Cardiomyopathy, Dilated: 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.Cardiomyopathy, Hypertrophic: 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).Cardiomyopathies: 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).Cardiomyopathy, Restrictive: 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.Takotsubo Cardiomyopathy: 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.Cardiomyopathy, Hypertrophic, Familial: 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.Chagas Cardiomyopathy: 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.Myocardium: 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.Cardiomyopathy, Alcoholic: 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).Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.Arrhythmogenic Right Ventricular Dysplasia: 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.Diabetic Cardiomyopathies: 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.Electrocardiography: 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.Ventricular Function, Left: 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.Myocarditis: 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.Ventricular Dysfunction, Left: 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.Heart Ventricles: 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.Heart Septum: This structure includes the thin muscular atrial septum between the two HEART ATRIA, and the thick muscular ventricular septum between the two HEART VENTRICLES.Heart Failure: 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.Ventricular Outflow Obstruction: 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.Myocardial Contraction: Contractile activity of the MYOCARDIUM.Myocytes, Cardiac: Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).Heart: The hollow, muscular organ that maintains the circulation of the blood.Stroke Volume: 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.Death, Sudden, Cardiac: 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)Cardiac Myosins: Myosin type II isoforms found in cardiac muscle.Peripartum Period: The period shortly before, during, and immediately after giving birth.Echocardiography, Doppler: 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.Ventricular Myosins: 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.Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.Tachycardia, Ventricular: 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).Sarcomeres: The repeating contractile units of the MYOFIBRIL, delimited by Z bands along its length.Endomyocardial Fibrosis: 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).Pedigree: 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.Myocardial Ischemia: 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).Myosin Heavy Chains: 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.Hypertrophy, Left Ventricular: 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.Arrhythmias, Cardiac: 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.Endocardium: The innermost layer of the heart, comprised of endothelial cells.Plakophilins: Members of the armadillo family of proteins that are found in DESMOSOMES and interact with various proteins including desmocadherins; DESMOPLAKIN; ACTIN FILAMENTS; and KERATINS.Heart Transplantation: The transference of a heart from one human or animal to another.Mutation: 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.Lamin Type A: A subclass of developmentally regulated lamins having a neutral isoelectric point. They are found to disassociate from nuclear membranes during mitosis.Ventricular Remodeling: 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.Troponin T: 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.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Cardiac Pacing, Artificial: Regulation of the rate of contraction of the heart muscles by an artificial pacemaker.Diastole: Post-systolic relaxation of the HEART, especially the HEART VENTRICLES.Heart Diseases: Pathological conditions involving the HEART including its structural and functional abnormalities.Puerperal Disorders: Disorders or diseases associated with PUERPERIUM, the six-to-eight-week period immediately after PARTURITION in humans.Sarcoglycans: A family of transmembrane dystrophin-associated proteins that play a role in the membrane association of the DYSTROPHIN-ASSOCIATED PROTEIN COMPLEX.Cardiomegaly: 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.Defibrillators, Implantable: 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.Death, Sudden: The abrupt cessation of all vital bodily functions, manifested by the permanent loss of total cerebral, respiratory, and cardiovascular functions.Magnetic Resonance Imaging, Cine: 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.Desmoglein 2: A CALCIUM-dependent adhesion molecule of DESMOSOMES that also plays a role in embryonic STEM CELL proliferation.Follow-Up Studies: 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.Systole: Period of contraction of the HEART, especially of the HEART VENTRICLES.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Disease Models, Animal: 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.Cardiac Catheterization: Procedures in which placement of CARDIAC CATHETERS is performed for therapeutic or diagnostic procedures.Glycogen Storage Disease Type IIb: 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.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Mutation, Missense: 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)Isolated Noncompaction of the Ventricular Myocardium: 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.Pregnancy Complications, Cardiovascular: 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.Desmin: 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.Dystrophin: 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.Treatment Outcome: 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.Ventricular Dysfunction: A condition in which HEART VENTRICLES exhibit impaired function.Adrenergic beta-Antagonists: 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.Mitral Valve: The valve between the left atrium and left ventricle of the heart.Heart Function Tests: Examinations used to diagnose and treat heart conditions.Mitral Valve Insufficiency: 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.Ablation Techniques: 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.3-Iodobenzylguanidine: 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.Prognosis: 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.Cardiotonic Agents: 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).Catheter Ablation: 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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Heart Block: 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.Predictive Value of Tests: 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.Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.Muscular Dystrophy, Duchenne: 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)Syncope: 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)Epicardial Mapping: 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.Tropomyosin: A protein found in the thin filaments of muscle fibers. It inhibits contraction of the muscle unless its position is modified by TROPONIN.Electrocardiography, Ambulatory: 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.Prospective Studies: 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.Ventricular Dysfunction, Right: 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.Connectin: 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.Myofibrils: 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 .Mitochondria, Heart: The mitochondria of the myocardium.Bundle-Branch Block: 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.Electrophysiologic Techniques, Cardiac: Methods to induce and measure electrical activities at specific sites in the heart to diagnose and treat problems with the heart's electrical system.Troponin I: One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.Myosins: 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, Doppler, Color: Echocardiography applying the Doppler effect, with the superposition of flow information as colors on a gray scale in a real-time image.Tachycardia: 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.Coxsackievirus Infections: 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.Pericarditis, Constrictive: 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.Case-Control Studies: 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.Coronary Circulation: The circulation of blood through the CORONARY VESSELS of the HEART.Propanolamines: AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.Heart-Assist Devices: 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.Retrospective Studies: 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.Pacemaker, Artificial: A device designed to stimulate, by electric impulses, contraction of the heart muscles. It may be temporary (external) or permanent (internal or internal-external).Natriuretic Peptide, Brain: 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.Genetic Testing: 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, Doppler, Pulsed: 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.IodobenzenesDesmocollins: A group of desmosomal cadherins with cytoplasmic tails that are divergent from those of classical CADHERINS. Their intracytoplasmic domains bind PLAKOGLOBIN; PLAKOPHILINS; and DESMOPLAKINS.DNA Mutational Analysis: Biochemical identification of mutational changes in a nucleotide sequence.LIM Domain Proteins: 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.Severity of Illness Index: Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.Magnetic Resonance Imaging: 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: Desmoplakins are cytoskeletal linker proteins that anchor INTERMEDIATE FILAMENTS to the PLASMA MEMBRANE at DESMOSOMES.Heart Conduction System: 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.Noonan Syndrome: 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.Receptors, Adrenergic, beta-1: 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.Desmosomes: 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)Ventricular Pressure: 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.Muscle Proteins: The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.Carbazoles: Benzo-indoles similar to CARBOLINES which are pyrido-indoles. In plants, carbazoles are derived from indole and form some of the INDOLE ALKALOIDS.Exercise Test: 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.Dobutamine: 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.Ventricular Premature Complexes: 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.Cardiac Output, Low: 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.Fatal Outcome: 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.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Heterozygote: An individual having different alleles at one or more loci regarding a specific character.Doxorubicin: Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.Diabetes Mellitus, Experimental: Diabetes mellitus induced experimentally by administration of various diabetogenic agents or by PANCREATECTOMY.Friedreich Ataxia: 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)Muscular Dystrophies: 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.Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.Ventricular Septum: 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.Penetrance: 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)Radionuclide Ventriculography: 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.Amyloidosis: 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.Mitochondrial Myopathies: A group of muscle diseases associated with abnormal mitochondria function.Sarcoplasmic Reticulum Calcium-Transporting ATPases: 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.Antibiotics, Antineoplastic: Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.Disease Progression: 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.Ventricular Fibrillation: 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.Heart Aneurysm: 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.Atrial Natriuretic Factor: 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.Sports: Activities or games, usually involving physical effort or skill. Reasons for engagement in sports include pleasure, competition, and/or financial reward.Anti-Arrhythmia Agents: 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.Risk Factors: 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.Trypanosoma cruzi: 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.Enterovirus B, Human: 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.Gadolinium DTPA: 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)Barth Syndrome: 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.Atrioventricular Block: Impaired impulse conduction from HEART ATRIA to HEART VENTRICLES. AV block can mean delayed or completely blocked impulse conduction.Enterovirus: 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".Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Calcium: 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.Contrast Media: Substances used to allow enhanced visualization of tissues.Papillary Muscles: Conical muscular projections from the walls of the cardiac ventricles, attached to the cusps of the atrioventricular valves by the chordae tendineae.Coronary Angiography: Radiography of the vascular system of the heart muscle after injection of a contrast medium.Body Surface Potential Mapping: 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)Survival Analysis: 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.Mice, Knockout: 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.Phonocardiography: 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.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Muscular Diseases: Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.Gated Blood-Pool Imaging: 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).Angiocardiography: Radiography of the heart and great vessels after injection of a contrast medium.gamma Catenin: 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.Mice, Inbred mdx: 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: 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.Ventricular Function, Right: The hemodynamic and electrophysiological action of the right HEART VENTRICLE.Heart Atria: The chambers of the heart, to which the BLOOD returns from the circulation.Mice, Inbred C57BLSyndrome: A characteristic symptom complex.Fabry Disease: 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.Survival Rate: 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.LEOPARD Syndrome: 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.Chronic Disease: 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)Amiodarone: 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.Ethanol: 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.Echocardiography, Stress: A method of recording heart motion and internal structures by combining ultrasonic imaging with exercise testing (EXERCISE TEST) or pharmacologic stress.Endocardial Fibroelastosis: 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.alpha-Crystallin B Chain: 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.Biological Markers: 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.Pericardium: 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.Exercise Tolerance: The exercise capacity of an individual as measured by endurance (maximal exercise duration and/or maximal attained work load) during an EXERCISE TEST.Totiviridae: A family of RNA viruses that infect fungi and protozoa. There are three genera: TOTIVIRUS; GIARDIAVIRUS; and LEISHMANIAVIRUS.Cardiac Complexes, Premature: 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.Myocardial Stunning: Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.Organ Size: The measurement of an organ in volume, mass, or heaviness.Risk Assessment: 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)Hypertrophy: 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).Receptors, Adrenergic, beta: 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.Oxidative Stress: 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).Cardiac Resynchronization Therapy: The restoration of the sequential order of contraction and relaxation of the HEART ATRIA and HEART VENTRICLES by atrio-biventricular pacing.Desmosomal Cadherins: A single-pass transmembrane glycoproteins that mediate CALCIUM-dependent CELL ADHESION and are core components of DESMOSOMES.Cardiotoxins: 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.Ventricular Function: The hemodynamic and electrophysiological action of the HEART VENTRICLES.

Coexistence of mitochondrial DNA and beta myosin heavy chain mutations in hypertrophic cardiomyopathy with late congestive heart failure. (1/1667)

OBJECTIVE: To investigate the possible coexistence of mitochondrial DNA (mtDNA) mutations in patients with beta myosin heavy chain (beta MHC) linked hypertrophic cardiomyopathy (HCM) who develop congestive heart failure. DESIGN: Molecular analysis of beta MHC and mtDNA gene defects in patients with HCM. SETTING: Cardiovascular molecular diagnostic and heart transplantation reference centre in north Italy. PATIENTS: Four patients with HCM who underwent heart transplantation for end stage heart failure, and after pedigree analysis of 60 relatives, eight additional affected patients and 27 unaffected relatives. A total of 111 unrelated healthy adult volunteers served as controls. Disease controls included an additional 27 patients with HCM and 102 with dilated cardiomyopathy. INTERVENTION: Molecular analysis of DNA from myocardial and skeletal muscle tissue and from peripheral blood specimens. MAIN OUTCOME MEASURES: Screening for mutations in beta MHC (exons 3-23) and mtDNA tRNA (n = 22) genes with denaturing gradient gel electrophoresis or single strand conformational polymorphism followed by automated DNA sequencing. RESULTS: One proband (kindred A) (plus seven affected relatives) had arginine 249 glutamine (Arg249Gln) beta MHC and heteroplasmic mtDNA tRNAIle A4300G mutations. Another unrelated patient (kindred B) with sporadic HCM had identical mutations. The remaining two patients (kindred C), a mother and son, had a novel beta MHC mutation (lysine 450 glutamic acid) (Lys450Glu) and a heteroplasmic missense (T9957C, phenylalanine (Phe)-->leucine (Leu)) mtDNA mutation in subunit III of the cytochrome C oxidase gene. The amount of mutant mtDNA was higher in the myocardium than in skeletal muscle or peripheral blood and in affected patients than in asymptomatic relatives. Mutations were absent in the controls. Pathological and biochemical characteristics of patients with mutations Arg249Gln plus A4300G (kindreds A and B) were identical, but different from those of the two patients with Lys450Glu plus T9957C(Phe-->Leu) mutations (kindred C). Cytochrome C oxidase activity and histoenzymatic staining were severely decreased in the two patients in kindreds A and B, but were unaffected in the two in kindred C. CONCLUSIONS: beta MHC gene and mtDNA mutations may coexist in patients with HCM and end stage congestive heart failure. Although beta MHC gene mutations seem to be the true determinants of HCM, both mtDNA mutations in these patients have known prerequisites for pathogenicity. Coexistence of other genetic abnormalities in beta MHC linked HCM, such as mtDNA mutations, may contribute to variable phenotypic expression and explain the heterogeneous behaviour of HCM.  (+info)

Altered crossbridge kinetics in the alphaMHC403/+ mouse model of familial hypertrophic cardiomyopathy. (2/1667)

A mutation in the cardiac beta-myosin heavy chain, Arg403Gln (R403Q), causes a severe form of familial hypertrophic cardiomyopathy (FHC) in humans. We used small-amplitude (0.25%) length-perturbation analysis to examine the mechanical properties of skinned left ventricular papillary muscle strips from mouse hearts bearing the R403Q mutation in the alpha-myosin heavy chain (alphaMHC403/+). Myofibrillar disarray with variable penetrance occurred in the left ventricular free wall of the alphaMHC403/+ hearts. In resting strips (pCa 8), dynamic stiffness was approximately 40% greater than in wild-type strips, consistent with elevated diastolic stiffness reported for murine hearts with FHC. At pCa 6 (submaximal activation), strip isometric tension was approximately 3 times higher than for wild-type strips, whereas at pCa 5 (maximal activation), tension was marginally lower. At submaximal calcium activation the characteristic frequencies of the work-producing (b) and work-absorbing (c) steps of the crossbridge were less in alphaMHC403/+ strips than in wild-type strips (b=11+/-1 versus 15+/-1 Hz; c= 58+/-3 versus 66+/-3 Hz; 27 degrees C). At maximal calcium activation, strip oscillatory power was reduced (0. 53+/-0.25 versus 1.03+/-0.18 mW/mm3; 27 degrees C), which is partly attributable to the reduced frequency b, at which crossbridge work is maximum. The results are consistent with the hypothesis that the R403Q mutation reduces the strong binding affinity of myosin for actin. Myosin heads may accumulate in a preforce state that promotes cooperative activation of the thin filament at submaximal calcium but blunts maximal tension and oscillatory power output at maximal calcium. The calcium-dependent effect of the mutation (whether facilitating or debilitating), together with a variable degree of fibrosis and myofibrillar disorder, may contribute to the diversity of clinical symptoms observed in murine FHC.  (+info)

Altered cardiac excitation-contraction coupling in mutant mice with familial hypertrophic cardiomyopathy. (3/1667)

Excitation-contraction coupling in cardiac muscle of familial hypertrophic cardiomyopathy (FHC) remains poorly understood, despite the fact that the genetic alterations are well defined. We characterized calcium cycling and contractile activation in trabeculae from a mutant mouse model of FHC (Arg403Gln knockin, alpha-myosin heavy chain). Wild-type mice of the same strain and age ( approximately 20 weeks old) served as controls. During twitch contractions, peak intracellular Ca2+ ([Ca2+]i) was higher in mutant muscles than in the wild-type (P < 0.05), but force development was equivalent in the two groups. Ca2+ transient amplitude increased dramatically in both groups as stimulation rate increased from 0.2 to 4 Hz. Nevertheless, developed force fell at the higher stimulation rates in the mutants but not in controls (P < 0.05). The steady-state force-[Ca2+]i relationship was less steep in mutants (Hill coefficient, 2.94 +/- 0.27 vs. 5.28 +/- 0.64; P > 0.003), with no changes in the [Ca2+]i required for 50% activation or maximal Ca2+-activated force. Thus, calcium cycling and myofilament properties are both altered in FHC mutant mice: more Ca2+ is mobilized to generate force, but this does not suffice to maintain contractility at high stimulation rates.  (+info)

Sudden death in hypertrophic cardiomyopathy: potential importance of altered autonomic control of vasculature. (4/1667)

Current evidence suggests that alterations in the autonomic function and abnormal vascular control play a significant role either as independent triggers themselves or as modifiers of ischaemia and tolerance to to arrhythmias. A combination of several factors--that is, arrhythmia, hypotension, altered autonomic function including vascular control, and ischaemia are therefore likely to act as triggers for sudden death. The relative contribution of each of these factors needs further detailed study.  (+info)

Effects of permanent dual-chamber pacing on mitral regurgitation in hypertrophic obstructive cardiomyopathy. (5/1667)

AIMS: To assess the effects of chronic dual-chamber pacing on mitral regurgitation in hypertrophic obstructive cardiomyopathy. METHODS AND RESULTS: Twenty-three patients with hypertrophic obstructive cardiomyopathy and mitral regurgitation. treated with DDD pacing for 16 +/- 14 months, were included in the study. Mitral regurgitation was assessed by Doppler-echocardiography using semi-quantitative analysis (grades I-IV) and by measuring the maximum regurgitant jet area/left atrial area ratio. At the end of follow-up, DDD pacing reduced the outflow gradient from 93 +/- 37 mmHg to 31 +/- 30 mmHg (P<0.0001). Nine of the 14 patients who initially had > or =grade II mitral regurgitation improved by at least one grade, two of them exhibiting dramatic improvement (from grade IV and III to grade I). The regurgitant jet area/left atrial area ratio was reduced with DDD pacing from 20 +/- 13% to 11 +/- 6% (P<0.0001). Patients who had significant mitral regurgitation despite pacing were those whose outflow gradient remained high or those with mitral valve organic abnormalities (mitral annulus calcification or mitral valve prolapse). In the absence of organic abnormalities other than leaflet elongation, there was a significant correlation between the gradient value achieved with DDD pacing and the extent of mitral regurgitation (P<0.05). CONCLUSION: In the absence of organic mitral valve abnormalities, DDD pacing reduces in parallel mitral regurgitation and left ventricular outflow gradient. In such patients therefore, significant mitral regurgitation is not a contraindication to pacing.  (+info)

Rapid progression of cardiomyopathy in mitochondrial diabetes. (6/1667)

Cardiac involvement and its clinical course in a diabetic patient with a mitochondrial tRNA(Leu)(UUR) mutation at position 3243 is reported in a 54-year-old man with no history of hypertension. At age 46, an electrocardiogram showed just T wave abnormalities. At age 49, it fulfilled SV1 + RV5 or 6>35 mm with strain pattern. At age 52, echocardiography revealed definite left ventricular (LV) hypertrophy, and abnormally increased mitochondria were shown in biopsied endomyocardial specimens. He was diagnosed as having developed hypertrophic cardiomyopathy associated with the mutation. However, at age 54, SV1 and RV5,6 voltages were decreased, and echocardiography showed diffuse decreased LV wall motion and LV dilatation. Because he had mitochondrial diabetes, the patient's heart rapidly developed hypertrophic cardiomyopathy, and then it seemed to be changing to a dilated LV with systolic dysfunction. Rapid progression of cardiomyopathy can occur in mitochondrial diabetes.  (+info)

A patient with hypertrophic cardiomyopathy accompanied by right ventricular dilation of unknown cause. (7/1667)

Hypertrophic cardiomyopathy (HCM) is a disease characterized by an unknown cause of hypertrophy in the left or right ventricle. The dilated phase of HCM shows disease conditions resembling dilated cardiomyopathy, such as ventricular dilation, thin ventricular wall, and reduction of the ejection fraction. A patient presented with left ventricular concentric hypertrophy accompanied by right ventricular dilatation of unknown cause. Right ventricular endomyocardial biopsy specimens showed characteristic myocardial disarray. Therefore, there is the possibility that the patient had right and left ventricular HCM in the process toward the dilated phase, in which dilatation first occurred in the right ventricle.  (+info)

Ca2+ sensitization and potentiation of the maximum level of myofibrillar ATPase activity caused by mutations of troponin T found in familial hypertrophic cardiomyopathy. (8/1667)

Human wild-type cardiac troponin T, I, C and five troponin T mutants (I79N, R92Q, F110I, E244D, and R278C) causing familial hypertrophic cardiomyopathy were expressed in Escherichia coli, and then were purified and incorporated into rabbit cardiac myofibrils using a troponin exchange technique. The Ca2+-sensitive ATPase activity of these myofibrillar preparations was measured in order to examine the functional consequences of these troponin mutations. An I79N troponin T mutation was found to cause a definite increase in Ca2+ sensitivity of the myofibrillar ATPase activity without inducing any significant change in the maximum level of ATPase activity. A detailed analysis indicated the inhibitory action of troponin I to be impaired by the I79N troponin T mutation. Two more troponin T mutations (R92Q and R278C) were also found to have a Ca2+-sensitizing effect without inducing any change in maximum ATPase activity. Two other troponin T mutations (F110I and E244D) had no Ca2+-sensitizing effects on the ATPase activity, but remarkably potentiated the maximum level of ATPase activity. These findings indicate that hypertrophic cardiomyopathy-linked troponin T mutations have at least two different effects on the Ca2+-sensitive ATPase activity, Ca2+-sensitization and potentiation of the maximum level of the ATPase activity.  (+info)

*Hypertrophic cardiomyopathy

... at Curlie (based on DMOZ) GeneReviews/NIH/NCBI/UW entry on Familial Hypertrophic Cardiomyopathy ... hypertrophic obstructive cardiomyopathy (HOCM) has also historically been known as idiopathic hypertrophic subaortic stenosis ( ... Hypertrophic Cardiomyopathy Association. Retrieved November 14, 2016. Colan, Steven (October 2010). "Hypertrophic ... A diagnosis of hypertrophic cardiomyopathy is based upon a number of features of the disease process. While there is use of ...

*Hypertrophic cardiomyopathy screening

Hypertrophic cardiomyopathy, or HCM, is the leading cause of sudden cardiac death (SCD) in young athletes. HCM is frequently ... While younger individuals are likely to have a more severe form of hypertrophic cardiomyopathy, the condition is seen in people ... Maron, B.J., Thompson, P.D. (2002). Hypertrophic Cardiomyopathy: Practical steps for preventing sudden death. The Physician and ... Maron BJ (March 2002). "Hypertrophic cardiomyopathy: a systematic review". Journal of the American Medical Association. 287 (10 ...

*Srihari S. Naidu

Hypertrophic Cardiomyopathy; Springer UK; https://www.amazon.co.uk/Hypertrophic-Cardiomyopathy-Srihari-Naidu/dp/1447149556 ... Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death among athletes, and a cause of heart failure at ... A co-author on the 2011 ACCF/AHA National Guideline on the Diagnosis and Management of Hypertrophic Cardiomyopathy, he is ... Naidu is Director of the Hypertrophic Cardiomyopathy National Center of Excellence - with offices in Long Island and ...

*Maine Coon

"Feline Hypertrophic Cardiomyopathy". Cat Fanciers' Association. Archived from the original on 13 May 2008. Retrieved 24 ... "Hypertrophic Cardiomyopathy Genetic Mutation Testing Service for Cats". Washington State University. Archived from the original ... The most severe threat is feline hypertrophic cardiomyopathy (HCM), the most common heart disease seen in cats, whether pure ... Professionals notice certain health problems in the breed including feline hypertrophic cardiomyopathy and hip dysplasia, but ...

*Haplogroup T (mtDNA)

Hypertrophic CardioMyopathy (HCM) also referred to as Hypertrophic Obstructive CardioMyopathy or HOCM is more likely to happen ... "Hypertrophic cardiomyopathy - Medical Encyclopedia". Medline Plus. National Library of Medicine. Retrieved 2015-10-03. Meet the ... Castro, M (2006). "Mitochondrial DNA haplogroups in Spanish patients with hypertrophic cardiomyopathy". Int J Cardiol. 112: 202 ...

*Premature ventricular contraction

Cardiomyopathy, hypertrophic or dilated; Certain medicines such as digoxin, which increases heart contraction or tricyclic ... In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses. ... One drawback comes from emerging data that suggests very frequent ventricular ectopy may be associated with cardiomyopathy ... cardiomyopathy) African American ethnicity- increased the risk of PVCs by 30% in comparison with the risk in white individuals ...

*Ragdoll

... and their Association with Hypertrophic Cardiomyopathy" (PDF). Vetogene.it. Retrieved 15 December 2017. "Hypertrophic ... Hypertrophic cardiomyopathy (HCM) is a common heart disease in all cats and is most commonly genetic in cause. The disease ... cardiomyopathy (HCM) in cats". Fabcats.org. Retrieved 15 December 2017. Ragdoll history according to the Ragdoll Fanciers Club ...

*ACTC1

The E101K missense mutation has been associated with Hypertrophic Cardiomyopathy and Left Ventricular Noncompaction. Another ... "Inherited and de novo mutations in the cardiac actin gene cause hypertrophic cardiomyopathy". Journal of Molecular and Cellular ... "Mutation in the alpha-cardiac actin gene associated with apical hypertrophic cardiomyopathy, left ventricular non-compaction, ... "Gene mutations in apical hypertrophic cardiomyopathy". Circulation. 112 (18): 2805-11. doi:10.1161/CIRCULATIONAHA.105.547448. ...

*Pacemaker syndrome

... 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 ...

*Barry A. Love

"Gregory M. Hirsch Hypertrophic Cardiomyopathy Center". Archived from the original on January 27, 2011. Retrieved November 9, ... Postrenal biopsy AVM leading to severe hypertension and dilated cardiomyopathy. Pediatr Nephrol. 2009 Dec;24(12):2459-62. Epub ...

*MYH10

... and progressive hypertrophic cardiomyopathy at 6 months. These data indicate that NM-IIB functions in ensuring the proper ...

*Cardiomegaly

Hypertrophic cardiomyopathy is typically an inherited condition. There are many techniques and tests used to diagnose an ... Other possible causes include: Heart Valve Disease Cardiomyopathy (disease to the heart muscle) Pulmonary Hypertension ... Dilated cardiomyopathy is the most common type of cardiomegaly. In this condition, the walls of the left and/or right ... peripartum cardiomyopathy) Kidney disease requiring dialysis Alcohol or cocaine abuse HIV infection Diabetes Treatments for ...

*Karthik Nagesh

Myocardial Infarction with hypertrophic Cardiomyopathy .Perinatology ;1999. Karthik Nagesh N.Ventilatory Therapy in the Neonate ...

*Shauna Bradley

Watson explained "Shauna's condition is called hypertrophic cardiomyopathy. It's generally found in athletes when there's too ...

*CSRP3

GeneReviews/NIH/NCBI/UW entry on Familial Hypertrophic Cardiomyopathy Overview Human CSRP3 genome location and CSRP3 gene ... and hypertrophic cardiomyopathy (HCM) [e.g. L44P, S46R, S54R/E55G, C58G, R64C, Y66C, Q91L, K42/fs165], while the most frequent ... CSRP3 mutations cause hypertrophic cardiomyopathy". Human Molecular Genetics. 17 (18): 2753-65. doi:10.1093/hmg/ddn160. PMID ... "Mutations in the human muscle LIM protein gene in families with hypertrophic cardiomyopathy". Circulation. 107 (10): 1390-5. ...

*Obscurin

A mutation in the OBSCN gene has been associated with hypertrophic cardiomyopathy and altered obscurin protein properties have ... An obscurin mutation Arg4344Gln was identified in patients with hypertrophic cardiomyopathy, which disrupted binding of ... "Structural analysis of obscurin gene in hypertrophic cardiomyopathy". Biochemical and Biophysical Research Communications. 362 ... "Structural analysis of obscurin gene in hypertrophic cardiomyopathy". Biochemical and Biophysical Research Communications. 362 ...

*Locus heterogeneity

Other examples are hypertrophic cardiomyopathy, osteogenesis imperfecta, Familial hypercholesterolemia. Allelic heterogeneity ...

*MYL2

GeneReviews/NIH/NCBI/UW entry on Familial Hypertrophic Cardiomyopathy Overview MYL2 Info with links in the Cell Migration ... MLC-2v dephosphorylation has also been reported in human patients carrying a rare form of familial hypertrophic cardiomyopathy ... Mutations in MYL2 have been associated with familial hypertrophic cardiomyopathy (FHC). Ten FHC mutations have been identified ... "Familial hypertrophic cardiomyopathy mutations in the regulatory light chains of myosin affect their structure, Ca2+ binding, ...

*JPH2

Mutations in JPH2 were identified in a cohort of patients with hypertrophic cardiomyopathy who lacked the traditional mutations ... 2007). "Mutations in JPH2-encoded junctophilin-2 associated with hypertrophic cardiomyopathy in humans". J Mol Cell Cardiol. 42 ... 2007). "Mutation of junctophilin type 2 associated with hypertrophic cardiomyopathy". J. Hum. Genet. 52 (6): 543-8. doi:10.1007 ... 2007). "Mutations in JPH2-encoded junctophilin-2 associated with hypertrophic cardiomyopathy in humans". J. Mol. Cell. Cardiol ...

*PYGB

Meanwhile, GPBB levels are elevated in patients with hypertrophic cardiomyopathy. Glycogen phosphorylase PYGL "PYGB ... is associated with pulmonary artery wedge pressure and left ventricle mass index in patients with hypertrophic cardiomyopathy ...

*TNNI3

cTnI mutations account for approximately 5% of familial hypertrophic cardiomyopathy cases and to date, more than 20 myopathic ... GeneReviews/NIH/NCBI/UW entry on Familial Hypertrophic Cardiomyopathy Overview. ... "Mutations in the cardiac troponin I gene associated with hypertrophic cardiomyopathy". Nature Genetics. 16 (4): 379-82. doi: ... "Investigation of a truncated cardiac troponin T that causes familial hypertrophic cardiomyopathy: Ca(2+) regulatory properties ...

*IRX4

2008). "Genetic analysis of the Irx4 gene in hypertrophic cardiomyopathy". Turk Kardiyol Dern Ars. 36 (2): 90-5. PMID 18497553 ...

*Chris Naumoff

Following further testing, Naumoff was diagnosed with hypertrophic cardiomyopathy (HCM). On 4 July 2016, he announced his ... hypertrophic cardiomyopathy, which led to the cancellation of the contract and Naumoff's subsequent retirement as a health ...

*ANKRD1

CARP has been implicated in several diseases, including dilated cardiomyopathy, hypertrophic cardiomyopathy, and several ... Mutations in ANKRD1 have also been associated with hypertrophic cardiomyopathy, and have shown to increase binding of CARP to ... Examination of the functional effects of CARP hypertrophic cardiomyopathy mutations in engineered heart tissue demonstrated ... mutations in hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 54 (4): 334-42. doi:10.1016/j.jacc. ...

*Myocardial disarray

A critical review Information from the Stanford Hypertrophic Cardiomyopathy Center. ... Aortic stenosis Congenital heart disease Hypertensive heart disease Hypertrophic cardiomyopathy The common factor amongst all ...

*List of ICD-9 codes 390-459: diseases of the circulatory system

Cardiomyopathy (425.0) Endomyocardial fibrosis (425.1) Hypertrophic obstructive cardiomyopathy (425.2) Obscure cardiomyopathy ... Alcoholic cardiomyopathy (425.7) Nutritional and metabolic cardiomyopathy (425.8) Cardiomyopathy in other diseases classified ... elsewhere (425.9) Secondary cardiomyopathy unspecified (426) Conduction disorders (426.0) Atrioventricular block, third degree ... of africa (425.3) Endocardial fibroelastosis (425.4) Other primary cardiomyopathies (425.5) ...
The angiographic features of the left ventricle were examined in patients with idiopathic hypertrophic subaortic stenosis who had clinical and hemodynamic evidence of obstruction. Of 36 combined hemodynamic and angiographic studies considered to be technically satisfactory, 33 showed a characteristic combination of abnormalities. In the frontal projection in systole, a linear radiolucent area extended across the left ventricular outflow tract 2 to 2.5 cm below the aortic annulus, at a level corresponding to the site of intraventricular pressure change. In the left oblique and lateral projections, the mitral leaflets did not swing posteriorly in a normal fashion, but projected into the outflow tract during mid and late systole. The radiolucent line, seen in the frontal views, was considered to represent contact of the leading edge of the leaflet with the hypertrophied muscular interventricular septum. The jet of mitral regurgitation, when present, was seen immediately below the anterior mitral ...
Only 10 years have elapsed since the concept of functional obstruction to left ventricular ejection was introduced to clinical medicine (1), and in the interim the features of obstructive cardiomyopathy, or idiopathic hypertrophic subaortic stenosis, have become generally recognized. It seems certain that the increasingly frequent recognition of this disease has resulted largely from wider application of left heart catheterization techniques; nevertheless, while the diagnosis initially was based on hemodynamic features peculiar to this disease, it has become possible with increasing experience to recognize and assess the severity of this lesion on clinical grounds alone (2).. Work originating in a ...
Introduction: Hypertrophic Obstructive Cardiomyopathy (HOCM) is associated with systolic anterior motion of the mitral valve, frequently leading to mitral regurgitation (MR). We hypothesized that after septal reduction with alcohol septal ablation (ASA), left ventricular outflow tract gradients would be reduced and mitral regurgitation would improve.. Methods: We reviewed echocardiograms at baseline and 3 month post ASA for 210 consecutive patients treated at the Medical University of South Carolina between 2000 and 2007 for whom complete echo data was available. For each echocardiogram the left atrial end-systolic volume index (LAESVI), resting left ventricular outflow tract (LVOT) gradient, degree of mitral regurgitation and mitral regurgitation jet area were assessed.. Results: Mitral regurgitation was seen in 70% of patients at baseline (Figure 1A). ASA significantly reduced regurgitation, with only 41% having mild or greater MR at three months (70% vs 41%, p=,0.001), and nearly eliminated ...
Although it is often considered a disease of the young, hypertrophic obstructive cardiomyopathy is commonly diagnosed in the elderly. Studies have also indicated that this condition may be more common in older patients than is generally recognised, supporting the notion that the elderly may be a large and neglected subset of patients with hypertrophic obstructive cardiomyopathy. Whiting and colleagues35 reported that 32% of patients presenting with hypertrophic cardiomyopathy were , 60 years of age, and in a community hospital based series published by Petrin and Tavel,36 83% of patients were , 50 years of age. Krasnow and Stein37 described 23 new cases of hypertrophic cardiomyopathy with 20 of the patients over the age of 50 years and 15 of these patients over the age of 60 years. Likewise, in a study by Lever and colleagues27 hypertrophic cardiomyopathy was more commonly diagnosed in patients ⩾ 65 years of age than in those , 40 years of age. Nevertheless, most information about the ...
TY - JOUR. T1 - Apical myectomy for patients with hypertrophic cardiomyopathy and advanced heart failure. AU - Nguyen, Anita. AU - Schaff, Hartzell V. AU - Nishimura, Rick A.. AU - Geske, Jeffrey B.. AU - Dearani, Joseph A.. AU - King, Katherine S.. AU - Ommen, Steve R.. PY - 2019/1/1. Y1 - 2019/1/1. N2 - Objective: In patients with apical hypertrophic cardiomyopathy, extensive apical hypertrophy may reduce left ventricular end-diastolic volume and contribute to diastolic dysfunction, angina, and ventricular arrhythmias. Transapical myectomy to augment left ventricular cavity size can increase stroke volume and decrease left ventricular end-diastolic pressure. In this study, we describe early outcomes of patients with apical hypertrophic cardiomyopathy after transapical myectomy and compare survival with that of patients with hypertrophic cardiomyopathy listed for heart transplantation. Methods: Between September 1993 and March 2017, 113 symptomatic patients with apical hypertrophic ...
Sakamoto T, Tei C, Murayama M, Ichiyasu H, Hada Y. Giant T wave inversion as a manifestation of asymmetrical apical hypertrophy (AAH) of the left ventricle: echocardiographic and ultrasono-cardiotomographic study. Jpn Heart J. 1976;17(5):611-29. PMID: 136532. DOI: https://doi.org/10.1536/ihj.17.611 Yamaguchi H, Ishimura T, Nishiyama S, Nagasaki F, Nakanishi S, Takatsu F, et al. Hypertrophic nonobstructive cardiomyopathy with giant negative T waves (apical hypertrophy): Ventriculographic and echocardiographic features in 30 patients. Am J Cardiol. 1979;44(3):401- 12. PMID: 573056. DOI: https://doi.org/10.1016/0002-9149(79)90388-6 Eriksson MJ, Sonnenberg B, Woo A, Rakowski P, Parker TG, Wigle ED, et al. Long-term outcome in patients with apical hypertropic cardiomyopathy. J Am Cardiol. 2002;39(4):638- 45. PMID: 11849863. DOI: https://doi.org/10.1016/s0735-1097(01)01778-8 Kitaoka H, Doi Y, Casey SA, Hitomi M, Furuno T, Maron BJ. Comparision of prevalence of apical hypertrophic cardiomyopathy in ...
TY - JOUR. T1 - Benefits of intraoperative echocardiography in the surgical management of hypertrophic cardiomyopathy. AU - Marwick, Thomas H.. AU - Stewart, William J.. AU - Lever, Harry M.. AU - Lytle, Bruce W.. AU - Rosenkranz, Eliot. AU - Duffy, Carol I.. AU - Salcedo, Ernesto E.. PY - 1992/11/1. Y1 - 1992/11/1. N2 - Objectives. The purpose of this study was to determine the role of intraoperative echocardiography in planning the site and extent of myectomy and in ensuring adequate control of the left ventricular outflow tract gradient. Background. Although intraoperative echocardiography has been found to be beneficial in patients undergoing valve repair, its impact on surgical decisions in patients undergoing septal myectomy for hypertrophic cardiomyopathy has not been described. Methods. In 50 patients undergoing septal myectomy over a 5-year period, epicardial echocardiography was performed before cardiopulmonary bypass to establish the extent of outflow tract obstruction, locate its ...
Familial hypertrophic cardiomyopathy is a genetically heterogeneous disease with variable clinical features that is inherited as autosomal dominant with variable penetrance. Recent developments in genetics of hereditary cardiomyopathy have not only enlightened many points about pathogenesis, but have also provided great benefit to diagnostic approaches of clinicians. Heterozygous mutation of c3691-3692insTTCA in MYBPC3 gene was identified in a pediatric patient with diagnosis of hypertrophic cardiomyopathy at clinic. Hypertrophy was observed in sister and father of the patient in echocardiography screening, and it was subsequently determined that they also had same mutation. This mutation has not previously been defined and reported previously in the literature as cause of hypertrophic cardiomyopathy.. Keywords: Echocardiography, hypertrophic cardiomyopathy, molecular genetics, MYBPC ...
TY - JOUR. T1 - Multidetector computerized tomography can guide and document alcohol septal ablation in hypertrophic obstructive cardiomyopathy. AU - Ghersin, Eduard. AU - Soto, Victor. AU - Heldman, Alan W.. PY - 2011/1/18. Y1 - 2011/1/18. UR - http://www.scopus.com/inward/record.url?scp=78751605593&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=78751605593&partnerID=8YFLogxK. U2 - 10.1161/CIRCULATIONAHA.110.975599. DO - 10.1161/CIRCULATIONAHA.110.975599. M3 - Article. C2 - 21242503. AN - SCOPUS:78751605593. VL - 123. JO - Circulation. JF - Circulation. SN - 0009-7322. IS - 2. ER - ...
The short-term results of PTSMA are excellent for the reduction of LVOT obstruction (13,17,32). Previous studies report that mean resting PGs significantly reduced from 60 mm Hg to 14 mm Hg after PTSMA (13,17,32), and other studies with longer follow-up (16,18,33)do not show any recurrence of obstruction over time. One- to two-year follow-up shows continued improvement in symptoms with a mean increase of over one NYHA functional class (16,18,33). More importantly, objective tests show increases of exercise time around 40% over follow-up (18). Recently, Lakkis et al. (18)reported results of a one-year follow-up study in 50 patients. In his study, resting PGs dropped significantly from average 74 ± 23 mm Hg to 6 ± 18 mm Hg, and dobutamine-induced gradient decreased from 84 ± 28 mm Hg to 30 ± 33 mm Hg. The exercise duration increased by 2 min at one year. Similar results were also found in our study, with both resting and provokable PGs significantly reduced immediately after the PTSMA and ...
Myocardial disarray, also known as myocyte disarray, is a term to describe the loss of the normal parallel alignment of myocytes (the muscle cells of the heart). Instead, the myocytes usually form circles around foci of connective tissue. Myocardial disarray is associated with myocardial fibrosis (the replacement of the myocytes with non-contractile scar tissue). Myocardial disarray can be seen in a number of disease states, including: Aortic stenosis Congenital heart disease Hypertensive heart disease Hypertrophic cardiomyopathy The common factor amongst all these diseases is that they all cause varying degrees of remodelling (myocardial fibrosis) of the ventricles. Myocardial disarray. A critical review Information from the Stanford Hypertrophic Cardiomyopathy ...
OBJECTIVE: Angina and the presence of myocardial ischaemia are common in hypertrophic cardiomyopathy. Dual chamber pacing results in clinical improvement in these patients. This study evaluates the effects of permanent dual chamber pacing on absolute regional myocardial perfusion and perfusion reserve. SETTING: University hospital. PATIENTS AND DESIGN: Six patients with hypertrophic cardiomyopathy and severe symptoms of angina received a dual chamber pacemaker. Absolute myocardial regional perfusion and perfusion reserve (dipyridamole 0.56 mg/kg) were measured by dynamic positron emission tomography with 13N-ammonia both during sinus rhythm and 3 months after pacemaker insertion. Results were compared with those from 28 healthy volunteers. RESULTS: Pacing resulted in a reduction of anginal complaints and a reduction in intraventricular pressure gradient from 65 (SD 30) mm Hg to 19 (10) mm Hg. During sinus rhythm, baseline perfusion was higher in patients with hypertrophic cardiomyopathy than ...
TY - JOUR. T1 - Dual chamber pacing relieves obstruction in japanese-variant hypertrophic cardiomyopathy. AU - Wever-Pinzon, Omar. AU - Romero, Jorge E.. AU - Cordova, Juan P.. PY - 2013/9. Y1 - 2013/9. N2 - Japanese-variant or apical hypertrophic cardiomyopathy (HCM) is a specific type of HCM, first described in Japan and initially thought to carry a benign prognosis. However, current evidence suggests that these patients experience severe symptoms and are at increased risk of ventricular arrhythmias and death, especially in the presence of an apical akinetic chamber. The management of patients who do not respond to medical therapy is challenging. We describe a patient with Japanesevariant HCM, with an apical akinetic chamber and severe symptoms who failed medical therapy. The use of dual chamber pacing relieved obstruction and significantly improved the patients symptoms.. AB - Japanese-variant or apical hypertrophic cardiomyopathy (HCM) is a specific type of HCM, first described in Japan and ...
This trial will investigate efficacy, safety, tolerability and dose ranging of MYK-461 in patients with symptomatic non-obstructive hypertrophic cardiomyopathy
We described a patient with familial non-obstructive hypertrophic cardiomyopathy and complete atrioventricular block. A 27-year-old male was admitted to our institution with syncope. Electrocardiography demonstrated complete atrioventricular block. Two-dimensional echocardiography revealed non-obstructive hypertrophic cardiomyopathy. A temporary transvenous ventricular pacemaker was inserted urgently, and subsequently replaced by a permanent dual-chamber pacemaker. Meanwhile, non-obstructive hypertrophic cardiomyopathy was diagnosed in the mother, the aunt and one of the brothers of the patient in the screening of the family, but atrioventricular conduction block was not detected in them. In the electrophysiological study of the mother, inducible ventricular tachycardia was detected. The reason for diversity of the arrhythmias in the members of the same family with hypertrophic cardiomyopathy may be explained by penetrance. The phenotype of the familial hypertrophic cardiomyopathy is influenced ...
TY - JOUR. T1 - Exercise gas exchange analysis in obstructive hypertrophic cardiomyopathy before and after myectomy (cardiopulmonary exercise test combined with exercise-echocardiography in HCM). AU - Bandera, F.. AU - Generati, G.. AU - Pellegrino, M.. AU - Secchi, F.. AU - Menicanti, L.. AU - Guazzi, M.. PY - 2015/1/15. Y1 - 2015/1/15. KW - Cardiopulmonary exercise test. KW - Exercise intolerance. KW - Exercise-echocardiography. KW - Hypertrophic cardiomyopathy. KW - Septal resection. UR - http://www.scopus.com/inward/record.url?scp=84916213770&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84916213770&partnerID=8YFLogxK. U2 - 10.1016/j.ijcard.2014.11.104. DO - 10.1016/j.ijcard.2014.11.104. M3 - Article. C2 - 25465307. AN - SCOPUS:84916213770. VL - 178. SP - 282. EP - 283. JO - International Journal of Cardiology. JF - International Journal of Cardiology. SN - 0167-5273. ER - ...
DISCUSSION. Recently, the advances in cardiopulmonary bypass and myocardial protection associated with the improvement of the surgical technique, and the postoperative cardiovascular surgery has caused the morbidity and mortality of septal myectomy to become progressively decreased. Currently, assistance units with extensive experience present a mortality rate between 1% and 2%, being able to reach zero in most favorable situations (9,12,13). In our experience, we had an in-hospital death (2.9%) and a survival rate of 87.9% with a mean follow-up of 9.6 years, equivalent to that observed in the international experience, with an 5-year overall survival ranging from 86% up to 96% and in 10 years between 70% and 90% [9,10,12,13]. The recent consensus of American and European Societies of Cardiology have highlighted the surgical septal myectomy as the "gold standard" to reduce the left ventricular outflow obstruction tract and to relief the symptoms in patients with hypertrophic obstructive ...
Presented by: Angelos G. Rigopoulos,1,2 Hubert Seggewiss,1 Ioannis C. Rizos2. 11st Department of Internal Medicine, Leopoldina Hospital, Schweinfurt, Germany. 22nd Department of Cardiology, University of Athens Medical School, Athens, Greece. Alcohol septal reduction in hypertrophic obstructive cardiomyopathy (HOCM) is indicated for patients with drug refractory symptoms or drug intolerance who have significant left ventricular obstruction.(1) On the other hand, several structural and functional changes including low-normal left ventricular (LV) ejection fraction, moderate to severe diastolic dysfunction, marked atrial dilatation, thinning of the LV walls, onset of atrial fibrillation, spontaneous reduction or loss of LV outflow obstruction, and LV apical aneurysms characterise an advanced stage of progression in the physical history of the disease which signifies adverse remodelling and clinical deterioration.(2) The benefit derived from septal reduction treatments in this stage is largely ...
Store Levitra Super Active+ at room temperature, between 68 and 77 degrees F (20 and 25 degrees C). Store away from heat, moisture, and light. Keep Levitra Super Active+ out of the reach of children and away from pets.. Warnings/Precautions. Levitra Super Active+ has vasodilator properties which may result in mild and transient decreases in blood pressure. Patients with left ventricular outflow obstruction, e.g., aortic stenosis and idiopathic hypertrophic subaortic stenosis, can be sensitive to the action of vasodilators including Type 5 phosphodiesterase inhibitors ...
Global Hypertrophic Cardiomyopathy Therapeutics Market - Key Trends With heart diseases emerging as one of the most common causes of mortality among men and women worldwide, Transparency Market Research (TMR) expects the demand for hypertrophic cardiomyopathy (HCM) therapeutics to surge considerably. Furthermore, the market is expected to gain significant impetus from successful government interventions aimed at spreading awareness about hypertrophic cardiomyopathy.. View Report-. https://www.transparencymarketresearch.com/hypertrophic-cardiomyopathy-therapeutics-market.html. TMR projects the global HCM therapeutics market to expand at a moderate 1.4% CAGR between 2015 and 2023. Despite witnessing positive opportunities, the rising demand for advanced medical devices could threaten the markets growth to an extent. Nevertheless, since the majority of HCM drugs are yet to get approved, the hypertrophic cardiomyopathy therapeutics market is likely to gain momentum post their approval in the near ...
0002] Hypertrophic cardiomyopathy ("HCM") is an often fatal but manageable disease. The incidence is reported to be about 1/400 (approximately 750,000) in the general U.S. population. The variable expressivity of this disease suggests it may be higher, making HCM the most common monogenic cardiac disorder in the U.S. Macon and McKenna et al., ACC/ESC Expert Consensus Document on Hypertrophic Cardiomyopathy, J of American College of Cardiology (2003) 42: 1-27. In addition, it is the most frequent cause of unexpected sudden death in teenagers and young adults. Elliott, Poloniecki et al., Sudden death in hypertrophic cardiomyopathy: Identification of high risk patients, J of American College of Cardiology (2000) 36: 2212-2218. The disease is characterized by a thickening of the heart muscle (hypertrophy) in the absence of hypertension or any other apparent cause. HCM is difficult to diagnose. Clinical presentation and progression of HCM varies widely among affected patients and the symptoms ...
IVS hypertrophy can occur as part of generalized LV hypertrophy, or it can occur in isolation, such as in asymmetric septal hypertrophy (ASH).5 In ASH, the ratio of the IVS thickness to the inferolateral (posterior) wall thickness is ,1.3. Although ASH is a characteristic feature of hypertrophic cardiomyopathy, it can also occur in the elderly due to hypertension or aortic stenosis. Excessive thickening can lead to LVOT obstruction in systole: this condition is termed hypertrophic obstructive cardiomyopathy.5 This obstruction can be further worsened with concomitant systolic anterior motion of the anterior leaflet of the mitral valve.. Surgical repair of hypertrophic cardiomyopathy with septal myectomy is generally performed for patients with severe LVOT obstruction: a gradient at rest ,30 mm Hg, IVS thickness ,18 mm, and evidence of systolic anterior motion.6 During septal myectomy, TEE can be used to evaluate the extent of resection required, determine the presence and severity of mitral ...
Compared to men, women with a hereditary heart condition called hypertrophic cardiomyopathy are substantially more likely to be diagnosed later in life and with more severe symptoms, an Italian study indicates. This occurs despite the fact that hypertrophic cardiomyopathy "should theoretically be present in males and females equally," Dr. Iacopo Olivotto commented to Reuters Health, because it is a genetic disease with an inheritance pattern that requires only one parent to have the condition. People with hypertrophic cardiomyopathy (HCM) suffer from progressive weakening of the heart, which becomes enlarged in an attempt to compensate ...
Patients with hypertrophic cardiomyopathy are not immune from nationwide problems of inactivity and obesity. This study suggests that these issues may in fact be exaggerated in patients with hypertrophic cardiomyopathy. This may be due to apprehension regarding exercise on the part of patients, as well as by exercise restrictions imposed by physicians. Well-designed, likely multicenter, prospective studies will be necessary to determine the risks and benefits of different exercise regimens on hypertrophic cardiomyopathy disease progression and complications.. ...
Hypertrophic cardiomyopathy (HCM) may be defined as left ventricular (LV) hypertrophy in the absence of an underlying cause such as systemic hypertension or valvular aortic stenosis.1 Left ventricular outflow tract obstruction (LVOTO) is caused by septal hypertrophy combined with abnormal systolic anterior motion (SAM) of the mitral valve, and this, in turn, produces variable degrees of mitral valve regurgitation (MR). LVOTO in HCM is distinct in morphology and prognosis from congenital membranous subaortic stenosis, which is rarely associated with SAM. Some patients with HCM will have symptoms due to mid ventricular obstruction. Hypertrophic obstructive cardiomyopathy (HOCM) is important for surgeons because obstruction may occur in over 70 percent of patients with HCM,2 and transaortic septal ...
Hypertrophic cardiomyopathy (HCM) has caused Cuttino Mobley to retire from the NBA. Hypertrophic cardiomyopathy occurs when the myocardium is enlarged, usually for an unknown reason. The disease distorts the morphology of the heart, and at times of high flow, can cause the outflow tract of the left ventricle to collapse, leading to sudden death. Specifically, the theory is that systolic anterior motion (SAM) of the anterior leaflet of the mitral valve, caused either by Venturi forces or drag, can lead to the obstruction. According to JAMA, "Hypertrophic cardiomyopathy is the most common cause of cardiovascular sudden death in young people, including trained competitive athletes (most commonly in basketball and football and in black athletes ...
Advanced EKGs - Sudden Cardiac Death (Hypertrophic cardiomyopathy, ARVD, Brugada syndrome, and CPVT) - lesson plan ideas from Spiral. Tagged under: brugada syndrome,catecholaminergic,polymorphic vt,polymoprhic ventricular tachycardia,arrhythmogenic ventricular dysplasia,sudden unexcepted death syndrome,sudden unexpected nocturnal death syndrome,hypertrophic cardiomyopathy,hypertrophic obstructive cardiomyopathy,hocm,commotio cordis,ekg,ecg,electrocardiogram
TY - JOUR. T1 - Hypertrophic cardiomyopathy. T2 - A review. AU - Hensley, Nadia. AU - Dietrich, Jennifer. AU - Nyhan, Daniel. AU - Mitter, Nanhi. AU - Yee, May Sann. AU - Brady, Mary Beth. PY - 2015/3/4. Y1 - 2015/3/4. N2 - Hypertrophic cardiomyopathy (HCM) is a relatively common disorder that anesthesiologists encounter among patients in the perioperative period. Fifty years ago, HCM was thought to be an obscure disease. Today, however, our understanding and ability to diagnose patients with HCM have improved dramatically. Patients with HCM have genotypic and phenotypic variability. Indeed, a subgroup of these patients exhibits the HCM genotype but not the phenotype (left ventricular hypertrophy). There are a number of treatment modalities for these patients, including pharmacotherapy to control symptoms, implantable cardiac defibrillators to manage malignant arrhythmias, and surgical myectomy and septal ablation to decrease the left ventricular outflow obstruction. Accurate diagnosis is vital ...
Anesthesia for elective cesarean section in a patient with idiopathic hypertrophic subaortic stenosis. She weighs 80 kg.. 1. Would a regional or a general be preferred? Explain your rationale.. 2. What local anesthetic and technique would you use for a regional?. 3. What is ion trapping, and what is its significance to obstetrics?. Ion trapping occurs in an acidic environment when ionized local anesthetic accumulates. It can be seen in the case of an acidic fetus, and leads to an increased concentration of local anesthetic in the fetal blood, and can jeopardize the fetal circulatory systems own response to asphyxia.. 4. What is the maximum dose of 0.25% bupivacaine that the surgeon can use for infiltration of the surgical incision site?. The maximum dose is 80 kg X 2mg/kg, which is 160 mg total. At 2.5 mg per cc, the total injected safe dose is 160 divided by 2.5, or 64 cc.. 5. Why is epinephrine added to local anesthetics?. To cause local vasoconstriction, decrease the vascular absorption of ...
HealthDay)-Racial differences in disease expression and adverse clinical outcomes exist between black and white patients with hypertrophic cardiomyopathy, according to a study published online Dec. 4 in JAMA Cardiology.. Lauren A. Eberly, M.D., from Brigham and Womens Hospital in Boston, and colleagues assessed data from the Sarcomeric Human Cardiomyopathy Registry (1989 through 2018) to evaluate the associations among race, disease expression, care provision, and clinical outcomes among patients with hypertrophic cardiomyopathy.. The researchers identified 2,467 patients with hypertrophic cardiomyopathy (8.3 percent black; 91.7 percent white). Black patients were younger at the time of diagnosis (mean age, 36.5 versus 41.9 years), had a higher prevalence of New York Heart Association (NYHA) class III or IV heart failure at presentation (22.6 versus 15.8 percent), had lower rates of genetic testing (54.1 versus 62.1 percent), and were less likely to have sarcomeric mutations identified by ...
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A quick reference on Obstructive hypertrophic cardiomyopathy, covering the clinical presentation, investigative approach, and key principles of management
Diagnosis and Management of Hypertrophic Cardiomyopathy : Diagnosis and Management of Hypertrophic Cardiomyopathy is a unique, multi-authored compendium of information regarding the complexities of clinical and genetic diagnosis, natural history, and management of hypertrophic cardiomyopathy (HCM)-the most common and important of the genetic cardiovascular diseases-as well as related issues impacting the health of trained athletes. Edited by Dr.
Another name for Hypertrophic Cardiomyopathy is Hypertrophic Cardiomyopathy. To better understand hypertrophic cardiomyopathy, it helps to understand ...
OBJECTIVE: To clarify the morphological basis of the limited coronary reserve in hypertrophic cardiomyopathy (HCM). BACKGROUND: Some of the symptoms in Hypertrophic cardiomyopathy (HCM), such as chest pain, dyspnea and arrhythmia, may be explained by myocardial ischemia. Many patients with HCM are known to exhibit these symptoms in the absence of atherosclerosis in the major coronary vessels. Decreased myocardial perfusion has been demonstrated in HCM, however, little is known about the myocardial capillary morphology in this disease. METHODS: Using immunohistochemistry and morphometry, we analysed capillaries and cardiomyocytes in myectomy specimens from 5 patients with HCM with moderate hypertrophy and left ventricular outflow tract obstruction and in 5 control hearts. RESULTS: The number of capillaries per cardiomyocyte (p,0.009) and number of capillaries per cardiomyocyte area unit, reflecting cardiomyocyte mass (p=0.009), were lower in individuals with HCM, i.e. indicating loss of ...
Introduction- Estrogen-related receptor gamma (ERRγ) is an orphan nuclear receptor that has biological roles mainly in metabolism and it controls metabolic switching in perinatal heart. In adult heart diseases, however, the functional roles of ERRγ have not yet been elucidated.. Hypothesis- In the present study, we aimed to characterize the role of ERRγ in cardiac hypertrophy. Here we show that ERRγ provokes cardiac hypertrophy by inducing GATA4 and that its inverse agonist, GSK-5182, prevents cardiac hypertrophy.. Methods and Results- The functional roles of ERRγ in association with development of cardiac hypertrophy were examined in primarily cultured cardiomyocytes, in animal models, and in heart samples from human hypertrophic cardiomyopathy patients. ERRγ expression was increased in hearts obtained from human hypertrophic cardiomyopathy patients and in both agonist-induced cellular models and aortic banding-induced animal models of cardiac hypertrophy. Transgenic overexpression in ...
A 63 year-old woman presented with fatigue and pro-gressive shortness of breath on exertion (class III NYHA). The patient reported remained asymptomatic until age 55, when she was diagnosed with severe subaortic stenosis. Transthoracic echocardiography, at that time, showed left ventricle (LV) hypertrophy - intraventricular septum (IVS) 13 mm and LV posterior wall (PP) 13 mm, LV outflow tract gradient of 107/43 mmHg, mitral regurgitation grade I-II and 50% ejection fraction (EF). There is no any data available related with the morphology of aortic or mitral valve. The patient had several cardiovascular risk factors, such as 6- year history of moderate hypertension, dyslipidemia, 6-year history of diabetes mellitus type II treated with oral antidiabetic agents and family history of sudden cardiac arrest (father died of sudden cardiac arrest when he was 65 years). She followed the treatment as prescribed in 2005 with betablockers and non-dihydropyridine calcium channel blocker and had a favorable ...
TY - JOUR. T1 - Contemporary Surgical Management of Hypertrophic Cardiomyopathy in the United States. AU - Wei, Lawrence M.. AU - Thibault, Dylan P.. AU - Rankin, J. Scott. AU - Alkhouli, Mohamad. AU - Roberts, Harold G.. AU - Vemulapalli, Sreekanth. AU - Yerokun, Babatunde. AU - Ad, Niv. AU - Schaff, Hartzell V.. AU - Smedira, Nicholas G.. AU - Takayama, Hiroo. AU - McCarthy, Patrick M. AU - Thourani, Vinod H.. AU - Ailawadi, Gorav. AU - Jacobs, Jeffrey P.. AU - Badhwar, Vinay. PY - 2019/2/1. Y1 - 2019/2/1. N2 - Background: The primary surgical therapy for hypertrophic cardiomyopathy with obstruction is septal myectomy (SM). The current outcomes of SM with and without concomitant mitral operations in the United States was examined using The Society of Thoracic Surgeons database. Methods: From July 2014 through June 2017, 4,274 SM operations were performed. Emergent status, endocarditis, aortic stenosis, and planned aortic valve operations were excluded. In the final cohort of 2,382 patients, ...
The prognosis of patients diagnosed as having hypertrophic cardiomyopathy at advanced age has not been well defined. This study details follow-up information obtained for 95 patients initially diagnosed as having hypertrophic cardiomyopathy at age ≥65 years. Seventy-five percent of patients were symptomatic, as defined by the presence of chest pain, dyspnea or syncope, and the mean ventricular septal thickness was 20 mm. The median duration of follow-up study was 4.2 years. The survival rate at 1 and 5 years was 95% and 76%, respectively, which was not significantly different from that of an age- and gender-matched control group. Of patients presenting with New York Heart Association functional class I or II dyspnea, only 18% progressed to class III or IV during the follow-up period. However, patients presenting with class III dyspnea had a 1 year mortality rate of 36%, significantly higher than that of control subjects (p < 0.003). Of the echocardiographic variables, indexed left atrial ...
Hypertrophic cardiomyopathy - Can you tell me the medical definition of hypertrophic obstructive cardiomyopathy? Defined. Most often the portion of the heart between the right and left ventricles (septum) is thickened. This narrows the region below the aortic valve and causes a portion of mitral valve to be sucked into this area during ventricular ejection (emptying). As a result there is narrowing of outflow leading to obsruction.
STUDY RATIONALE:. Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterized by histopathologic findings of cardiac myocyte disarray and fibrosis, and clinical manifestations of unexplained left ventricular hypertrophy (LVH), diastolic dysfunction, and an increased risk for sudden death. It is a common disorder affecting approximately 1 in 1000 individuals in the general population. Dominantly-acting mutations in contractile proteins-genes encoding the elements of the sarcomere apparatus-- have been shown to be the genetic etiology of HCM. Contemporary management strategies for HCM focus on identification of individuals at high risk for sudden death and management of symptoms. There is no current therapy available which address disease prevention or phenotypic attenuation.. Dysregulation of intracellular calcium handling is a fundamental and early manifestation of sarcomere mutations. Animal models of HCM demonstrated abnormal Ca2+ cycling prior to the development of myocyte disarray ...
By the end of this presentation, viewers will be able to: Learning objectives: Recognize dynamic nature of left ventricular outflow obstruction and the various provocative maneuvers that should be utilized in symptomatic patients without significant resting outflow gradient....
Late gadolinium enhancement in hypertrophic cardiomyopathy: When should we use it in risk stratification of our patients? Hypertrophic cardiomyopathy (HCM) is associated with complications including heart failure and sudden cardiac death (SCD). The ...
Familial hypertrophic cardiomyopathy (FHCM) is an autosomal dominant disease with protean clinical manifestations, ranging from asymptomatic to that of severe heart failure or sudden death. There ist no known parameter in individuals with hypertrophic cardiomyopathy (HCM) that predicts a specific clinical event. This is particularly troublesome for premature sudden death that frequently occurs in young athletes without prior symptoms. Recent identifications of mutations in the beta-myosin heavy chain (betaMHC) gene that co-segregate with the inheritance of the disease provides an opportunity to determine whether certain mutations are more likely to induce a particular clinical event. In this study we analyzed the genotype and phenotype of individuals from two unrelated families with HCM in which the affected individuals have the same missense mutation in exon 13 (G1208A) of the coding sequence for betaMHC. Results: We studied 54 individuals from the two families, 21 were affected with HCM of ...
TY - JOUR. T1 - Echocardiography-guided genetic testing in hypertrophic cardiomyopathy. T2 - Septal morphological features predict the presence of myofilament mutations. AU - Binder, Josepha. AU - Ommen, Steve R.. AU - Gersh, Bernard J.. AU - Van Driest, Sara L.. AU - Tajik, A. Jamil. AU - Nishimura, Rick A.. AU - Ackerman, Michael J.. PY - 2006/4. Y1 - 2006/4. N2 - OBJECTIVE: To examine the relationship among age, septal morphological subtype, and presence of hypertrophic cardiomyopathy (HCM)-associated myofilament mutations. PATIENTS AND METHODS: Comprehensive mutation analysis of the 8 HCM susceptibility genes that encode the myofilaments of the cardiac sarcomere was performed previously in 382 unrelated patients with HCM. Blinded to genotype status, we used echocardiography to characterize the left ventricular morphological features. Multivariate regression was used to assess the relationship among morphological subtypes, clinical data, and genetic variables. RESULTS: The mean ± SD age of ...
This is the business view business. Hypertrophic cardiomyopathy Is a condition in which the heart muscle becomes thick. The thickening makes it harder for blood to leave the heart forcing the heart to work harder to pump blood. Hypertrophic cardiomyopathy is often asymmetrical, meaning one ...
... (HCM) is a genetically transmitted disease that directly affects the heart muscle.
Familial hypertrophic cardiomyopathy, also known as FHC or HCM, is a rare condition best known publicly for its association with sudden death among young athletes. It is estimated that about 1 in 500 people have HCM and the associated thickening of the heart muscle (hypertrophy). An irregular heartbeat (arrhythmia) may lead to collapse and death during or after an athletic competition. There are usually no symptoms of a heart condition before the sudden collapse, which is also called sudden cardiac death or SCD. Fortunately, SCD occurs to a very small fraction of those carrying HCM mutations. Ordinary screening does not pick up this condition. A family history of sudden death before age 50 may be the only clue that a child or teenager needs a closer medical check before starting a sport. Most HCM appears to be inherited in a dominant fashion. Family members who carry the same genes may not have cardiac hypertrophy; those who do have hypertrophy can be treated clinically, and they will ...
In a pathbreaking proof of concept experimental study, MYBPC3 gene mutation causing hypertrophic cardiomyopathy has been corrected in human embryos using CRISPR-Cas9 gene editing technique.
Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric left ventricular hypertrophy, diastolic dysfunction and myocardial disarray. HCM is caused by mutations in sarcomeric genes, but in 40 of patients, the mutation is not yet identified. We hypothesized that FHL1, encoding four-and-a-half-LIM domains 1, could be another disease gene since it has been shown to cause distinct myopathies, sometimes associated with cardiomyopathy. We evaluated 121 HCM patients, devoid of a mutation in known disease genes. We identified three novel variants in FHL1 (c.134delA/K45Sfs, c.459CA/C153X and c.827GC/C276S). Whereas the c.459CA variant was associated with muscle weakness in some patients, the c.134delA and c.827GC variants were associated with isolated HCM. Gene transfer of the latter variants in C2C12 myoblasts and cardiac myocytes revealed reduced levels of FHL1 mutant proteins, which could be rescued by proteasome inhibition. Contractility measurements after adeno-associated virus transduction ...
Background: Heterogeneous phenotypic expression in hypertrophic cardiomyopathy (HCM) results in challenging risk stratification. Risk stratification is limited due to lack of hypertrophy visualized by transthoracic echocardiography (TTE) particularly of the lateral wall and apical hypertrophy. Cardiac magnetic resonance (CMR) provides better visualization and more accurate assessment of LV wall thickness and mass. In addition, the role of LV mass in risk stratification of HCM has not been clearly understood.. Objective: There were two main objectives of the study. Firstly, to investigate the effect of maximum LV wall thickness (LVWTmax) measured by MRI and TTE on the 5-year ESC risk of sudden cardiac death. Secondly, to investigate the relationship of indexed LVmass on CMR with the incidence of insertion of an implantable cardioverter defibrillator (ICD).. Methods: HCM subjects were retrospectively analysed for a mean duration of 5.7 ± 3.3 years in a single tertiary centre. LVmass and LVWTmax ...
Hypertrophic cardiomyopathy (HCM) accounts for 42% of childhood cardiomyopathy, with a prevalence of 0.47/100,000 and mortality rates in the region of 1- 2%.1-3 A small minority of children with HCM complain of symptoms attributable to left ventricular outflow obstruction (LVOTO). Medical management of LVOTO involves the use of beta blockers, calcium channel antagonists and disopyramide. In those with refractory symptoms, surgical myomectomy remains the gold standard4,5 but this can be technically challenging in children and few centres have the necessary experience. In adults, alcohol septal ablation can be an alternative to surgery, but there is a general consensus that it should not be used in children due to concerns relating pro-arrhythmia and technical limitations.4,5 Isolated case reports and a case series published earlier this year have suggested that an alternative technique, endocardial radiofrequency septal ablation (RFSA) may be useful in the paediatric setting.6,7 ...
Intra- and interatrial electromechanical delay (AEMD) can be used to evaluate the development of atrial fibrillation (AF). Percutaneous transluminal septal myocardial ablation (PTSMA) is an alternative therapy for patients with hypertrophic obstructi
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Hypertrophic cardiomyopathy (HCM) was first described by Donald Teare et al. in 1957 in a series of eight patients with asymmetric septal hypertrophy.1 Later in that decade, Morrow and Braunwald described three cases of a clinical syndrome mimicking aortic stenosis, which was solved by resection of the subaortic interventricular septum.2. HCM has been reported in several countries, in individuals of both sexes with varied racial and ethnic backgrounds, with or without resting left ventricular obstruction, but with similar genotypic abnormalities. Its estimated incidence is 1 per 500 individuals in the general population (0.2%), but delay in diagnosis is common. HCM is an important public health problem due to sudden cardiac death (SCD), heart failure (HF), atrial fibrillation and ventricular arrhythmias that occur in the course of the disease.3. HCM is a monogenic disease caused by a mutation in one of the 13 or more genes encoding the protein components of the sarcomere. It has an autosomal ...
The Syrian cardiomyopathic hamster (BIO14.6), that develops both muscular dystrophy and progressive cardiomyopathy, is widely used as an animal model of autosomal recessive cardiomyopathy mimicking human hypertrophic cardiomyopathy, and five genes have been proposed as strong candidates for the cause of cardiomyopathy. We recently mapped the cardiomyopathy locus of the hamster to the centromeric region of chromosome 9qa2.1-b1 by construction of a genetic linkage map of the Syrian hamster. Thus, we analyzed the loci of the five candidate genes, α tropomyosin, cardiac troponin T, adhalin, calpain 3 and cardiac myosin binding protein-C, by the FISH method, and found that these genes were mapped on the distal portion of chromosome 12qa5 and 4pa2 and the proximal portion of chromosomes 9qb7, 1qc1.1 and 1qb3, respectively. These results provide strong evidence that the five candidate genes previously proposed are not related to the hamster cardiomyopathy.. ...
Familial hypertrophic cardiomyopathy 12 information including symptoms, diagnosis, misdiagnosis, treatment, causes, patient stories, videos, forums, prevention, and prognosis.
Background: Hypertrophic cardiomyopathy (HCM) is often caused by sarcomere gene mutations, resulting in left ventricular hypertrophy (LVH), myocardial fibrosis, and increased risk of sudden cardiac death and heart failure. Studies in mouse models of sarcomeric HCM demonstrated that early treatment with an angiotensin receptor blocker (ARB) reduced development of LVH and fibrosis. In contrast, prior human studies using ARBs for HCM have targeted heterogeneous adult cohorts with well-established disease. The VANISH trial is testing the safety and feasibility of disease-modifying therapy with an ARB in genotyped HCM patients with early disease. Methods: A randomized, placebo-controlled, double-blind clinical trial is being conducted in sarcomere mutation carriers, 8 to 45 years old, with HCM and no/minimal symptoms, or those with early phenotypic manifestations but no LVH. Participants are randomly assigned to receive valsartan 80 to 320 mg daily (depending on age and weight) or placebo. The ...
The literature shows that genetic testing could stimulate solidarity among family members, but also lead to major conflicts. To prevent negative effects, clinical geneticists and ethicists have stressed the importance of good communication within families. In this qualitative study, we followed six extended families in the southern and eastern Netherlands involved in genetic testing for familial hypertrophic cardiomyopathy for three and a half years. In total 57 members of these families were interviewed in depth, most more than once. Our analysis shows that genetic testing does affect families, but that families perform a lot of balancing work in order to prevent genetic testing from becoming too all-encompassing. There is much more continuity in family life than is often thought. Moreover, as these families demonstrate different styles of family work, establishing a single norm of good communication in clinical genetics might in fact be more harmful for family life than genetic testing ...
In most cases, hypertrophic cardiomyopathy will not have an impact on daily life. Some people do not have any symptoms and do not need treatment.. But that does not mean the condition cannot be serious. Hypertrophic cardiomyopathy is the most common cause of sudden unexpected death in childhood and in young athletes.. The main heart chambers can become stiff, leading to back pressure on the smaller collecting chambers. This can sometimes worsen the symptoms of heart failure and lead to abnormal heart rhythms (atrial fibrillation).. Blood flow from the heart may be reduced or restricted (called obstructive hypertrophic cardiomyopathy). Also, the mitral heart valve can become leaky, causing blood to leak backwards. Find out more about mitral regurgitation.. Youll also be at greater risk of developing a heart infection (endocarditis).. These heart changes can cause dizziness, chest pain, shortness of breath and temporary loss of consciousness.. If you have severe hypertrophic cardiomyopathy, ...
Hypertrophic cardiomyopathy (HCM) is an inherited disease of heart muscle that can be caused by mutations in sarcomere proteins. Clinical diagnosis depends on an abnormal thickening of the heart, but the earliest signs of disease are hyperdynamic contraction and impaired relaxation. Whereas some in vitro studies of power generation by mutant and wild-type sarcomere proteins are consistent with mutant sarcomeres exhibiting enhanced contractile power, others are not. We identified a small molecule, MYK-461, that reduces contractility by decreasing the adenosine triphosphatase activity of the cardiac myosin heavy chain. Here we demonstrate that early, chronic administration of MYK-461 suppresses the development of ventricular hypertrophy, cardiomyocyte disarray, and myocardial fibrosis and attenuates hypertrophic and profibrotic gene expression in mice harboring heterozygous human mutations in the myosin heavy chain. These data indicate that hyperdynamic contraction is essential for HCM ...
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Learn about the treatment options available for hypertrophic cardiomyopathy, including alcohol septal ablation, an innovative minimally invasive procedure we offer for cardiomyopathy that improves blood flow out of the heart.
Familial hypertrophic cardiomyopathy (HCM) is caused by mutations in 9 sarcomeric protein genes. The most commonly affected is beta-myosin heavy chain (MYH7), where missense mutations cluster in the head and neck regions and directly affect motor function. Comparable mutations have not been described in the light meromyosin (LMM) region of the myosin rod, nor would these be expected to directly affect motor function. We studied 82 probands with HCM in whom no mutations had been found in MYH7 exons encoding the head and neck regions of myosin nor in the other frequently implicated disease genes. Primers were designed to amplify exons 24 to 40 of MYH7. These amplimers were subjected to temperature modulated heteroduplex analysis by denaturing high-performance liquid chromatography. An Ala1379Thr missense mutation in exon 30 segregated with disease in three families and was not present in 200 normal chromosomes. The mutation occurred on two haplotypes, indicating that it was not a polymorphism linked with
Hypertrophic cardiomyopathy is a primary myocardial disorder with an autosomal dominant pattern of inheritance, characterized by an asymmetric thickening (hypertrophy) of the muscle of the left ventricle. In approximately 25% of patients there is a narrowing (obstruction) of the left ventricular outflow tract. The estimated prevalence of HCM in the general population is 1 in 500. Men and women are equally affected. Most patients are asymptomatic. Shortness of breath, chest pain, palpitations or fainting may occur. Exercise-dependent cardiac arrhythmias can lead to sudden death. Athletes with HCM are generally discouraged from competitive sports. ...
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We sought to evaluate the relation between atrial fibrillation (AF) and the extent of myocardial scarring together with left ventricular (LV) and atrial parameters assessed by late gadolinium-enhancement (LGE) cardiovascular magnetic resonance (CMR) in patients with hypertrophic cardiomyopathy (HCM). AF is the most common arrhythmia in HCM. Myocardial scarring is also identified frequently in HCM. However, the impact of myocardial scarring assessed by LGE CMR on the presence of AF has not been evaluated yet. 87 HCM patients underwent LGE CMR, echocardiography and regular ECG recordings. LV function, volumes, myocardial thickness, left atrial (LA) volume and the extent of LGE, were assessed using CMR and correlated to AF. Additionally, the presence of diastolic dysfunction and mitral regurgitation were obtained by echocardiography and also correlated to AF. Episodes of AF were documented in 37 patients (42%). Indexed LV volumes and mass were comparable between HCM patients with and without AF. However,
Although mutations in cMyBP‐C are one of the most frequent causes of hypertrophic cardiomyopathy on a per gene basis with ,150 individual mutations being documented, the majority of these mutations (≈60%) result not in a full‐length, mutated protein, but in a truncated peptide and these mutated alleles exhibit autosomal dominance.29, 30 We have shown that a truncated form of cMyBP‐C is produced from endogenous, normal cMyBP‐C as a result of ischemia-reperfusion injury and/or general cardiovascular stress and is generated from Ca2+ activated μ‐calpain activity.2 This fragment is stable, can be expressed inducibly in cardiomyocytes and causes cardiac disease, fibrosis, and eventually heart failure and death.4 This model displays pathology that is often seen in human cardiac fibrosis and myocardial disease: the hearts develop hypertrophy and show extensive interstitial fibrosis and perivascular fibrosis while maintaining systolic function. Thus, in terms of a fibrotic response, the ...
Hypertrophic cardiomyopathy (HCM) is a condition in which a portion of the heart becomes thickened without an obvious cause. This results in the heart being less able to pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications include heart failure, an irregular heartbeat, and sudden cardiac death. HCM is most commonly inherited from a persons parents. It is often due to mutations in certain genes involved with making heart muscle proteins. Other causes may include Fabry disease, Friedreichs ataxia, and certain medications such as tacrolimus. It is type of cardiomyopathy, a group of diseases that primarily affects the heart muscle. Diagnosis often involves an electrocardiogram, echocardiogram, and stress testing. Genetic testing may also be done. Treatment may include the use of beta blockers, diuretics, or disopyramide. An implantable cardiac defibrillator may be recommended in those ...
MYBPC3 encodes the cardiac isoform of myosin-binding protein C. Myosin-binding protein C is a myosin-associated protein found in the cross-bridge-bearing zone (C region) of A bands in striated muscle. MYBPC3, the cardiac isoform, is expressed exclussively in heart muscle. MYBPC gene is linked to CMH4 and demonstrated a splice donor mutationin 1 family with familial hypertrophic cardiomyopathy and a duplication mutation in a second. Both mutations were predicted to disrupt the high-affinity, C-terminal myosin-binding domain of cardiac MyBP-C. Again, findings demonstrated that as in the case of the 3 forms that had been defined in molecular terms previously, familial hypertrophic cardiomyopathy is a disease of the sarcomere.
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Evolution of dilated cardiomyopathy from hypertrophic obstructive cardiomyopathy in a child.: Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM)
... (HCM) is far and away the most common form of heart disease in the cat. Diagnosis of HCM means that there is a primary disease process causing the myocytes of the heart to behave inappropriately, and leads to enlargement of the heart, primarily of the left ventricle (the main muscular chamber that pumps blood to the body). Secondary hypertrophic diseases of the heart may be caused by hyperthyroidism or hypertension, and lead to signs that mimic HCM, but if addressed early may be reversible by treating the underlying condition. Primary HCM is not reversible, and has been shown to have a genetic link, particularly in Main Coons. Unfortunately, genotyping is not yet available. It is not yet possible to isolate the gene that causes HCM in cats, but through studying family trees, it has been shown to be an autosomal dominant gene in some Main Coons and likely other breeds as well. In cats, HCM presents with a high degree of phenotypic heterogeneity from patient to ...
1 Answer - Posted in: cardiomyopathy, hypertrophic cardiomyopathy, pain - Answer: I have hcm and back pain and fibro. I know that there are pain meds ...
- Hypertrophic cardiomyopathy is a condition in which a portion of the heart muscle is abnormally thick. This can make it harder for blood to flow into and out of the heart and cause other problems.
BACKGROUND: Interpretation of the athletes ECG is based on differentiation between benign ECG changes and potentially pathological abnormalities. The aim of the study was to compare the 2010 European Society of Cardiology (ESC) and the 2017 International criteria for differential diagnosis between hypertrophic cardiomyopathy (HCM) and athletes heart. METHODS: The study populations included 200 patients with HCM and 563 athletes grouped as follows: group 1, including normal ECG and isolated increase of QRS voltages, which are considered non-pathologic according to ESC and International criteria; group 2, including left atrial enlargement or left axis deviation in isolation and Q-waves with an amplitude ≥4 mm but ,25% of the ensuing R-wave and a duration ,0 ...
Live/real time three-dimensional transthoracic echocardiography in hypertrophic cardiomyopathy with mid-left ventricular obstruction and apical aneurysm. Multiplanar reconstruction (MPR) mode. A small appearing thrombus (right upper panel, red box) has been cropped (green line) to demonstrate its full extent (left upper panel, green box).
Hypertrophic Cardiomyopathy, Sudden Death, and Endocarditis. A small number of people with HCM have an increased risk of sudden cardiac death. People at risk include.: Those who have family members who have had sudden cardiac death. Young people with HCM who have had several episodes of fainting. Those who have an abnormal blood pressure response with exercise. Adults who have a history of arrhythmia with a fast heart rate. Those with severe symptoms and poor heart function. If you have two or more risk factors for sudden cardiac death, your doctor will treat you with medications to prevent arrhythmias or with an ICD. Most people with HCM are at low risk for sudden cardiac death. Talk to your doctor about any concerns you may have. How Can I Prevent Endocarditis? People with obstructive HCM may be at increased risk for infective endocarditis, a potentially life-threatening condition ...
Hypertrophic cardiomyopathy (HCM) is a primary myocardial disorder with an autosomal dominant pattern of inheritance that is characterized by hypertrophy of the left ventricles with histological features of myocyte hypertrophy, myfibrillar disarray, and interstitial fibrosis. HCM is one of the most common inherited cardiac disorders, with a prevalence in young adults of 1 in 500. Hundreds of mutations in the genes that encode protein constituents of the sarcomere have been identified in HCM. These mutations increase the Ca2+ sensitivity of cardiac myofilaments. Increased myofilament Ca2+ sensitivity is expected to increase the ATP utilization by actomyosin at submaximal Ca2+ concentrations, which might cause an imbalance in energy supply and demand in the heart under severe stress. The inefficient use of ATP suggests that an inability to maintain normal ATP levels could be the central abnormality. This theory might be supported by the discovery of the role of a mutant PRKAG2 gene in HCM, which ...
Hypertrophic cardiomyopathy (HCM) is a primary myocardial disorder with an autosomal dominant pattern of inheritance that is characterized by hypertrophy of the left ventricles with histological features of myocyte hypertrophy, myfibrillar disarray, and interstitial fibrosis. HCM is one of the most common inherited cardiac disorders, with a prevalence in young adults of 1 in 500. Hundreds of mutations in the genes that encode protein constituents of the sarcomere have been identified in HCM. These mutations increase the Ca2+ sensitivity of cardiac myofilaments. Increased myofilament Ca2+ sensitivity is expected to increase the ATP utilization by actomyosin at submaximal Ca2+ concentrations, which might cause an imbalance in energy supply and demand in the heart under severe stress. The inefficient use of ATP suggests that an inability to maintain normal ATP levels could be the central abnormality. This theory might be supported by the discovery of the role of a mutant PRKAG2 gene in HCM, which ...
Hypertrophic cardiomyopathy (HCM) is a genetically determined heart muscle disease caused by mutations in one of several sarcomere genes which encode components of the contractile apparatus. (See.)HCM is characterized by an enormous diversity in both
http://www.ncbi.nlm.nih.gov/pubmed/24819852 Eur Heart J Cardiovasc Imaging. 2014 May 12. [Epub ahead of print] A comprehensive evaluation of myocardial fibrosis in hypertrophic cardiomyopathy with cardiac magneticresonance imaging: linking genotype with fibrotic phenotype. Ellims AH1, Iles LM, Ling LH, Chong B, Macciocca I, Slavin GS, Hare JL, Kaye DM, Marasco SF, McLean CA, James PA, du Sart…
A 66-year-old woman was referred to our service because of a presyncope on effort and dyspnoea of exercise. Blood pressure was 130/85 mmHg, heart rate 78/min, with a left parasternal systolic murmur grade 4/6 and no clinical signs of pulmonary or systemic venous congestion. ECG showed sinus rhythm and left ventricular (LV) hypertrophy with strain. Echocardiography showed LV hypertrophy (interventricular septum 18 mm, posterior wall 15 mm in diastole); reduced LV cavity (diastolic LV diameter 36 mm, systolic LV diameter 18 mm), with good ejection fraction. Anatomic M mode showed anterior systolic motion of both mitral valves (Panel A- white arrows = early systole; red arrows = late systole). 3D echo confirmed the anterior displacement of both valve leafl ets (Panel B - white and red arrows) and crossover of mitral valves (Panel C - red arrow). The mitral leaflets appear elongated (Panel C-red arrow), oversized for the left ventricular size and together with the asymmetrical hypertrophy of the ...
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Aims To explore the cost-effectiveness of alternative methods of screening family members for hypertrophic cardiomyopathy (HCM), the most common monogenic cardiac disorder and the most frequent cause of sudden cardiac death (SCD) in young people. Methods and results Economic decision model comparing cascade screening by genetic, as opposed to clinical methods. The incremental cost per life year saved was 14,397 euro for the cascade genetic compared with the cascade clinical approach. Genetic diagnostic strategies are more likely to be cost-effective than clinical tests alone. The costs for cascade molecular genetic testing were slightly higher than clinical testing in the short run, but this was largely because the genetic approach is more effective and identifies more individuals at risk. Conclusion The use of molecular genetic information in the diagnosis and management of HCM is a cost-effective approach to the primary prevention of SCD in these patients.
Although hypertrophic cardiomyopathy is common (about 1 in 500 people have it), it affects each person differently. Some people have no symptoms their entire lives while others face serious risks of stroke or sudden cardiac death.. If you have symptoms or a family history of HCM, you may need an echocardiograph (ECG). Echocardiographs use ultrasound technology to look at the heart as it beats. Talk to your doctor about whether an echocardiograph is the right choice for you and your family.. ...
Early screening for a genetic variant that predisposes people to hypertrophic cardiomyopathy could help reduce the incidence of sudden cardiac death.
Published: 01 Mar 2019 , Last Updated: 01 Mar 2019 15:15:05 Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease in humans (1 in 500) and cats (1 in 7). The disease is strikingly similar in the two species, although the feline prevalence is much higher. HCM is characterized by significant clinical heterogeneity making the diagnosis challenging. Cats with subclinical disease can be difficult to identify without specialist testing; cats with severe disease can develop heart failure, painful paralysis due to thromboembolic complications, or they die suddenly and unexpectedly causing distress to cat owners and frustration to veterinarians.. In both humans and cats HCM is heritable. Previous studies in the Maine coon and Ragdoll cat breeds have identified two genetic risk factors also known to affect humans. However, these risk factors are not segregating among other cat breeds.At the RVC, a new scientific research project has just started with the goal of enhancing our ...
Dr Shivanee Shah. A 32-year-old man, Nikhil (name changed), brought his 2 sons to the one-of-its-kind Hypertrophic Cardiomyopathy Centre at Amrita Institute of Medical Sciences (AIMS), Kochi, to be screened for hypertrophic cardiomyopathy (HCM). While Nikhils boys, aged 6 and 2, had no obvious symptoms, he himself had been an HCM patient since his teen years and had come to ascertain the fate of his children. The HCM history went beyond Nikhil; his mother also had been diagnosed with the same condition, and at the age of 28, had sadly collapsed while working and died of sudden cardiac arrest.. Nikhil, the only son, had undergone ECG and echo studies at VSM Hospital, Mavelikkara, and was diagnosed with HCM. During a follow-up examination, it was observed that his condition had worsened considerably, and by age 17, his myocardial thickness had increased to such an extent that there were overt signs of obstructive hypertrophic cardiomyopathy that could no longer be controlled by medication. Nikhil ...
This work proposes an image processing methodology to distinguish fibrotic from normal tissue by the assessment of the local mechanical properties of the myocardium in magnetic resonance tagging images. The procedure uses the information provided by short axis images of the above mentioned modality to estimate the Green-Lagrange strain tensor; a modified method based on the Harmonic Phase is employed for motion estimation. The method has been applied to the analysis of the local deformation patterns in a set of patients affected by hypertrophic cardiomyopathy in order to find the agreement between hyperenhanced zones in late enhancement images and areas in the myocardium with abnormal tensor values (both the radial and the circumferential components as well as the shearing component have been accounted for). The agreement is measured taken as ground truth manual segmentation of late enhancement images carried out by two cardiologists. Finally, a set of example images illustrate the agreement ...
Hypertrophic cardiomyopathy, or HCM, is the most common heart disease diagnosed in cats. It is a disease that affects the heart muscle, causing the muscle to become thickened and ineffective in pumping the blood through the heart and the rest of the body.
Marcela suffered from hypertrophic cardiomyopathy. This is a heart disease which required her to have a heart transplant. Organ donors are needed very much. Recipients go on to lead nornal lives.
Hypertrophic cardiomyopathy (HCM) is an inherited disease of the heart muscle. HCM can cause the wall of the heart muscle to thicken.More about this condition.
Looking for online definition of Feline hypertrophic cardiomyopathy in the Medical Dictionary? Feline hypertrophic cardiomyopathy explanation free. What is Feline hypertrophic cardiomyopathy? Meaning of Feline hypertrophic cardiomyopathy medical term. What does Feline hypertrophic cardiomyopathy mean?
Figure 3. Delayed contrast enhancement short axis.. Conclusion: The CMR findings confirm, on one hand, the clinical suspicion of apical hypertrophic cardiomyopathy, by showing asymmetrically increased myocardial wall thickness of the apical region, with evidence of intramyocardial fibrosis of the hypertrophied segment. On the other hand, the study also shows the coexistence of a second pattern of DCE, characteristic, in this case, of endomyocardial fibrosis, involving both, the right and left ventricular apical regions.. Perspective: Idiopathic hypereosinophilic syndrome (HES) is rare and frequently involves the heart with development of endomyocardial fibrosis, a characteristic restrictive cardiomyopathy with uni- or biventricular endocardial fibrous tissue proliferation, preferably in the apical region and inflow tract, which leads to diastolic dysfunction and, not infrequently, to embolic phenomena arising from an overlying intracavitary thrombus.(1) Although the diagnosis was initially ...
Classically, chronic intestinal angina is caused by a reduction in mesenteric blood flow [1], and the pathophysiology of most cases is atherosclerotic stenosis of the celiac and mesenteric arteries. Arterial dissection, fibromuscular dysplasia, and vasculitis are included as rare etiologies of arterial narrowing, and the median arcuate ligament of the diaphragm can compress the celiac artery and disturb blood flow (median arcuate ligament syndrome) [5, 6]. Intestinal circulation consists of an abundant collateral blood supply, and chronic intestinal ischemia is associated with high-grade stenosis or occlusion of two or more of the three major vessels: the celiac artery, the superior and inferior mesenteric arteries [7, 8]. In our case, the arterial lesions were relatively mild compared with previous reports [9, 10]; thus, we hypothesized that our patients major symptoms were not due to his arterial lesions alone.. Specifically, our patients symptoms depended greatly on his hemodynamic ...
Medical information, Alcoholic cardiomyopathy. Definition of Alcoholic cardiomyopathy, symptoms of Alcoholic cardiomyopathy, treatment of Alcoholic cardiomyopathy, and prevention of Alcoholic cardiomyopathy. Exams and Tests Alcoholic cardiomyopathy.
TY - JOUR. T1 - Linkage analysis of left ventricular outflow tract malformations (aortic valve stenosis, coarctation of the aorta, and hypoplastic left heart syndrome). AU - McBride, Kim L.. AU - Zender, Gloria A.. AU - Fitzgerald-Butt, Sara M.. AU - Koehler, Daniel. AU - Menesses-Diaz, Andres. AU - Fernbach, Susan. AU - Lee, Kwanghyuk. AU - Towbin, Jeffrey A.. AU - Leal, Suzanne. AU - Belmont, John W.. PY - 2009/1/15. Y1 - 2009/1/15. N2 - The left ventricular outflow tract (LVOT) malformations aortic valve stenosis (AVS), coarctation of the aorta (CoA), and hypoplastic left heart syndrome (HLHS) are significant causes of infant mortality. These three malformations are thought to share developmental pathogenetic mechanisms. A strong genetic component has been demonstrated earlier, but the underlying genetic etiologies are unknown. Our objective was to identify genetic susceptibility loci for the broad phenotype of LVOT malformations. We genotyped 411 microsatellites spaced at an average of 10 cM ...
hereditary galactose intolerance, Lapp lactase deficiency or malabsorption syndrome glucose-galactose.Precautions: renovascular hypertension, bilateral renal artery stenosis, renal artery stenosis only - risk of severe hypotension and renal failure; CHF decompensation, hypotension; chronic renal insufficiency (creatinine clearance (CC) of less than 60 ml / min); significant hypovolemia and hyponatremia (due to salt-free diet and / or previous therapy with diuretics, dialysis, vomiting, diarrhea), cerebrovascular disease (including cerebrovascular insufficiency, coronary heart disease, coronary insufficiency) - the risk of excessive reduction of blood pressure; stenosis of the aortic or mitral valve, hypertrophic obstructive cardiomyopathy, hemodialysis using vysokoprotochnyh nitron polyacrylic membrane - the risk of anaphylactoid reactions; condition after kidney transplantation - is no clinical experience;apheresis procedure to low density lipoprotein (LDL), simultaneous desensitizing therapy ...
Pulmonary veno-occlusive disease: not recommended. PAH secondary to sickle cell anemia (risk of vaso-occlusive crisis). Underlying conditions that could be affected by vasodilatory effects (eg, concomitant antihypertensive therapy, BP,90/50, fluid depletion, severe left ventricular outflow obstruction, autonomic dysfunction). Risk of non-arteritic anterior ischemic optic neuropathy; monitor for sudden vision loss. Retinitis pigmentosa. Anatomical penile deformation. Predisposition to priapism. Severe hepatic impairment. Active peptic ulcer. Bleeding disorders. Elderly. Pregnancy. Nursing mothers.. ...
It is suggested that Borrelia burgdorferi infection could be associated with dilated cardiomyopathy (IDC). Stanek et al. were able to cultivate Borrelia burgdorferi from myocardial biopsy tissue of a patient with longstanding dilated cardiomyopathy. Here we present a study in which we examined the effect of standard antibiotic treatment on the left ventricular ejection fraction (LVEF) in patients with dilated cardiomyopathy associated with Borrelia burgdorferi infection. In this study we assessed the serum (IgG, IgM Elisa) and history of 46 IDC patients with specific regard to Borrelia burgdorferi infection (mean LVEF 30.4 +/- 1.3%, measured by cardiac catheterization and echocardiography with the length-area-volume method). All 46 patients received standard treatment for dilated cardiomyopathy: ACE inhibitors, digitalis, and diuretics. Eleven (24%) patients showed positive serology and a history of Borrelia burgdorferi infection; nine of these also had a typical history of tick bite and ...
Results:. Alcoholic patients with cardiomyopathy had less muscle strength than did alcoholic patients with normal cardiac function, patients with idiopathic dilated cardiomyopathy, and patients with coronary heart disease (all P , 0.01). Among alcoholic patients with cardiomyopathy, 20 of 24 (83%) had histologic findings of skeletal myopathy compared with 1 of 24 (4%) alcoholic patients with normal cardiac function (P , 0.001). Interstitial fibrosis occurred in all cardiac biopsy specimens, hypertrophy of the myocytes occurred in 95%, and myocytolysis occurred in 83%. Those patients with more severe cellular hypertrophy and interstitial fibrosis of the myocardium had a greater decrease in deltoid muscle strength and had worse histologic myopathy. ...

Number 15-05: Endomyocardial fibrosis associated with apical hypertrophic cardiomyopathy. - Society for Cardiovascular Magnetic...Number 15-05: Endomyocardial fibrosis associated with apical hypertrophic cardiomyopathy. - Society for Cardiovascular Magnetic...

Number 15-05: Endomyocardial fibrosis associated with apical hypertrophic cardiomyopathy.. Case from: Veronica Aliaga, MD, ... Conclusion: The CMR findings confirm, on one hand, the clinical suspicion of apical hypertrophic cardiomyopathy, by showing ... Cardiovascular magnetic resonance in the evaluation of hypertrophic and infiltrative cardiomyopathies. Heart Fail Clin. 2009 ... Loeffler endocarditis mimicking apical hypertrophic cardiomyopathy. Circulation 2009 Jul 7;120:82-85. ...
more infohttp://scmr.org/page/COW1505/Number-15-05-Endomyocardial-fibrosis-associated-with-apical-hypertroph.htm

Systemic disease and the heart: Effects of enzyme-replacement therapy in patients with Anderson-Fabry disease: a prospective...Systemic disease and the heart: Effects of enzyme-replacement therapy in patients with Anderson-Fabry disease: a prospective...

Familial Hypertrophic Cardiomyopathy with Atypical Location. Guler, Ahmet; Tigen, Kursat M.; Aung, Soe M.; Karabay, Can Yucel; ... Apical Hypertrophic Cardiomyopathy. Ates, Mehmet; Kwong, Raymond Y.; Lipton, Martin J.; Tatli, Servet; Stainback, Raymond F ... Background: Patients with hypertrophic cardiomyopathy (HCM) exhibit a difference in left ventricular outflow tract (LVOT) ... The article describes the clinical case of a 25-year-old woman who was diagnosed with familial hypertrophic cardiomyopathy (HCM ...
more infohttp://connection.ebscohost.com/c/articles/43671861/systemic-disease-heart-effects-enzyme-replacement-therapy-patients-anderson-fabry-disease-prospective-long-term-cardiac-magnetic-resonance-imaging-study

Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

[A condition in which the myocardium is hypertrophied without an obvious cause. The hypertrophy is generally asymmetric and may be associated with obstruction of the ventricular outflow tract.]
more infohttps://www.ebi.ac.uk/ols/ontologies/NCIT/terms?iri=http%3A%2F%2Fpurl.obolibrary.org%2Fobo%2FNCIT_C34449

Hypertrophic Cardiomyopathy | OHSUHypertrophic Cardiomyopathy | OHSU

The Hypertrophic Cardiomyopathy Clinic at OHSU is the first of its kind in Oregon dedicated to treating this complicated ... Hypertrophic Cardiomyopathy The Hypertrophic Cardiomyopathy (HCM) Clinic at OHSU is the first of its kind in Oregon dedicated ... What is hypertrophic cardiomyopathy?. Dr. Stephen Heitner, cardiologist at the OHSU Knight Cardiovascular Institute, talks ... Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiac condition, is difficult to diagnose and affects each ...
more infohttps://www.ohsu.edu/knight-cardiovascular-institute/hypertrophic-cardiomyopathy

Hypertrophic Cardiomyopathy ScreeningHypertrophic Cardiomyopathy Screening

Hypertrophic cardiomyopathy is a genetic condition in which the heart fails to pump normally due to the muscular walls of the ... www.bhf.org.uk/heart-health/conditions/cardiomyopathy/hypertrophic-cardiomyopathy. Further Reading. *All Hypertrophic ... Hypertrophic Cardiomyopathy Screening. News-Medical. https://www.news-medical.net/health/Hypertrophic-Cardiomyopathy-Screening ... Hypertrophic cardiomyopathy is a genetic condition in which the heart fails to pump normally due to the muscular walls of the ...
more infohttps://www.news-medical.net/health/Hypertrophic-Cardiomyopathy-Screening.aspx

Hypertrophic Cardiomyopathy TreatmentsHypertrophic Cardiomyopathy Treatments

Hypertrophic cardiomyopathy is a genetic disease of the heart muscles that reduces the hearts ability to pump blood around the ... www.bhf.org.uk/heart-health/conditions/cardiomyopathy/hypertrophic-cardiomyopathy. Further Reading. *All Hypertrophic ... http://www.cardiomyopathy.org/hypertrophic-cardiomyopathy/intro *https://www.heart.org/HEARTORG/Conditions/More/Cardiomyopathy/ ... Hypertrophic Cardiomyopathy Treatments. News-Medical. https://www.news-medical.net/health/Hypertrophic-Cardiomyopathy- ...
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Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

... (HCM) is a genetic condition that causes your heart walls to thicken. ... Hypertrophic Cardiomyopathy Symptoms. Often, people with HCM dont have any symptoms until sudden cardiac death occurs. If you ... Although hypertrophic cardiomyopathy is common (about 1 in 500 people have it), it affects each person differently. Some people ... This testing helps us find genes that put your family at risk of hypertrophic cardiomyopathy. This lets you or your family get ...
more infohttps://www.emoryhealthcare.org/heart-vascular/hypertrophic-cardiomyopathy.html

Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

Diagnosis and management of valve disease in patients with hypertrophic cardiomyopathy *Aortic valve disease ...
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Hypertrophic Cardiomyopathy - Newly diagnosed?Hypertrophic Cardiomyopathy - Newly diagnosed?

... cardiomyopathy, hypertrophic cardiomyopathy - Answer: Youve got to keep your bp down. Im on a beta ... ... Home › Q & A › Questions › Hypertrophic Cardiomyopathy -.... Hypertrophic Cardiomyopathy - Newly diagnosed?. Asked. 8 Feb 2014 ... cardiomyopathy, hypertrophic cardiomyopathy, side effect, medicine, statin, cholesterol, diagnosis. Details:. Simvastatin for ... Hypertrophic Cardiomyopathy - I just been diagnosed with hcm a couple of months ago I am scared?. Posted 3 Mar 2016 • 1 answer ...
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Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser ...
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Hypertrophic cardiomyopathy: MedlinePlus Medical EncyclopediaHypertrophic cardiomyopathy: MedlinePlus Medical Encyclopedia

Hypertrophic cardiomyopathy (HCM) is a condition in which the heart muscle becomes thick. Often, only one part of the heart is ... In some cases, the condition may develop into dilated cardiomyopathy. People with hypertrophic cardiomyopathy are at higher ... Cardiomyopathy - hypertrophic (HCM); IHSS; Idiopathic hypertrophic subaortic stenosis; Asymmetric septal hypertrophy; ASH; HOCM ... Hypertrophic cardiomyopathy (HCM) is a condition in which the heart muscle becomes thick. Often, only one part of the heart is ...
more infohttps://medlineplus.gov/ency/article/000192.htm

Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

... , Hypertrophic Obstructive Cardiomyopathy, Idiopathic Hypertrophic Subaortic Stenosis, IHSS, HOCM. ... Hypertrophic Cardiomyopathy. Hypertrophic Cardiomyopathy Aka: Hypertrophic Cardiomyopathy, Hypertrophic Obstructive ... Cardiomyopathy;hypertrophic, hypertrophic cardiomyopathy (HCM), cardiomyopathy hypertrophic, obstructive cardiomyopathy, ... Hypertrophic, Obstructive Cardiomyopathy, Hypertrophic, hypertrophic myocardiopathy, Hypertrophic Cardiomyopathy, Hypertrophic ...
more infohttps://fpnotebook.com/CV/Myocardium/HyprtrphcCrdmypthy.htm

Hypertrophic Cardiomyopathy: Read About TreatmentHypertrophic Cardiomyopathy: Read About Treatment

Read about how Hypertrophic cardiomyopathy (HCM) is associated with thickening of the heart muscle, most commonly at the septum ... What lifestyle changes are recommended to treat hypertrophic cardiomyopathy?. *What medications are used for hypertrophic ... Hypertrophic cardiomyopathy (HCM) can run in families, but the condition may also be acquired as a part of aging or high blood ... Hypertrophic cardiomyopathy (HCM) is associated with thickening of the heart muscle, most commonly at the septum between the ...
more infohttps://www.rxlist.com/cardiomyopathy_hypertrophic/article.htm

Hypertrophic Cardiomyopathy Overview - Mayo ClinicHypertrophic Cardiomyopathy Overview - Mayo Clinic

A single copy of these materials may be reprinted for noncommercial personal use only. "Mayo," "Mayo Clinic," "MayoClinic.org," "Mayo Clinic Healthy Living," and the triple-shield Mayo Clinic logo are trademarks of Mayo Foundation for Medical Education and Research. ...
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Hypertrophic cardiomyopathy: MedlinePlus Medical Encyclopedia ImageHypertrophic cardiomyopathy: MedlinePlus Medical Encyclopedia Image

Hypertrophic cardiomyopathy is the thickening of the muscles that make up the heart. The thickening may interfere with the ... Hypertrophic cardiomyopathy is the thickening of the muscles that make up the heart. The thickening may interfere with the ...
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hypertrophic cardiomyopathy | MomsTeamhypertrophic cardiomyopathy | MomsTeam

Home » hypertrophic cardiomyopathy. hypertrophic cardiomyopathy. Illinois Concussion Class Action Lawsuit: More Questions Than ... About 50 young athletes go into sudden cardiac arrest each year and die from a rare congenital heart defect called hypertrophic ... cardiomyopathy (HCM ). While some parent groups advocate for routine electrocardiogram (ECG) screening for youth athletes, ...
more infohttp://www.momsteam.com/hypertrophic-cardiomyopathy

Hypertrophic Cardiomyopathy CenterHypertrophic Cardiomyopathy Center

Cleveland Clinics Hypertrophic Cardiomyopathy Center is a multidisciplinary specialty treatment group dedicated to the ... Hypertrophic Cardiomyopathy Center Hypertrophic Cardiomyopathy Center Diagnoses and treats hypertrophic cardiomyopathy (HCM) in ... Experts in hypertrophic cardiomyopathy explain symptoms of HCM, how it is diagnosed and treated.. Hypertrophic cardiomyopathy ( ... The Hypertrophic Cardiomyopathy Center Cardiologist will provide you with a diagnosis and plan of care within 1 to 2 days, ...
more infohttps://my.clevelandclinic.org/departments/heart/depts/hypertrophic-cardiomyopathy

Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

UVA is Virginias only designated HCM Center of Excellence by the Hypertrophic Cardiomyopathy Association. Learn more about our ... Hypertrophic Cardiomyopathy. Hypertrophic cardiomyopathy is a genetic disease that leads to abnormal thickening of the heart ... Hypertrophic cardiomyopathy (HCM) is a genetic disease that leads to abnormal thickening of the heart muscle, which makes it ... UVA is Virginias only designated HCM Center of Excellence by the Hypertrophic Cardiomyopathy Association. We offer ...
more infohttps://uvahealth.com/services/heart-vascular-center/hypertrophic-cardiomyopathy

Hypertrophic Cardiomyopathy | Conditions | UCSF HealthHypertrophic Cardiomyopathy | Conditions | UCSF Health

Hypertrophic cardiomyopathy (HCM) is an inherited disease of the heart muscle. HCM can cause the wall of the heart muscle to ... Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy (HCM) is an inherited disease of the heart muscle. HCM can cause the ... Our Approach to Hypertrophic Cardiomyopathy. Over the past decades, UCSF has helped pioneer breakthroughs in the understanding ... and treatment of genetic heart disorders such as hypertrophic cardiomyopathy. Patients have access to world-class care at our ...
more infohttps://www.ucsfhealth.org/conditions/hypertrophic-cardiomyopathy

Hypertrophic cardiomyopathy: Natural history and prognosisHypertrophic cardiomyopathy: Natural history and prognosis

Hypertrophic cardiomyopathy (HCM) is a genetically determined heart muscle disease caused by mutations in one of several ... Patient education: Hypertrophic cardiomyopathy in adults (The Basics). *Patient education: Hypertrophic cardiomyopathy in ... Hypertrophic cardiomyopathy: Medical therapy. *Hypertrophic cardiomyopathy: Morphologic variants and the pathophysiology of ... Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation. *Hypertrophic cardiomyopathy: Gene mutations ...
more infohttp://www.uptodate.com/contents/hypertrophic-cardiomyopathy-natural-history-and-prognosis

Hypertrophic Cardiomyopathy - Make an AppointmentHypertrophic Cardiomyopathy - Make an Appointment

... from your primary care physician or cardiologist and would like to make an appointment with the Hypertrophic Cardiomyopathy ...
more infohttps://www.emoryhealthcare.org/centers-programs/hypertrophic-cardiomyopathy-program/appointment.html

Nifedipine in hypertrophic cardiomyopathy. | CirculationNifedipine in hypertrophic cardiomyopathy. | Circulation

Thank you for your interest in spreading the word on Circulation.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. ...
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UPMC Establishes Hypertrophic Cardiomyopathy Center

		UPMC Establishes Hypertrophic Cardiomyopathy Center

UPMC has established a center to treat patients with hypertrophic cardiomyopathy (HCM), a condition in which the heart muscle ... UPMC Establishes Hypertrophic Cardiomyopathy Center. PITTSBURGH, March 8, 2010 - UPMC has established a center to treat ... Extreme cases of hypertrophic cardiomyopathy may lead to heart failure, or even sudden death. However, most patients do not ... "Hypertrophic cardiomyopathy is a genetic disease that affects more than 600,000 people in the United States, but only 20 ...
more infohttp://www.upmc.com/media/newsreleases/2010/pages/upmc-establishes-hypertrophic-cardiomyopathy-center.aspx

Hypertrophic Cardiomyopathy - DrugBankHypertrophic Cardiomyopathy - DrugBank

Also known as: Hypertrophic Cardiomyopathies / Hypertrophic cardiomyopathy / Cardiomyopathy, Hypertrophic / HOCM Hypertrophic ... Cardiomyopathy / Hypertrophic obstructive cardiomyopathy / Obstructive cardiomyopathy / Hypertrophic subaortic stenosis ( ...
more infohttps://www.drugbank.ca/indications/DBCOND0028068

Hypertrophic cardiomyopathy - Symptoms and causes - Mayo ClinicHypertrophic cardiomyopathy - Symptoms and causes - Mayo Clinic

Hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy. Illustrations of a normal heart (left) and a heart with hypertrophic ... The severity of hypertrophic cardiomyopathy varies widely. Most people with hypertrophic cardiomyopathy have a form of the ... obstructive hypertrophic cardiomyopathy).. Sometimes hypertrophic cardiomyopathy occurs without significant blocking of blood ... Hypertrophic cardiomyopathy is usually inherited. Theres a 50 percent chance that the children of a parent with hypertrophic ...
more infohttps://www.mayoclinic.org/diseases-conditions/hypertrophic-cardiomyopathy/symptoms-causes/syc-20350198?mc_id=us&