardiomyopathy-ppcm/ ...
Familial restrictive cardiomyopathy. MedlinePlus Genetics provides information about Familial restrictive cardiomyopathy. More ... Familial hypertrophic cardiomyopathy. Mutations in the TNNT2 gene can cause familial hypertrophic cardiomyopathy, a condition ... Familial dilated cardiomyopathy. Mutations in the TNNT2 gene have been found in people with a heart condition called familial ... Familial dilated cardiomyopathy is a condition that weakens and enlarges the heart, preventing it from pumping blood ...
Wen, Y., Xu, Y., Wang, Y., Pinto, J., Potter, J., & Kerrick, W. (2009). Functional Effects of a Restrictive-Cardiomyopathy- ... Wen, Y., Xu, Y., Wang, Y., Pinto, J., Potter, J., & Kerrick, W. (2009). Functional Effects of a Restrictive-Cardiomyopathy- ... The human cardiac troponin I (hcTnI) mutation R145W has been associated with restrictive cardiomyopathy. In this study, ... Functional Effects of a Restrictive-Cardiomyopathy-Linked Cardiac Troponin I Mutation (R145W) in Transgenic Mice. ...
Explore more about Restrictive Cardiomyopathy Epidemiology at: Restrictive Cardiomyopathy Epidemiology Insights. Restrictive ... Restrictive Cardiomyopathy: An Overview. Restrictive cardiomyopathy refers to a set of changes in how the heart muscle ... Restrictive Cardiomyopathy Market The Restrictive Cardiomyopathy market outlook of the report helps to build a detailed ... Restrictive Cardiomyopathy Epidemiology The Restrictive Cardiomyopathy epidemiology section provides insights into the ...
Inherited restrictive cardiomyopathy in a 74-year-old woman: A case of Fabrys disease. American heart journal. 1995 Jan;129(1 ... Inherited restrictive cardiomyopathy in a 74-year-old woman : A case of Fabrys disease. In: American heart journal. 1995 ; Vol ... Inherited restrictive cardiomyopathy in a 74-year-old woman: A case of Fabrys disease. / Hillsley, Russell E.; Hernandez, ... Hillsley, R. E., Hernandez, E., Steenbergen, C., Bashore, T. M., & Harrison, J. K. (1995). Inherited restrictive cardiomyopathy ...
Restrictive cardiomyopathy. This is the least common type of cardiomyopathy. It can occur for no known reason. Sometimes its ... The cause of cardiomyopathy depends on the type:. *Dilated cardiomyopathy. The cause of this most common type of cardiomyopathy ... Heart disease symptoms caused by diseased heart muscle (cardiomyopathy). Early stages of cardiomyopathy may not cause ... Hypertrophic cardiomyopathy. This type is usually passed down through families (inherited).. * ...
Restrictive cardiomyopathy * Prolonged hypovolemic or septic shock * Ventricular interdependence * External compression by ...
Ischemic Cardiomyopathy In patients with ischemic cardiomyopathy, TTE may show segmental areas of systolic dysfunction that are ... and restrictive physiology (Figure 2a). Longitudinal myocardial strain polar maps (measured by speckle-tracking ... Dilated Cardiomyopathy. Dilated cardiomyopathy (DCM) is characterized by dilated LV cavity size, LV systolic dysfunction, and ... Hypertrophic Cardiomyopathy. In hypertrophic cardiomyopathy (HCM), the most common site of hypertrophy is where the basal ...
Familial restrictive cardiomyopathy Familial restrictive cardiomyopathy is a genetic form of heart disease. For the heart to ... X-linked dilated cardiomyopathy X-linked dilated cardiomyopathy is a form of heart disease. Dilated cardiomyopathy enlarges and ... Familial dilated cardiomyopathy Familial dilated cardiomyopathy is a genetic form of heart disease. It occurs when heart ( ... Cardiomyopathy (National Library of Medicine) Cardiomyopathy is the name for diseases of the heart muscle. These diseases ...
Hypertrophic or restrictive cardiomyopathy. *Single ventricle heart disease. *Coronary allograft vasculopathy and retransplant ...
Cardiomyopathies and Myocarditis. 5.5.1. Dilated Cardiomyopathy (CMP). 5.5.2. Restrictive Cardiomyopathy ...
24 Hypertrophic Cardiomyopathy. 25 Restrictive Cardiomyopathy. 26 Heart Failure: Acute (In-hospital) Management. 27 Heart ... 22 LV dysfunction and Dilated Cardiomyopathy: Etiologies and Evaluation. 23 Heart Failure with Preserved Ejection Fraction. ...
Characteristics of subjects with alcoholic cardiomyopathy and sudden cardiac death Siiri Hietanen, Johanna Herajärvi, Juhani ...
... active obstructive or restrictive pulmonary disease; or active autoimmune diseases such as rheumatoid arthritis. -Patients will ... QT prolongation and cardiomyopathy); active cardiac arrhythmias (Active atrial fibrillation is not allowed, but resolved atrial ...
Cardiomyopathy with restrictive physiology in sickle cell disease. JACC Cardiovasc Imaging 2016; 9: 243-252. ... restrictive cardiomyopathy has been better recognised and described in clinical and experimental studies [68]. These data ...
Restrictive Cardiomyopathy. Reticulocytosis. Synonym: Increased Immature Red Blood Cells. Synonym: Increased Number of Immature ...
Title: Novel Missense Variant in MYL2 Gene Associated With Hypertrophic Cardiomyopathy Showing High Incidence of Restrictive ... Novel Missense Variant in MYL2 Gene Associated With Hypertrophic Cardiomyopathy Showing High Incidence of Restrictive ... Novel Missense Variant in MYL2 Gene Associated With Hypertrophic Cardiomyopathy Showing High Incidence of Restrictive ... Molecular basis of force-pCa relation in MYL2 cardiomyopathy mice: Role of the super-relaxed state of myosin. Yuan CC, et al. ...
Allelic with hereditary cardiomyopathy syndromes (CMD 1G, CMH 9, EOMFC [early onset myopathy with fatal cardiomyopathy]). ... Progression to wheelchair by the teenage years and restrictive respiratory failure (even when patients are ambulant) is common ... Cardiomyopathy occurs in about 50%. Presentation with an isolated, dilated cardiomyopathy has been described. ... The disease is also allelic with dilated cardiomyopathy 1G, autosomal recessive congenital myopathy with lethal cardiomyopathy ...
1. Significant Restrictive or Obstructive Lung Disease 2. Ischemic heart disease 3. Left ventricular dysfunction 4. Acute ... 5. Cardiomyopathy (dilated, hypertrophic, or non-idiopathic) 6. Significant renal or hepatic dysfunction 7. Disabling stroke 8 ...
Primary cardiac lymphoma presenting clinically as restrictive cardiomyopathy.. Fujisaki J; Tanaka T; Kato J; Saito T; Yano K; ...
Such disorders include restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease, and acute cor pulmonale. ... patients with hypertrophic cardiomyopathy, patients with renal or hepatic dysfunction, and other patients who are volume- ...
"4. Heart failure associated with unexplained restrictive cardiomyopathy. (Level of Evidence: C) " ... "3. Heart failure associated with suspected anthracycline cardiomyopathy. (Level of Evidence: C) " ... Complications may be as high as 6% as observed in a series where 546 patients with cardiomyopathy underwent right ventricular ... Wu LA, Lapeyre AC, Cooper LT (2001). "Current role of endomyocardial biopsy in the management of dilated cardiomyopathy and ...
Im in my early 20s and I have Restrictive Cardiomyopathy. I have always known about my heart not being able to function ... Being introduced to Cardiomyopathy UK has been a huge help as, I got to learn more about restrictive cardiomyopathy by the ... Im in my early 20s and I have Restrictive Cardiomyopathy.. I have always known about my heart not being able to function ... Cardiomyopathy was first mentioned at the age of eleven and did not mean that much to me at that time. By this age, my family ...
  • The image above shows a healthy heart and a heart muscle that is larger and thicker because of hypertrophic cardiomyopathy. (nih.gov)
  • Mutations in the TNNT2 gene can cause familial hypertrophic cardiomyopathy, a condition characterized by thickening (hypertrophy) of the cardiac muscle. (nih.gov)
  • Although some people with hypertrophic cardiomyopathy have no obvious health effects, all affected individuals have an increased risk of heart failure and sudden death. (nih.gov)
  • Most TNNT2 gene mutations in familial hypertrophic cardiomyopathy change single protein building blocks (amino acids) in the cardiac troponin T protein. (nih.gov)
  • However, it is unclear how the gene mutations lead to the features of familial hypertrophic cardiomyopathy. (nih.gov)
  • Hypertrophic cardiomyopathy: the genetic determinants of clinical disease expression. (nih.gov)
  • Hypertrophic cardiomyopathy is thought to be the most common inherited or genetic heart disease. (cdc.gov)
  • Myocardial strain imaging, a reproducible measure of LV systolic function, can identify subclinical LV dysfunction and patterns that suggest specific cardiomyopathies (eg, ischemic cardiomyopathy, amyloidosis, hypertrophic cardiomyopathy, chemotherapy-induced cardiotoxicity). (medscape.com)
  • Hypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. (nih.gov)
  • Mutations in this gene are associated with hypertrophic cardiomyopathy 10 and infant-onset myopathy. (nih.gov)
  • Novel Missense Variant in MYL2 Gene Associated With Hypertrophic Cardiomyopathy Showing High Incidence of Restrictive Physiology. (nih.gov)
  • Induced Pluripotent Stem Cell-Derived Cardiomyocytes from a Patient with MYL2-R58Q-Mediated Apical Hypertrophic Cardiomyopathy Show Hypertrophy, Myofibrillar Disarray, and Calcium Perturbations. (nih.gov)
  • Current research is being conducted on the relationship between Myosin light chain 3 and a multitude of diseases and disorders, including familial hypertrophic cardiomyopathy, congestive heart failure, restrictive cardiomyopathy, dilated cardiomyopathy, diabetes mellitus, and renal failure. (novusbio.com)
  • Arrhythmogenic cardiomyopathy usually affects teens or young adults, and it raises the risk for cardiac arrest . (nih.gov)
  • While this type of cardiomyopathy occurs at many ages, in children and young adults with this condition there may be no symptoms, yet they are at high risk of sudden cardiac death. (cdc.gov)
  • A family history of cardiomyopathy, heart failure or sudden cardiac arrest. (cdc.gov)
  • The human cardiac troponin I (hcTnI) mutation R145W has been associated with restrictive cardiomyopathy. (fsu.edu)
  • Thanks to technologic advances in cardiac imaging, multimodality studies provide insight into the pathophysiology of both ischemic and nonischemic cardiomyopathy. (medscape.com)
  • In this overview based on the latest research, we discuss the integral role of comprehensive imaging studies, particularly transthoracic echocardiography (TTE) and cardiac magnetic resonance imaging (CMR), in differentiating potential causes of HF and diagnosing various cardiomyopathies. (medscape.com)
  • 18. Primary cardiac lymphoma presenting clinically as restrictive cardiomyopathy. (nih.gov)
  • Cardiac failure is the most common cardiovascular manifestation cardiomyopathy (HCM), restrictive cardiomyopathy (RCM), in urban Africa. (who.int)
  • Mutations in the TNNT2 gene have been found in people with a heart condition called familial dilated cardiomyopathy. (nih.gov)
  • Familial dilated cardiomyopathy is a condition that weakens and enlarges the heart, preventing it from pumping blood efficiently. (nih.gov)
  • Familial dilated cardiomyopathy increases the risk of heart failure and premature death. (nih.gov)
  • Familial dilated cardiomyopathy is a genetic form of heart disease. (nih.gov)
  • 76%). Of 50 pedigrees analysed, 14 (28%) were positive and likely to be indicative of familial dilated cardiomyopathy (DCM), and 9 (18%) patients were at intermediate risk of familial disease. (who.int)
  • Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a form of heart disease that usually appears in adulthood. (nih.gov)
  • 1] Dilated cardiomyopathy (DCM), defined as left arrhythmogenic right ventricular cardiomyopathy (ARVC) and LV ventri cular (LV) dilatation and systolic dysfunction, is a major cause non-compaction cardiomyopathy (LVNCC). (who.int)
  • Another type of cardiomyopathy - called peripartum cardiomyopathy - can occur during or after pregnancy. (nih.gov)
  • Peripartum cardiomyopathy is rare but serious. (nih.gov)
  • Peripartum cardiomyopathy (PPCM) is a rare form of heart failure that can occur near the end of pregnancy or up to a year after giving birth. (cdc.gov)
  • Peripartum cardiomyopathy is a rare disorder in which a pregnant woman's heart becomes weakened and enlarged. (nih.gov)
  • The principal utility of CMR and its advantage over echocardiography for cardiomyopathy is its use of late gadolinium enhancement (LGE) , which visualizes myocardial tissue and detects scar, fibrosis, or infiltration. (medscape.com)
  • Further, T2* mapping, another parametric imaging approach, can detect and quantify myocardial iron deposition, primarily to assess iron overload cardiomyopathy. (medscape.com)
  • DelveInsight's "Restrictive Cardiomyopathy Market Insights, Epidemiology, and Market Forecast-2032" report delivers an in-depth understanding of Restrictive Cardiomyopathy, historical and forecasted epidemiology as well as the Restrictive Cardiomyopathy market trends in the United States, EU5 (Germany, Spain, Italy, France, and United Kingdom), and Japan. (jamshedpurreporter.in)
  • Although the cause of cardiomyopathy is sometimes unknown, certain diseases or conditions can lead to cardiomyopathy. (cdc.gov)
  • Cardiomyopathy is the name for diseases of the heart muscle. (nih.gov)
  • Genetic or inherited types of cardiomyopathy cannot be prevented, but adopting or following a healthier lifestyle can help control symptoms and complications. (cdc.gov)
  • 7] Genetic conditions of heart failure in adults between the third and fourth decades of with dilated cardiomyopathy as a presenting feature include the life. (who.int)
  • Contact your health care provider if you have symptoms of restrictive cardiomyopathy. (medlineplus.gov)
  • Some people who have cardiomyopathy never have symptoms, while others may show signs as the disease progresses. (cdc.gov)
  • Familial disease is implicated in 20 - 50% of cases of idiopathic dilated cardiomyopathy (IDCM) worldwide. (who.int)
  • Transthoracic echocardiography , the most widely available initial standard of care test for ventricular dysfunction, can help differentiate ischemic and nonischemic etiologies of cardiomyopathies. (medscape.com)
  • Forma de enfermedad del MIOCARDIO en la que las paredes ventriculares son excesivamente rígidas, impidiendo el llenado ventricular. (bvsalud.org)
  • An aclinical Havanese dog was diagnosed with a membranous restrictive ventricular septal defect. (bvsalud.org)
  • This rare type of cardiomyopathy occurs when the left ventricle develops muscle that is both smooth, as it should be, and loose, like a thick web. (nih.gov)
  • Restrictive cardiomyopathy is when the walls of the lower chambers of your heart (called the ventricles) are too rigid to expand as they fill with blood . (webmd.com)
  • Restrictive cardiomyopathy may affect either or both of the lower heart chambers (ventricles). (medlineplus.gov)
  • In patients with ischemic cardiomyopathy, TTE may show segmental areas of systolic dysfunction that are typically localized to a coronary distribution. (medscape.com)
  • Based on the 1989 U.S. National Health Inter- ter 7, adults with diabetes are more likely than those view Survey (NHIS), 3% of men and women without diabetes to have hypert en sion and age 18-44 years who reported having diabetes dyslipidemia (low levels of high-density lipoprotein, also reported having ischemic heart disease. (nih.gov)
  • When cardiomyopathy occurs, the normal muscle in the heart can thicken, stiffen, thin out, or fill with substances the body produces that do not belong in the heart muscle. (cdc.gov)
  • Cardiomyopathy occurs when there is damage to the heart. (nih.gov)
  • Contact to receive a sample @ Restrictive Cardiomyopathy Market Outlook 2032 . (jamshedpurreporter.in)
  • The Restrictive Cardiomyopathy market outlook of the report helps to build a detailed comprehension of the historical, current, and forecasted Restrictive Cardiomyopathy market trends by analyzing the impact of current Restrictive Cardiomyopathy therapies on the market and unmet needs, and drivers, barriers, and demand for better technology. (jamshedpurreporter.in)
  • Clinical and functional characterization of TNNT2 mutations identified in patients with dilated cardiomyopathy. (nih.gov)
  • These functional results help to explain the mechanisms by which these mutations give rise to a restrictive phenotype. (fsu.edu)
  • Cardiomyopathy can be acquired-developed because of another disease, condition, or factor-or inherited. (cdc.gov)
  • If you have an underlying disease or condition that can cause cardiomyopathy, early treatment of that condition can help prevent the disease from developing. (cdc.gov)
  • Cardiomyopathy is disease in which the heart muscle becomes weakened, stretched, or has another structural problem. (nih.gov)
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  • Molecular basis of force-pCa relation in MYL2 cardiomyopathy mice: Role of the super-relaxed state of myosin. (nih.gov)
  • In some cases, restrictive cardiomyopathy may be confused with something called constrictive pericarditis . (webmd.com)
  • Restrictive cardiomyopathy may appear similar to constrictive pericarditis . (medlineplus.gov)
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  • Treatment also depends on which type of cardiomyopathy you have. (cdc.gov)
  • Few treatments are known to work well for restrictive cardiomyopathy. (medlineplus.gov)
  • Visit our Pregnancy and Cardiomyopathy page to learn what raises your risk and how to recognize the warning signs. (nih.gov)
  • The frequency of clearly abnormal serum values of 15 parameters analysed, however, was low even in patients with signs of restrictive cardiomyopathy. (helsinki.fi)
  • People with restrictive cardiomyopathy may be heart transplant candidates. (medlineplus.gov)
  • The Restrictive Cardiomyopathy report provides insights into different therapeutic candidates in Phase II, and Phase III stages. (jamshedpurreporter.in)
  • The Restrictive Cardiomyopathy market report provides current treatment practices, emerging drugs, the market share of the individual therapies, and the current and forecasted Restrictive Cardiomyopathy market size from 2019 to 2032, segmented by seven major markets. (jamshedpurreporter.in)
  • The Report also covers current Restrictive Cardiomyopathy treatment practice/algorithm, market drivers, market barriers, and unmet medical needs to curate the best opportunities and assesses the underlying potential of the Restrictive Cardiomyopathy market. (jamshedpurreporter.in)
  • Learn more about Restrictive Cardiomyopathy, treatment algorithms in different geographies, and patient journeys. (jamshedpurreporter.in)
  • Restrictive cardiomyopathy is a rare condition. (medlineplus.gov)
  • The condition causing the cardiomyopathy is treated when it can be found. (medlineplus.gov)
  • As I was getting older and living with cardiomyopathy, I started to take on more of my responsibilities with my condition. (cardiomyopathy.org)
  • Transthyretin amyloid cardiomyopathy is a rare type of restrictive cardiomyopathy that is more common in African-American men. (nih.gov)
  • This is more common in males and is the most common form of cardiomyopathy in children. (cdc.gov)
  • How common is cardiomyopathy? (cdc.gov)
  • Dilated cardiomyopathy is more common in blacks than in whites and in males than in females. (cdc.gov)
  • Friedreich's ataxia, Barth syndrome, mitochondrial myopathies and cardiomyopathy (IDCM) was the second most common form of numerous inborn errors of metabolism. (who.int)
  • In a case of restrictive cardiomyopathy, the heart muscle is of normal size or slightly enlarged. (medlineplus.gov)
  • If you are diagnosed with cardiomyopathy, your doctor may tell you to change your diet and physical activity, reduce stress, avoid alcohol and other drugs, and take medicines. (cdc.gov)
  • This section focuses on the uptake rate of the potential Restrictive Cardiomyopathy drugs recently launched in the Restrictive Cardiomyopathy market or expected to be launched in 2019-2032. (jamshedpurreporter.in)
  • The analysis covers the Restrictive Cardiomyopathy market uptake by drugs, patient uptake by therapies, and sales of each drug. (jamshedpurreporter.in)
  • Restrictive Cardiomyopathy Drugs Uptake helps in understanding the drugs with the most rapid uptake and the reasons behind the maximal use of new drugs and allows the comparison of the drugs based on Restrictive Cardiomyopathy market share and size, which again will be useful in investigating factors important in market uptake and in making financial and regulatory decisions. (jamshedpurreporter.in)
  • Being introduced to Cardiomyopathy UK has been a huge help as, I got to learn more about restrictive cardiomyopathy by the massive support from the panel members and all the advice at the conferences explaining about different aspects of cardiomyopathy. (cardiomyopathy.org)
  • Some people live long, healthy lives with cardiomyopathy. (nih.gov)
  • The Restrictive Cardiomyopathy epidemiology section provides insights into the historical and current Restrictive Cardiomyopathy patient pool and forecasted trends for seven individual major countries. (jamshedpurreporter.in)
  • This part of the Restrictive Cardiomyopathy market report also provides the diagnosed patient pool, trends, and assumptions. (jamshedpurreporter.in)