Cardiomyopathy, Hypertrophic, Familial
Arrhythmogenic Right Ventricular Dysplasia
Ventricular Function, Left
Ventricular Dysfunction, Left
Ventricular Outflow Obstruction
Death, Sudden, Cardiac
Myosin Heavy Chains
Hypertrophy, Left Ventricular
Lamin Type A
Cardiac Pacing, Artificial
Magnetic Resonance Imaging, Cine
Disease Models, Animal
Glycogen Storage Disease Type IIb
Isolated Noncompaction of the Ventricular Myocardium
Pregnancy Complications, Cardiovascular
Mitral Valve Insufficiency
Predictive Value of Tests
Muscular Dystrophy, Duchenne
Ventricular Dysfunction, Right
Electrophysiologic Techniques, Cardiac
Echocardiography, Doppler, Color
Natriuretic Peptide, Brain
Echocardiography, Doppler, Pulsed
LIM Domain Proteins
Severity of Illness Index
Magnetic Resonance Imaging
Heart Conduction System
Receptors, Adrenergic, beta-1
Ventricular Premature Complexes
Cardiac Output, Low
Diabetes Mellitus, Experimental
Sarcoplasmic Reticulum Calcium-Transporting ATPases
Atrial Natriuretic Factor
Enterovirus B, Human
Body Surface Potential Mapping
Gated Blood-Pool Imaging
Mice, Inbred mdx
Ventricular Function, Right
alpha-Crystallin B Chain
Cardiac Complexes, Premature
Receptors, Adrenergic, beta
Cardiac Resynchronization Therapy
Cardiac sympathetic activity estimated by 123I-MIBG myocardial imaging in patients with dilated cardiomyopathy after beta-blocker or angiotensin-converting enzyme inhibitor therapy. (1/2423)Impaired cardiac sympathetic activity can be evaluated by 123I-metaiodobenzylguanidine (MIBG) imaging. METHODS: We studied the significance of MIBG imaging for 24 patients (age 58+/-12 y) with dilated cardiomyopathy (DCM). We compared 12 patients (group A) treated with metoprolol (dose from 30-60 mg/d) with 12 patients treated with angiotensin-converting enzyme (ACE) inhibitors. Patients were studied before treatment, after 5 mo of treatment (only in group A) and after 1 y of treatment. Cardiac MIBG uptake was assessed as the heart-to-mediastinum activity ratio (H/M) and total defect score (TDS) from anterior planar and SPECT MIBG images, which were acquired in 4 h after tracer injection. New York Heart Association (NYHA) class and left ventricular ejection fraction (LVEF) calculated by echocardiography were also assessed. RESULTS: TDS decreased in both groups (in group A, from 30+/-7 through 23+/-9 to 18+/-10; P < 0.01, in group B, from 30+/-6 to 24+/-8; P < 0.01) and H/M was increased in both groups (in group A, from 1.87+/-0.31 through 2.03+/-0.28 to 2.14+/-0.29; P < 0.01, in group B, from 1.82+/-0.28 to 1.94+/-0.26; P < 0.05). But TDS and H/M were more improved in group A than in group B (P < 0.05). LVEF was significantly increased in only group A (from 38+/-6 through 43+/-8 to 49%+/-9%; P < 0.01). NYHA improved in both groups (in group A, from mean 2.5 through 2.1 to 1.8; P < 0.01, in group B, from mean 2.6 to 2.1; P < 0.05) but was more improved in group A than in group B (P < 0.05). CONCLUSION: Cardiac function, symptom and cardiac sympathetic activity evaluated by MIBG images improved after the beta-blocker therapy more than with the treatment that used ACE inhibitors. (+info)
Sympathetic nerve alterations assessed with 123I-MIBG in the failing human heart. (2/2423)Norepinephrine (NE) reuptake function is impaired in heart failure and this may participate in myocyte hyperstimulation by the neurotransmitter. This alteration can be assessed by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. METHODS: To determine whether the impairment of neuronal NE reuptake was reversible after metoprolol therapy, we studied 18 patients (43+/-7 y) with idiopathic dilated cardiomyopathy who were stabilized at least for 3 mo with captopril and diuretics. Patients underwent, before and after 6 mo of therapy with metoprolol, measurements of radionuclide left ventricular ejection fraction (LVEF), maximal oxygen consumption and plasma NE concentration. The cardiac adrenergic innervation function was scintigraphically assessed with MIBG uptake and release measurements on the planar images obtained 20 min and 4 h after tracer injection. To evaluate whether metoprolol had a direct interaction with cardiac MIBG uptake and release, six normal subjects were studied before and after a 1-mo metoprolol intake. RESULTS: In controls, neither cardiac MIBG uptake and release nor circulating NE concentration changed after the 1-mo metoprolol intake. Conversely, after a 6-mo therapy with metoprolol, patients showed increased cardiac MIBG uptake (129%+/-10% versus 138%+/-17%; P = 0.009), unchanged cardiac MIBG release and decreased plasma NE concentration (0.930+/-412 versus 0.721+/-0.370 ng/mL; P = 0.02). In parallel, patients showed improved New York Heart Association class (2.44+/-0.51 versus 2.05+/-0.23; P = 0.004) and increased LVEF (20%+/-8% versus 27%+/-8%; P = 0.0005), whereas maximal oxygen uptake remained unchanged. CONCLUSION: Thus, a parallel improvement of myocardial NE reuptake and of hemodynamics was observed after a 6-mo metoprolol therapy, suggesting that such agents may be beneficial in heart failure by directly protecting the myocardium against excessive NE stimulation. (+info)
Regional patterns of myocardial sympathetic denervation in dilated cardiomyopathy: an analysis using carbon-11 hydroxyephedrine and positron emission tomography. (3/2423)OBJECTIVE: To assess presynaptic function of cardiac autonomic innervation in patients with advanced congestive heart failure using positron emission tomography (PET) and the recently developed radiolabelled catecholamine analogue carbon-11 hydroxyephedrine (HED) as a marker for neuronal catecholamine uptake function. DESIGN AND PATIENTS: 29 patients suffering from dilated cardiomyopathy with moderate to severe heart failure were compared with eight healthy controls. Perfusion scan was followed by HED dynamic PET imaging of cardiac sympathetic innervation. The scintigraphic results were compared with markers of disease severity and the degree of sympathetic dysfunction assessed by means of heart rate variability. RESULTS: In contrast to nearly normal perfusions, mean (SD) HED retention in dilated cardiomyopathy patients was abnormal in 64 (32)% of the left ventricle. Absolute myocardial HED retention was 10.7 (1.0)%/min in controls v 6.2 (1.6)%/min in dilated cardiomyopathy patients (p < 0.001). Moreover, significant regional reduction of HED retention was demonstrated in apical and inferoapical segments. HED retention was significantly correlated with New York Heart Association functional class (r = -0.55, p = 0. 002) and ejection fraction (r = 0.63, p < 0.001), but not, however, with plasma noradrenaline concentrations as well as parameters of heart rate variability. CONCLUSIONS: In this study, using PET in combination with HED in patients with dilated cardiomyopathy, not only global reduction but also regional abnormalities of cardiac sympathetic tracer uptake were demonstrated. The degree of abnormality was positively correlated to markers of severity of heart failure. The pathogenetic mechanisms leading to the regional differences of neuronal damage as well as the prognostic significance of these findings remain to be defined. (+info)
Endogenous plasma endothelin concentrations and coronary circulation in patients with mild dilated cardiomyopathy. (4/2423)OBJECTIVE: To determine whether increased plasma concentrations of endothelin-1 (ET-1) and big endothelin (BET) play a role in the regulation of coronary circulation in patients with idiopathic dilated cardiomyopathy (IDCM). SETTING: Tertiary referral centre for cardiac diseases. PATIENTS: Fourteen patients (eight male/six female; mean (SD) age 59 (9) years) with IDCM (ejection fraction 36 (9)%) and five normotensive subjects (two male/three female; age 52 (7) years) serving as controls were studied. METHODS: Functional status was classified according to New York Heart Association (NYHA) class. Endogenous ET-1 and BET plasma concentrations from the aorta and the coronary sinus were determined by radioimmunoassay. Coronary blood flow, using the inert chromatographic argon method, myocardial oxygen consumption, and coronary sinus oxygen content under basal conditions were determined. RESULTS: In the aorta, mean (SD) concentrations of ET-1 (IDCM 0.76 (0.25) v controls 0.31 (0.06) fmol/ml; p = 0.002) and BET (IDCM 3.58 (1.06) v controls 2.11 (0.58) fmol/ml; p = 0.014) were increased in patients with IDCM. Aortic ET-1 concentrations correlated positively with NYHA class (r = 0. 731; p < 0.001), myocardial oxygen consumption (r = 0.749; p < 0. 001), and coronary blood flow (r = 0.645; p = 0.003), but inversely with coronary sinus oxygen content (r = -0.633; p = 0.004), which was significantly decreased in IDCM patients (IDCM 4.68 (1.05) v controls 6.70 (1.06) vol%; p = 0.003). CONCLUSIONS: The coronary circulation in patients with IDCM is exposed to an increased endothelin load. ET-1 concentrations correlate with functional deterioration. A decrease of the coronary sinus content of oxygen suggests a mismatch between coronary blood flow and metabolic demand. Thus, ET-1 might be a marker of a disequilibrium between myocardial oxygen demand and coronary blood flow in IDCM. (+info)
Familial dilated cardiomyopathy locus maps to chromosome 2q31. (5/2423)BACKGROUND: Inherited gene defects are an important cause of dilated cardiomyopathy. Although the chromosome locations of some defects and 1 disease gene (actin) have been identified, the genetic etiologies of most cases of familial dilated cardiomyopathy remain unknown. METHODS AND RESULTS: We clinically evaluated 3 generations of a kindred with autosomal dominant transmission of dilated cardiomyopathy. Nine surviving and affected individuals had early-onset disease (ventricular chamber dilation during the teenage years and congestive heart failure during the third decade of life). The disease was nonpenetrant in 2 obligate carriers. To identify the causal gene defect, linkage studies were performed. A new dilated cardiomyopathy locus was identified on chromosome 2 between loci GCG and D2S72 (maximum logarithm of odds [LOD] score=4.86 at theta=0). Because the massive gene encoding titin, a cytoskeletal muscle protein, resides in this disease interval, sequences encoding 900 amino acid residues of the cardiac-specific (N2-B) domain were analyzed. Five sequence variants were identified, but none segregated with disease in this family. CONCLUSIONS: A dilated cardiomyopathy locus (designated CMD1G) is located on chromosome 2q31 and causes early-onset congestive heart failure. Although titin remains an intriguing candidate gene for this disorder, a disease-causing mutation is not present in its cardiac-specific N2-B domain. (+info)
From myocarditis to cardiomyopathy: mechanisms of inflammation and cell death: learning from the past for the future. (6/2423)A progression from viral myocarditis to dilated cardiomyopathy has long been hypothesized, but the actual extent of this progression has been uncertain. However, a causal link between viral myocarditis and dilated cardiomyopathy has become more evident than before with the tremendous developments in the molecular analyses of autopsy and endomyocardial biopsy specimens, new techniques of viral gene amplification, and modern immunology. The persistence of viral RNA in the myocardium beyond 90 days after inoculation, confirmed by the method of polymerase chain reaction, has given us new insights into the pathogenesis of dilated cardiomyopathy. Moreover, new knowledge of T-cell-mediated immune responses in murine viral myocarditis has contributed a great deal to the understanding of the mechanisms of ongoing disease processes. Apoptotic cell death may provide the third concept to explain the pathogenesis of dilated cardiomyopathy, in addition to persistent viral RNA in the heart tissue and an immune system-mediated mechanism. Beneficial effects of alpha1-adrenergic blocking agents, carteolol, verapamil, and ACE inhibitors have been shown clinically and experimentally in the treatment of viral myocarditis and dilated cardiomyopathy. Antiviral agents should be more extensively investigated for clinical use. The rather discouraging results obtained to date with immunosuppressive agents in the treatment of viral myocarditis indicated the importance of sparing neutralizing antibody production, which may be controlled by B cells, and raised the possibility of promising developments in immunomodulating therapy. (+info)
Echo derived variables predicting exercise tolerance in patients with dilated and poorly functioning left ventricle. (7/2423)OBJECTIVE: To determine whether resting echo derived measurements predict exercise tolerance and its interrelation with heart rate response and ventilation drive in patients with systolic left ventricular disease. DESIGN: Prospective echocardiographic examination followed by cardiopulmonary exercise testing. SETTING: A tertiary referral centre for cardiac diseases. SUBJECTS: 21 patients (11 with coronary artery disease, 10 with idiopathic dilated cardiomyopathy) with end diastolic dimension > 6.4 cm, shortening fraction < 25%, and in sinus rhythm. There were 11 age matched normal controls. RESULTS: In the patients, peak oxygen consumption (mVo2) correlated with right ventricular long axis excursion (r = 0.62); 65% of the variance in mVo2 was predictable using a multivariate model with right ventricular long axis excursion and peak lengthening rate, and peak mitral atrial filling velocity as independent variables. Aetiology was not an independent predictor, although the right ventricular long axis excursion (mean (SD)) was greater in patients with idiopathic dilated cardiomyopathy than in those with coronary artery disease (2.4 (0.5) cm v 1.6 (0.5) cm, p < 0.001). Peak heart rate correlated with duration of mitral regurgitation (r = -0.52) and the slope of ventilation against CO2 production correlated with M mode isovolumic relaxation time (r = 0.61). CONCLUSIONS: In patients with systolic left ventricular dysfunction, more than half the variance in exercise tolerance can be predicted by factors measured on echocardiography at rest, particularly right ventricular long axis excursion. (+info)
Effects of dilated cardiomyopathy on the diaphragm in the Syrian hamster. (8/2423)This study aimed to elucidate changes in respiratory muscles and their mechanism in cardiomyopathy. The contractile properties and histology of the diaphragm, as well as serum levels of insulin-like growth factor (IGF)-1, were examined in 10 hamsters with idiopathic dilated cardiomyopathy (CM) and 10 controls. At 28 weeks, body weight in CM was reduced compared with controls (114+/-10 versus 144+/-14 g, p<0.0001). The ratio of diaphragm to body weight was significantly higher in CM than in controls (0.228+/-0.015 versus 0.182+/-0.017, p<0.0001). In vitro, maximal diaphragmatic twitch (303+/-63 versus 455+/-119 g x cm(-2)) and tetanic tensions (1,555+/-369 versus 2,204+/-506 g x cm(-2)) were significantly lower in CM than in controls (p<0.005). The half-relaxation time was significantly shorter in CM (19+/-1 ms) than in controls (24+/-3 ms, p<0.0005). Fatiguability at 25 Hz was significantly less in CM (28%) than in controls (42%, p<0.0001). Diaphragm and gastrocnemius adenosine triphosphatase staining showed type I fibre atrophy in CM, associated with an increase in the number of type I fibres in the diaphragm. Histological examination of both muscles revealed an abnormal muscular pattern. Finally, serum levels of IGF-1 were 47% lower in the CM group than in controls (p<0.0001) and were clearly related to the changes in the contractile properties and histology of the diaphragm. In conclusion, cardiomyopathy in hamsters: 1) depressed the force-generating capacity and shortened the relaxation of the hamster diaphragm; 2) induced type I fibre atrophy in combination with a myopathic pattern; and 3) was associated with a significant reduction in serum levels of insulin-like growth factor-1, related to the diaphragmatic changes. Whether these changes are primary myopathic or secondary to heart failure remains to be elucidated. (+info)
Dilated cardiomyopathy is a medical condition characterized by the enlargement and weakening of the heart muscle, specifically the ventricles, which are the lower chambers of the heart responsible for pumping blood out to the rest of the body. This enlargement causes the heart to become weakened and unable to pump blood efficiently, leading to symptoms such as shortness of breath, fatigue, and swelling in the legs and ankles. Dilated cardiomyopathy can be caused by a variety of factors, including genetics, infections, alcohol and drug abuse, and certain medications. It can also be a complication of other heart conditions, such as hypertension or coronary artery disease. Diagnosis of dilated cardiomyopathy typically involves a physical examination, electrocardiogram (ECG), echocardiogram, and other imaging tests. Treatment may include medications to improve heart function, lifestyle changes such as a heart-healthy diet and exercise, and in some cases, surgery or heart transplantation.
Hypertrophic cardiomyopathy (HCM) is a type of heart disease characterized by the thickening of the heart muscle, particularly the walls of the left ventricle. This thickening can obstruct blood flow through the heart, leading to symptoms such as shortness of breath, chest pain, and fatigue. HCM can be caused by genetic mutations or be acquired as a result of other medical conditions or environmental factors. It is a common condition, affecting an estimated 1 in 500 people worldwide. Treatment for HCM may include medications, lifestyle changes, and in some cases, surgery or other procedures to improve blood flow and reduce the risk of complications.
Cardiomyopathies are a group of heart diseases that affect the heart muscle (myocardium). These diseases can cause the heart to become enlarged, thickened, or rigid, which can lead to problems with the heart's ability to pump blood effectively. There are several different types of cardiomyopathies, including: 1. Hypertrophic cardiomyopathy: This is a condition in which the heart muscle becomes abnormally thick, which can make it difficult for the heart to pump blood. 2. Dilated cardiomyopathy: This is a condition in which the heart muscle becomes weakened and enlarged, which can cause the heart to pump blood less effectively. 3. Arrhythmogenic right ventricular cardiomyopathy (ARVC): This is a condition in which the heart muscle in the right ventricle becomes abnormal and can cause irregular heart rhythms. 4. Non-ischemic dilated cardiomyopathy: This is a type of dilated cardiomyopathy that is not caused by a lack of blood flow to the heart muscle. 5. Idiopathic left ventricular hypertrophy: This is a condition in which the left ventricle of the heart becomes abnormally thick, which can make it difficult for the heart to pump blood. Cardiomyopathies can be inherited or acquired, and they can range from mild to severe. Treatment for cardiomyopathies depends on the specific type and severity of the condition, and may include medications, lifestyle changes, and in some cases, surgery.
Cardiomyopathy, restrictive is a type of heart disease that affects the heart's ability to pump blood effectively. In restrictive cardiomyopathy, the heart muscle becomes stiff and thickened, making it difficult for the heart to relax and fill with blood. This can lead to a decrease in the amount of blood that the heart is able to pump out to the rest of the body, which can cause symptoms such as shortness of breath, fatigue, and swelling in the legs and ankles. There are several different types of restrictive cardiomyopathy, including infiltrative cardiomyopathy, fibrotic cardiomyopathy, and endomyocardial fibrosis. The exact cause of restrictive cardiomyopathy is often unknown, but it can be caused by a variety of factors, including viral infections, exposure to toxins, and certain genetic conditions. Treatment for restrictive cardiomyopathy typically involves managing symptoms and addressing any underlying causes of the condition. In some cases, medications or surgery may be necessary to improve heart function and prevent complications.
Takotsubo Cardiomyopathy, also known as stress-induced cardiomyopathy or broken heart syndrome, is a rare but potentially life-threatening condition that affects the heart muscle. It is characterized by a sudden and temporary weakening of the heart's ability to pump blood, often triggered by a severe emotional or physical stressor. The condition is named after the Japanese word "takotsubo," which means octopus pot, because the shape of the heart's left ventricle during an episode of Takotsubo Cardiomyopathy resembles the shape of an octopus pot. Symptoms of Takotsubo Cardiomyopathy can include chest pain, shortness of breath, rapid heartbeat, and fatigue. The condition is usually diagnosed through an electrocardiogram (ECG), echocardiogram, and other imaging tests. Treatment for Takotsubo Cardiomyopathy typically involves medications to manage symptoms and prevent complications, such as heart failure or arrhythmias. In some cases, hospitalization may be necessary. The condition usually resolves on its own within a few weeks to months, although some people may experience long-term changes in their heart function.
Cardiomyopathy, Hypertrophic, Familial is a type of heart disease that is caused by genetic mutations that affect the structure and function of the heart muscle. It is characterized by the thickening of the heart muscle, particularly in the walls of the left ventricle, which is the main pumping chamber of the heart. This thickening can lead to a decrease in the heart's ability to pump blood effectively, which can cause symptoms such as shortness of breath, chest pain, and fatigue. Familial hypertrophic cardiomyopathy is an inherited form of the disease, meaning that it is passed down from parents to their children through their genes. It is estimated that up to 1 in 500 people worldwide may have this condition, and it is more common in males than females. While the disease can be severe and life-threatening in some cases, many people with familial hypertrophic cardiomyopathy are able to lead normal, active lives with appropriate medical care and management.
Chagas cardiomyopathy is a type of heart disease caused by the Trypanosoma cruzi parasite, which is commonly transmitted to humans through the bite of infected triatomine bugs, also known as "kissing bugs." The parasite infects the heart muscle and can cause inflammation, scarring, and damage to the heart over time. This can lead to a variety of symptoms, including chest pain, shortness of breath, fatigue, and swelling in the legs and feet. In severe cases, Chagas cardiomyopathy can lead to heart failure, arrhythmias, and even sudden death. The disease is most common in Latin America, but it can also occur in other parts of the world where the parasite is present.
Cardiomyopathy, alcoholic, is a type of heart disease that occurs as a result of long-term heavy alcohol consumption. It is characterized by the weakening and thickening of the heart muscle, which can lead to reduced heart function and an increased risk of heart failure. Alcohol can damage the heart muscle in several ways, including by causing inflammation, disrupting the normal electrical activity of the heart, and interfering with the body's ability to repair damaged tissue. Over time, these effects can lead to the development of alcoholic cardiomyopathy. Symptoms of alcoholic cardiomyopathy may include shortness of breath, fatigue, swelling in the legs and ankles, and chest pain. Treatment typically involves stopping alcohol consumption, addressing any underlying medical conditions, and making lifestyle changes such as eating a healthy diet and getting regular exercise. In some cases, medications or surgery may also be necessary to manage symptoms and prevent complications.
Arrhythmogenic Right Ventricular Dysplasia (ARVD) is a genetic heart disorder that affects the right ventricle of the heart. It is characterized by the replacement of healthy heart muscle with fibrous scar tissue, which can lead to abnormal heart rhythms and heart failure. ARVD is often diagnosed in young adults and children, and it can be life-threatening if not treated. The exact cause of ARVD is not fully understood, but it is believed to be related to mutations in certain genes that are involved in the development and maintenance of heart muscle. Treatment for ARVD typically involves medications to control abnormal heart rhythms and lifestyle changes to reduce the risk of sudden cardiac death. In some cases, surgery may be necessary to remove damaged heart muscle or implant a device to regulate the heart's rhythm.
Diabetic cardiomyopathy is a type of heart disease that occurs in people with diabetes. It is characterized by changes in the structure and function of the heart muscle, which can lead to heart failure. The exact cause of diabetic cardiomyopathy is not fully understood, but it is thought to be related to the long-term effects of high blood sugar levels on the heart. Other risk factors for diabetic cardiomyopathy include high blood pressure, high cholesterol, and smoking. Treatment for diabetic cardiomyopathy typically involves managing blood sugar levels, blood pressure, and cholesterol, as well as medications to improve heart function and prevent further damage to the heart.
Myocarditis is an inflammation of the heart muscle (myocardium) that can be caused by a viral or bacterial infection, autoimmune disorders, or other factors. It can lead to swelling and damage to the heart muscle, which can affect its ability to pump blood effectively. Symptoms of myocarditis can include chest pain, shortness of breath, fatigue, and an irregular heartbeat. Treatment for myocarditis depends on the underlying cause and may include medications, rest, and lifestyle changes. In severe cases, hospitalization and supportive care may be necessary. Myocarditis can be a serious condition and can lead to complications such as heart failure, arrhythmias, and sudden cardiac death.
Ventricular dysfunction, left, is a medical condition in which the left ventricle of the heart is unable to pump blood efficiently. The left ventricle is responsible for pumping oxygen-rich blood from the heart to the rest of the body. When it is not functioning properly, it can lead to a variety of symptoms, including shortness of breath, fatigue, and chest pain. There are several causes of left ventricular dysfunction, including heart attacks, high blood pressure, coronary artery disease, and heart valve problems. Treatment for left ventricular dysfunction depends on the underlying cause and may include medications, lifestyle changes, and in some cases, surgery. Left ventricular dysfunction can be a serious condition and requires prompt medical attention.
Heart failure, also known as congestive heart failure, is a medical condition in which the heart is unable to pump enough blood to meet the body's needs. This can lead to a buildup of fluid in the lungs, liver, and other organs, causing symptoms such as shortness of breath, fatigue, and swelling in the legs and ankles. Heart failure can be caused by a variety of factors, including damage to the heart muscle from a heart attack, high blood pressure, or long-term damage from conditions such as diabetes or coronary artery disease. It can also be caused by certain genetic disorders or infections. Treatment for heart failure typically involves medications to improve heart function and reduce fluid buildup, as well as lifestyle changes such as a healthy diet, regular exercise, and avoiding smoking and excessive alcohol consumption. In some cases, surgery or other medical procedures may be necessary to treat the underlying cause of the heart failure or to improve heart function.
Ventricular outflow obstruction (VOO) is a condition in which there is a blockage or narrowing of the blood vessels that carry blood away from the heart's ventricles. This can cause the ventricles to work harder to pump blood, which can lead to an increase in blood pressure and strain on the heart. VOO can be caused by a variety of factors, including congenital heart defects, heart valve problems, and certain heart diseases. It can also be caused by damage to the heart muscle or blood vessels as a result of a heart attack or other cardiovascular disease. Symptoms of VOO may include shortness of breath, chest pain, fatigue, and swelling in the legs and ankles. Treatment for VOO depends on the underlying cause and may include medications, lifestyle changes, or surgery.
In the medical field, "Death, Sudden, Cardiac" refers to a sudden and unexpected death that is caused by a problem with the heart. This type of death is often referred to as sudden cardiac death (SCD) and can occur in people of all ages, including children and young adults. SCD is typically caused by an arrhythmia, which is an abnormal heartbeat that can disrupt the flow of blood to the brain and other vital organs. Other factors that can contribute to SCD include coronary artery disease, heart failure, and inherited heart conditions. Symptoms of SCD may include sudden collapse, loss of consciousness, and difficulty breathing. Treatment for SCD typically involves cardiopulmonary resuscitation (CPR) and the use of a defibrillator to shock the heart back into a normal rhythm. However, because SCD is sudden and often fatal, prevention is key, and people who are at risk may be prescribed medications or undergo procedures to reduce their risk of experiencing a cardiac event.
Cardiac myosins are a type of myosin protein found in the heart muscle cells (cardiomyocytes) of mammals. They are responsible for the contraction and relaxation of the heart muscle, which is essential for pumping blood throughout the body. Cardiac myosins are composed of two main components: a heavy chain and several light chains. The heavy chain contains the motor domain, which is responsible for the movement of the myosin head along the actin filament, and the binding site for ATP (adenosine triphosphate), which provides the energy for the contraction. There are several different types of cardiac myosins, including cardiac myosin heavy chain (MYH7), cardiac myosin light chain 2 (MYL2), and cardiac myosin light chain 3 (MYL3). These different types of myosins are expressed in different regions of the heart and may have different functions. Abnormalities in cardiac myosins can lead to various heart diseases, such as hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmias. Understanding the structure and function of cardiac myosins is important for developing new treatments for these conditions.
Ventricular myosins are a type of myosin proteins that are found in the ventricles of the heart. These proteins are responsible for the contraction of the heart muscle, which is necessary for pumping blood throughout the body. Ventricular myosins are made up of two main components: a heavy chain and a light chain. The heavy chain is responsible for binding to the actin filaments in the heart muscle, while the light chain helps to regulate the contraction of the muscle. Ventricular myosins are essential for maintaining a healthy heart and ensuring that blood is pumped efficiently throughout the body.
Fibrosis is a medical condition characterized by the excessive accumulation of fibrous connective tissue in the body. This tissue is made up of collagen fibers, which are responsible for providing strength and support to tissues. Fibrosis can occur in any part of the body, but it is most commonly seen in the lungs, liver, heart, and kidneys. It can be caused by a variety of factors, including injury, infection, inflammation, and chronic diseases such as diabetes and scleroderma. The accumulation of fibrous tissue can lead to a range of symptoms, depending on the affected organ. For example, in the lungs, fibrosis can cause shortness of breath, coughing, and chest pain. In the liver, it can lead to liver failure and other complications. In the heart, it can cause heart failure and arrhythmias. Fibrosis is often a progressive condition, meaning that it can worsen over time if left untreated. Treatment options depend on the underlying cause of the fibrosis and the severity of the symptoms. In some cases, medications or surgery may be used to slow the progression of the disease or to manage symptoms.
Tachycardia, ventricular refers to an abnormally fast heart rate that originates from the ventricles, which are the lower chambers of the heart. This type of tachycardia is also known as ventricular tachycardia (VT) and can be a serious medical condition that requires prompt medical attention. Ventricular tachycardia can be caused by a variety of factors, including heart disease, electrolyte imbalances, and certain medications. It can also be a complication of other medical conditions, such as heart attacks, heart failure, and myocarditis. The symptoms of ventricular tachycardia can vary depending on the severity and duration of the episode. Common symptoms include palpitations, shortness of breath, dizziness, and fainting. In some cases, ventricular tachycardia can lead to more serious complications, such as cardiac arrest, which can be life-threatening. Treatment for ventricular tachycardia typically involves medications to slow down the heart rate and restore a normal rhythm. In some cases, electrical cardioversion or catheter ablation may be necessary to eliminate the abnormal heart rhythm. It is important to seek medical attention immediately if you suspect you or someone else may be experiencing ventricular tachycardia.
Endomyocardial fibrosis (EMF) is a rare, progressive, and often fatal disease that affects the heart muscle. It is characterized by the accumulation of fibrous tissue within the endocardium, the inner lining of the heart, which can lead to thickening and stiffening of the heart muscle, impairing its ability to pump blood effectively. EMF can affect any part of the heart, but it most commonly affects the left ventricle, which is responsible for pumping oxygen-rich blood to the rest of the body. The disease can also affect the right ventricle, which pumps oxygen-poor blood to the lungs, and the atria, which are the upper chambers of the heart. The exact cause of EMF is not fully understood, but it is thought to be related to chronic inflammation and scarring of the heart muscle. Risk factors for developing EMF include hypertension, diabetes, and parasitic infections such as schistosomiasis. Symptoms of EMF can include shortness of breath, chest pain, fatigue, and swelling in the legs and ankles. Diagnosis is typically made through a combination of physical examination, imaging tests such as echocardiography or cardiac MRI, and biopsy of the affected tissue. Treatment for EMF may include medications to manage symptoms and improve heart function, such as diuretics to reduce fluid buildup and ACE inhibitors or beta blockers to lower blood pressure and reduce the workload on the heart. In severe cases, surgery may be necessary to remove the fibrous tissue or repair damaged heart valves.
Myocardial ischemia is a medical condition that occurs when the blood flow to the heart muscle is reduced or blocked, leading to a lack of oxygen and nutrients to the heart cells. This can cause chest pain or discomfort, shortness of breath, and other symptoms. Myocardial ischemia is often caused by atherosclerosis, a condition in which plaque builds up in the arteries, narrowing or blocking the flow of blood. It can also be caused by other factors, such as heart valve problems or blood clots. Myocardial ischemia can be a serious condition and requires prompt medical attention to prevent heart attack or other complications.
Myosin heavy chains (MHCs) are the largest subunit of the myosin motor protein, which is responsible for muscle contraction. There are multiple isoforms of MHCs, each with different properties and functions. In the medical field, MHCs are important for understanding muscle diseases and disorders. For example, mutations in MHC genes can lead to conditions such as nemaline myopathy, which is a group of muscle disorders characterized by muscle weakness and stiffness. Additionally, changes in MHC expression levels have been observed in various types of cancer, including breast, prostate, and colon cancer. MHCs are also important for understanding muscle development and regeneration. During muscle development, different MHC isoforms are expressed at different stages, and changes in MHC expression can affect muscle function and regeneration. Understanding the regulation of MHC expression is therefore important for developing therapies for muscle diseases and injuries.
Hypertrophy, Left Ventricular refers to the thickening of the left ventricle, which is the main pumping chamber of the heart. This thickening can occur due to an increase in the workload on the heart, such as high blood pressure or a condition called aortic stenosis, or due to an underlying genetic disorder. Left ventricular hypertrophy can lead to heart failure, arrhythmias, and an increased risk of heart attack. It is typically diagnosed through an echocardiogram, a test that uses sound waves to create images of the heart. Treatment may include medications to lower blood pressure and reduce workload on the heart, as well as lifestyle changes such as exercise and a healthy diet. In severe cases, surgery may be necessary.
Arrhythmias, cardiac refer to abnormal heart rhythms that are not synchronized with the electrical signals that control the heartbeat. These abnormal rhythms can be caused by a variety of factors, including structural abnormalities of the heart, damage to the heart muscle, or problems with the electrical conduction system of the heart. Arrhythmias can range from relatively harmless to life-threatening. Some common types of cardiac arrhythmias include atrial fibrillation, ventricular tachycardia, and atrial flutter. Symptoms of arrhythmias may include palpitations, shortness of breath, dizziness, or fainting. Treatment for arrhythmias may involve medications, lifestyle changes, or medical procedures such as catheter ablation or implantation of a pacemaker or defibrillator.
Plakophilins are a family of proteins that play a crucial role in the formation and maintenance of desmosomes, which are specialized cell-cell junctions found in many tissues throughout the body. Desmosomes are responsible for providing mechanical strength and stability to tissues, particularly in areas that experience high levels of stress or strain, such as the skin, heart, and muscles. Plakophilins are transmembrane proteins that span the plasma membrane and anchor intermediate filaments, which are part of the cytoskeleton, to the desmosome. They are also involved in the regulation of desmosome assembly and disassembly, as well as the stability of the desmosomal plaque, which is the central component of the desmosome. Mutations in plakophilin genes have been linked to a number of human diseases, including arrhythmogenic right ventricular cardiomyopathy (ARVC), a disorder that can cause sudden cardiac death, and epidermolysis bullosa simplex (EBS), a skin disorder characterized by blistering and scarring.
Lamin Type A is a type of protein that is found in the nuclear lamina, a mesh-like structure that surrounds the nucleus of a cell. The nuclear lamina plays a crucial role in maintaining the shape and integrity of the nucleus, as well as in regulating gene expression and DNA replication. Lamin Type A is synthesized in the endoplasmic reticulum and then transported to the nucleus, where it is assembled into a filamentous network that forms the nuclear lamina. Lamin Type A is also involved in the formation of interphase chromatin fibers, which help to organize and compact the DNA within the nucleus. Mutations in the gene that encodes Lamin Type A can lead to a group of genetic disorders known as laminopathies, which are characterized by a range of symptoms including muscle weakness, bone deformities, and developmental delays. These disorders are caused by defects in the structure or function of the nuclear lamina, which can disrupt normal cellular processes and lead to tissue damage and dysfunction.
Ventricular remodeling refers to the structural and functional changes that occur in the heart's ventricles (the lower chambers of the heart) in response to various factors such as heart disease, injury, or genetic predisposition. These changes can include thickening of the heart muscle, enlargement of the ventricles, and changes in the electrical activity of the heart. Ventricular remodeling can lead to a variety of heart conditions, including heart failure, arrhythmias, and sudden cardiac death. It is a complex process that involves multiple cellular and molecular mechanisms, including inflammation, fibrosis, and changes in gene expression. In the medical field, ventricular remodeling is an important area of research, as it can help identify new targets for the prevention and treatment of heart disease. Treatment options for ventricular remodeling may include medications, lifestyle changes, and in some cases, surgical interventions.
Troponin T is a protein that is found in cardiac muscle cells. It plays a critical role in the regulation of muscle contraction. When cardiac muscle cells are damaged or injured, troponin T is released into the bloodstream. This can be detected through a blood test and is often used as an indicator of a heart attack or other heart-related conditions. Troponin T levels can also be used to monitor the effectiveness of treatment for heart conditions and to predict the risk of future heart problems.
Heart diseases refer to a group of medical conditions that affect the heart and blood vessels. These conditions can range from minor to severe and can affect the heart's ability to pump blood effectively, leading to a variety of symptoms and complications. Some common types of heart diseases include: 1. Coronary artery disease: This is the most common type of heart disease, which occurs when the arteries that supply blood to the heart become narrowed or blocked due to the buildup of plaque. 2. Heart failure: This occurs when the heart is unable to pump enough blood to meet the body's needs. 3. Arrhythmias: These are abnormal heart rhythms that can cause the heart to beat too fast, too slow, or irregularly. 4. Valvular heart disease: This occurs when the heart valves become damaged or diseased, leading to problems with blood flow. 5. Congenital heart disease: This refers to heart defects that are present at birth. 6. Inflammatory heart disease: This includes conditions such as pericarditis and myocarditis, which cause inflammation of the heart. 7. Heart infections: These include conditions such as endocarditis and myocarditis, which can cause damage to the heart muscle and valves. Treatment for heart diseases depends on the specific condition and may include medications, lifestyle changes, and in some cases, surgery. Early detection and treatment are important for improving outcomes and reducing the risk of complications.
Puerperal disorders refer to a group of medical conditions that occur during the postpartum period, which is the time immediately following childbirth. These disorders can affect the mother's physical and mental health and can be life-threatening if left untreated. Some common puerperal disorders include: 1. Postpartum hemorrhage: This is the most common cause of maternal mortality worldwide and occurs when there is excessive bleeding after childbirth. 2. Infection: Infections such as endometritis, pelvic inflammatory disease, and sepsis can occur after childbirth and can be life-threatening if left untreated. 3. Puerperal fever: This is a fever that occurs within the first week after childbirth and can be caused by infection. 4. Postpartum depression: This is a mood disorder that can occur after childbirth and can affect the mother's ability to care for herself and her baby. 5. Postpartum psychosis: This is a rare but serious mental health disorder that can occur after childbirth and can cause hallucinations, delusions, and mood swings. 6. Breastfeeding difficulties: Many new mothers experience difficulties breastfeeding, which can lead to stress and anxiety. 7. Postpartum thyroiditis: This is an autoimmune disorder that can occur after childbirth and can cause symptoms such as fatigue, weight gain, and depression. Prompt diagnosis and treatment of puerperal disorders are essential to ensure the health and well-being of the mother and her baby.
Sarcoglycans are a group of proteins that are involved in muscle function and are found in the sarcolemma, which is the plasma membrane of muscle cells. They are part of a larger group of proteins called dystrophin-associated glycoproteins (DAGs) that play a critical role in maintaining the structural integrity of muscle fibers. Sarcoglycans are important for maintaining the stability of the muscle sarcolemma, which helps to prevent the loss of calcium ions from the muscle cell and maintain proper muscle function. Mutations in the genes that encode for sarcoglycans can lead to a group of inherited muscle disorders known as sarcoglycanopathies, which are characterized by muscle weakness, wasting, and degeneration. These disorders can range in severity from mild to life-threatening and can affect both skeletal and cardiac muscles.
Cardiomegaly is a medical condition characterized by an enlarged heart. The term "cardiomegaly" comes from the Greek words "kardia," meaning heart, and "mega," meaning large. Cardiomegaly can be caused by a variety of factors, including hypertension, valvular heart disease, myocardial infarction (heart attack), cardiomyopathy (disease of the heart muscle), and certain genetic disorders. The diagnosis of cardiomegaly is typically made through imaging tests such as echocardiography, chest X-rays, or computed tomography (CT) scans. Cardiomegaly can lead to a variety of complications, including heart failure, arrhythmias, and increased risk of stroke. Treatment depends on the underlying cause of the cardiomegaly and may include medications, lifestyle changes, and in some cases, surgery.
In the medical field, "Death, Sudden" refers to an unexpected and rapid loss of life, typically occurring within minutes to hours of the onset of symptoms. Sudden death can be caused by a variety of factors, including heart attacks, strokes, sudden arrhythmias, severe allergic reactions, and other medical emergencies. It is often characterized by the absence of warning signs or symptoms, and can occur in both young and old individuals. Sudden death is a serious medical emergency that requires immediate attention and intervention to prevent further harm or loss of life.
Desmoglein 2 (DSG2) is a protein that is expressed on the surface of cells in the skin and mucous membranes. It is a component of desmosomes, which are specialized structures that help to anchor cells together and provide mechanical strength to tissues. DSG2 plays a critical role in maintaining the integrity of the skin and other epithelial tissues, and mutations in the gene that encodes DSG2 can lead to a number of inherited disorders that affect the skin and other organs. These disorders, which are collectively known as desmogleinopathies, can cause a range of symptoms, including skin rashes, hair loss, and blistering.
In the medical field, "Disease Models, Animal" refers to the use of animals to study and understand human diseases. These models are created by introducing a disease or condition into an animal, either naturally or through experimental manipulation, in order to study its progression, symptoms, and potential treatments. Animal models are used in medical research because they allow scientists to study diseases in a controlled environment and to test potential treatments before they are tested in humans. They can also provide insights into the underlying mechanisms of a disease and help to identify new therapeutic targets. There are many different types of animal models used in medical research, including mice, rats, rabbits, dogs, and monkeys. Each type of animal has its own advantages and disadvantages, and the choice of model depends on the specific disease being studied and the research question being addressed.
Glycogen Storage Disease Type IIb (GSD IIb) is a rare genetic disorder that affects the body's ability to break down glycogen, a complex carbohydrate that stores energy in the liver and muscles. People with GSD IIb have a deficiency in the enzyme glucose-6-phosphatase, which is necessary for the breakdown of glycogen. As a result, glycogen accumulates in the liver and muscles, leading to a variety of symptoms and complications. The symptoms of GSD IIb can vary widely depending on the severity of the condition and the age at which it is diagnosed. Common symptoms include fatigue, muscle weakness, and liver enlargement. In severe cases, GSD IIb can lead to liver failure, which can be life-threatening. There is currently no cure for GSD IIb, but treatment is focused on managing the symptoms and complications of the condition. This may include dietary changes, such as a low-carbohydrate diet, and medications to help regulate blood sugar levels. In some cases, liver transplantation may be necessary to treat liver failure.
Isolated noncompaction of the ventricular myocardium (INVM) is a rare congenital heart defect that affects the ventricles, which are the main pumping chambers of the heart. INVM is characterized by an abnormal thickening of the ventricular myocardium, which is the muscular layer of the heart that contracts to pump blood. In INVM, the myocardium has a "spongy" or "clefted" appearance, with deep trabeculations (ridges) and shallow recesses (clefts) between them. This abnormal thickening of the myocardium can lead to reduced blood flow and increased pressure in the heart, which can cause symptoms such as shortness of breath, fatigue, and chest pain. INVM is usually diagnosed using echocardiography, a type of ultrasound that allows doctors to visualize the heart and its structures. Treatment for INVM may include medications to control symptoms and prevent complications, or surgery to repair or replace the affected heart structures.
Pregnancy complications, cardiovascular refers to medical conditions that affect the cardiovascular system of a pregnant woman and can potentially harm her or her developing fetus. These complications can include hypertension (high blood pressure), gestational diabetes, preeclampsia, and heart disease. These conditions can lead to serious complications such as preterm labor, fetal growth restriction, and even maternal death if not properly managed. It is important for pregnant women to receive regular prenatal care and to inform their healthcare provider of any pre-existing medical conditions or risk factors for cardiovascular complications.
Desmin is a type of intermediate filament protein that is primarily found in muscle cells, particularly in the sarcomeres of skeletal and cardiac muscles. It is a key component of the cytoskeleton, providing structural support and helping to maintain the shape and integrity of the muscle cell. Desmin is also involved in the regulation of muscle contraction and relaxation, as well as in the repair and regeneration of muscle tissue. In addition, it has been implicated in a number of muscle-related diseases and disorders, including desmin-related myopathy, which is a group of inherited muscle disorders characterized by muscle weakness and atrophy. In the medical field, desmin is often used as a diagnostic marker for muscle diseases and disorders, and it is also studied as a potential target for the development of new treatments for these conditions.
Dystrophin is a protein that plays a crucial role in maintaining the structural integrity of muscle fibers in the human body. It is encoded by the DMD gene, which is located on the X chromosome. Dystrophin is responsible for linking the inner and outer layers of muscle fibers, providing them with stability and preventing them from tearing during muscle contraction. When the DMD gene is mutated or absent, dystrophin cannot be produced, leading to a deficiency in the protein. This deficiency is the underlying cause of Duchenne muscular dystrophy (DMD), a severe and progressive muscle-wasting disorder that primarily affects boys. DMD is characterized by muscle weakness and wasting, which can lead to difficulty walking, breathing, and even death in severe cases. In addition to DMD, dystrophin deficiency can also cause other forms of muscular dystrophy, such as Becker muscular dystrophy and dilated cardiomyopathy.
Ventricular dysfunction is a medical condition in which the heart's ventricles, the lower chambers responsible for pumping blood out of the heart, are unable to function properly. This can result in a decrease in the amount of blood that is pumped out of the heart with each beat, leading to symptoms such as shortness of breath, fatigue, and swelling in the legs and ankles. There are several types of ventricular dysfunction, including systolic dysfunction, which occurs when the ventricles are unable to contract effectively, and diastolic dysfunction, which occurs when the ventricles are unable to relax and fill with blood properly. Ventricular dysfunction can be caused by a variety of factors, including heart disease, heart attack, high blood pressure, and certain genetic conditions. Treatment for ventricular dysfunction typically involves medications to improve heart function and lifestyle changes such as a healthy diet and regular exercise. In severe cases, surgery may be necessary.
Mitral Valve Insufficiency (MVI) is a medical condition in which the mitral valve, which is located between the left atrium and left ventricle of the heart, does not close properly. This allows blood to flow back from the left ventricle into the left atrium, which can lead to an overload of blood in the left atrium and a decrease in the amount of blood flowing to the rest of the body. MVI can be caused by a variety of factors, including damage to the valve from infection, rheumatic fever, or high blood pressure, or it can be a result of a congenital defect. Symptoms of MVI may include shortness of breath, fatigue, chest pain, and swelling in the legs and ankles. Treatment for MVI may include medications to manage symptoms and improve heart function, or surgery to repair or replace the damaged valve.
3-Iodobenzylguanidine (MIBG) is a synthetic analog of norepinephrine that is used in the medical field for diagnostic and therapeutic purposes. It is a radiolabeled compound that is commonly used in imaging studies to detect and evaluate certain types of tumors, particularly pheochromocytomas and neuroblastomas, which are tumors of the adrenal gland and sympathetic nervous system, respectively. In diagnostic imaging, MIBG is typically administered as a radiolabeled compound, such as 131I-MIBG, which is taken up by cells that have high levels of norepinephrine uptake. The radiolabeled compound is then detected using a gamma camera to create images of the distribution of the compound in the body. This can help to identify the location and size of tumors, as well as to determine whether the tumor is producing excess hormones. MIBG is also used in therapeutic applications, particularly for the treatment of certain types of neuroblastoma. In this context, MIBG is administered as a non-radiolabeled compound, and its mechanism of action is thought to involve the inhibition of catecholamine synthesis and release by the tumor cells. This can help to reduce the production of excess hormones and slow the growth of the tumor.
Heart block is a condition in which the electrical signals that regulate the heartbeat are slowed or blocked as they travel through the heart's conduction system. This can cause the heart to beat too slowly (bradycardia) or irregularly, which can lead to symptoms such as dizziness, fainting, and shortness of breath. There are three main types of heart block: first-degree, second-degree, and third-degree. First-degree heart block is the mildest form and usually does not cause any symptoms. Second-degree heart block is more serious and can cause symptoms, especially if it is caused by an underlying heart condition. Third-degree heart block is the most serious form and can lead to life-threatening complications if not treated promptly. Heart block can be caused by a variety of factors, including damage to the heart muscle, certain medications, and inherited conditions. Treatment options depend on the severity of the heart block and the underlying cause. In some cases, a pacemaker may be necessary to regulate the heartbeat.
Duchenne Muscular Dystrophy (DMD) is a genetic disorder that affects muscle strength and function. It is caused by mutations in the dystrophin gene, which is responsible for producing a protein called dystrophin that helps to maintain the integrity of muscle fibers. Without dystrophin, muscle fibers become damaged and break down, leading to progressive muscle weakness and wasting. DMD primarily affects boys and is usually diagnosed in early childhood. The symptoms of DMD typically begin with difficulty in walking and running, which worsen over time. As the disease progresses, affected individuals may experience difficulty in climbing stairs, getting up from a seated position, and even breathing. The disease can also affect the heart and respiratory muscles, leading to serious complications. There is currently no cure for DMD, but there are treatments available that can help manage symptoms and improve quality of life. These may include physical therapy, assistive devices, and medications to help manage muscle stiffness and pain. In some cases, a heart transplant may be necessary to treat complications related to heart muscle damage.
Syncope is a medical condition characterized by a temporary loss of consciousness due to a lack of blood flow to the brain. It is also known as fainting or passing out. Syncope can be caused by a variety of factors, including low blood pressure, heart problems, anemia, dehydration, or certain medications. Symptoms of syncope may include dizziness, lightheadedness, weakness, and loss of consciousness. Treatment for syncope depends on the underlying cause and may include lifestyle changes, medications, or medical procedures.
Tropomyosin is a protein that plays a crucial role in regulating muscle contraction in the medical field. It is a part of the thin filament of muscle fibers and helps to control the interaction between actin and myosin, the two proteins responsible for muscle contraction. In a relaxed muscle, tropomyosin covers the binding sites on actin that allow myosin to attach and generate force. When a muscle is stimulated to contract, calcium ions bind to troponin, a protein that is associated with tropomyosin. This binding causes a conformational change in tropomyosin, exposing the binding sites on actin and allowing myosin to attach and generate force. Tropomyosin is also involved in the regulation of muscle relaxation. When the muscle is no longer stimulated to contract, calcium ions are removed from troponin, causing tropomyosin to return to its original position and cover the binding sites on actin once again, preventing further muscle contraction. Disruptions in tropomyosin function can lead to muscle disorders such as nemaline myopathy, a condition characterized by muscle weakness and stiffness.
Ventricular dysfunction, right refers to a medical condition where the right ventricle of the heart is not functioning properly. The right ventricle is responsible for pumping blood from the heart to the lungs, where it receives oxygen and gets rid of carbon dioxide. When the right ventricle is not functioning properly, it can lead to a decrease in the amount of blood that is pumped to the lungs, which can cause a variety of symptoms and complications. There are several different causes of right ventricular dysfunction, including heart valve problems, heart muscle damage, and heart rhythm disorders. Treatment for right ventricular dysfunction depends on the underlying cause and may include medications, lifestyle changes, and in some cases, surgery. It is important to seek medical attention if you are experiencing symptoms of right ventricular dysfunction, as early diagnosis and treatment can help to improve outcomes and prevent complications.
In the medical field, "connectin" typically refers to a type of protein that plays a crucial role in the formation and maintenance of connective tissue. Connective tissue is a type of tissue that provides support, strength, and protection to the body's organs and tissues. Connectins are found in a variety of connective tissues, including tendons, ligaments, and cartilage. Connectins are large, complex proteins that are made up of multiple subunits. They are responsible for providing strength and flexibility to connective tissue, as well as helping to maintain the structural integrity of tissues. Connectins are also involved in the process of tissue repair and regeneration, as they help to facilitate the growth and differentiation of new cells. There are several different types of connectins, including collagen, elastin, and fibronectin. Each type of connectin has a unique structure and function, and they work together to provide the body's connective tissue with the strength, flexibility, and resilience it needs to function properly.
A Bundle-Branch Block (BBB) is a type of heart rhythm disorder that occurs when there is a disruption in the electrical signals that control the contraction of the heart muscle. The heart has two main electrical pathways, called the right and left bundle branches, which carry electrical signals from the sinoatrial node (the heart's natural pacemaker) to the ventricles (the lower chambers of the heart) and cause them to contract and pump blood. A Bundle-Branch Block occurs when there is a delay or blockage in the electrical signals that travel through the bundle branches, causing the ventricles to contract asynchronously or with an abnormal rhythm. This can lead to a variety of symptoms, including palpitations, shortness of breath, dizziness, and fainting. There are two main types of Bundle-Branch Block: Right Bundle-Branch Block (RBBB) and Left Bundle-Branch Block (LBBB). RBBB is more common and usually has no symptoms, while LBBB is less common and can cause more serious symptoms, such as fainting or heart failure. Treatment for Bundle-Branch Block depends on the underlying cause and the severity of the symptoms. In some cases, no treatment may be necessary, while in others, medications or electrical cardioversion may be used to restore a normal heart rhythm. In severe cases, surgery may be necessary to correct the blockage.
Troponin I is a protein that is found in cardiac muscle cells. It plays a key role in regulating muscle contraction by controlling the interaction between actin and myosin filaments. When troponin I is activated, it allows myosin to bind to actin and initiate muscle contraction. Troponin I levels can be measured in the blood to help diagnose and monitor heart muscle damage or injury, such as in cases of myocardial infarction (heart attack). High levels of troponin I in the blood are a strong indicator of heart muscle damage and can be used to guide treatment decisions and predict outcomes.
Myosins are a family of motor proteins that are responsible for muscle contraction in animals. They are found in almost all eukaryotic cells, including muscle cells, and play a crucial role in the movement of intracellular organelles and vesicles. In muscle cells, myosins interact with actin filaments to generate force and movement. The process of muscle contraction involves the binding of myosin heads to actin filaments, followed by the movement of the myosin head along the actin filament, pulling the actin filament towards the center of the sarcomere. This sliding of actin and myosin filaments past each other generates the force required for muscle contraction. There are many different types of myosins, each with its own specific function and localization within the cell. Some myosins are involved in the movement of organelles and vesicles within the cytoplasm, while others are involved in the movement of chromosomes during cell division. Myosins are also involved in a variety of other cellular processes, including cell migration, cytokinesis, and the formation of cell junctions.
Tachycardia is a medical condition characterized by an abnormally fast heart rate, typically defined as a resting heart rate of 100 beats per minute or higher. The normal resting heart rate for adults is generally considered to be between 60 and 100 beats per minute. Tachycardia can be classified into several types based on the underlying cause, including: 1. Sinus tachycardia: This is the most common type of tachycardia, and it occurs when the heart rate is faster than normal but still within a normal range for the individual's age, fitness level, and other factors. 2. Atrial fibrillation: This is a type of arrhythmia characterized by irregular and rapid heartbeats that originate in the atria (upper chambers) of the heart. 3. Ventricular tachycardia: This is a type of arrhythmia characterized by rapid and irregular heartbeats that originate in the ventricles (lower chambers) of the heart. Tachycardia can be caused by a variety of factors, including stress, anxiety, caffeine or other stimulants, dehydration, electrolyte imbalances, certain medications, and underlying medical conditions such as heart disease, thyroid disorders, or lung disease. Treatment for tachycardia depends on the underlying cause and may include medications, lifestyle changes, or medical procedures such as cardioversion or catheter ablation.
Coxsackievirus infections are a group of viral infections caused by the Coxsackievirus family of viruses. These viruses are highly contagious and can cause a range of symptoms, including fever, rash, and swelling of the hands and feet. In some cases, Coxsackievirus infections can also cause more serious complications, such as meningitis, encephalitis, and myocarditis. These infections are most common in children, but can also affect adults. Treatment for Coxsackievirus infections typically involves supportive care to manage symptoms and prevent complications. In severe cases, antiviral medications may be used to help control the infection.
Pericarditis, Constrictive is a rare condition in which the pericardium, the sac-like tissue surrounding the heart, becomes thickened and scarred, leading to constriction of the heart's ability to fill and pump blood effectively. This constriction can cause a buildup of fluid around the heart, which can lead to symptoms such as shortness of breath, fatigue, and swelling in the legs and abdomen. Treatment for pericarditis, constrictive may include medications to reduce inflammation and fluid buildup, as well as surgery to remove the thickened pericardium or to create an opening in the sac to allow the heart to expand and pump more effectively.
Propanolamines are a class of organic compounds that contain a tertiary amine group attached to a propane chain. They are commonly used as pharmaceuticals and as active ingredients in over-the-counter cold and allergy medications. There are several different types of propanolamines, including pseudoephedrine, phenylephrine, and triprolidine. These drugs work by constricting blood vessels in the nasal passages and sinuses, reducing inflammation, and relieving congestion. They are also used to treat other conditions such as high blood pressure, heart failure, and certain types of asthma. Propanolamines can have side effects, including dizziness, dry mouth, and insomnia. They can also interact with other medications, so it is important to tell your doctor about all the medications you are taking before starting to use propanolamines. In some cases, propanolamines may be contraindicated for certain individuals, such as those with certain heart conditions or high blood pressure.
Natriuretic Peptide, Brain (NPB) is a hormone that is produced by the brain and released into the bloodstream. It is a member of the natriuretic peptide family, which also includes atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). NPB has several functions in the body, including regulating blood pressure, fluid balance, and heart rate. It works by inhibiting the release of renin, a hormone that stimulates the production of angiotensin II, which in turn constricts blood vessels and increases blood pressure. NPB also has a role in the regulation of the autonomic nervous system, which controls heart rate and blood pressure. It can stimulate the release of nitric oxide, a molecule that helps to relax blood vessels and lower blood pressure. In the medical field, NPB is being studied as a potential diagnostic tool for various cardiovascular diseases, including heart failure and hypertension. It may also have therapeutic potential for these conditions, as it has been shown to improve cardiac function and reduce blood pressure in animal models.
Iodobenzenes are organic compounds that contain an iodine atom bonded to a benzene ring. They are commonly used in the medical field as antithyroid drugs, particularly in the treatment of hyperthyroidism. Iodobenzenes work by inhibiting the production of thyroid hormones by the thyroid gland. They are also used as contrast agents in diagnostic imaging procedures, such as computed tomography (CT) scans. In addition, iodobenzenes have been studied for their potential use in the treatment of other conditions, such as cancer and viral infections.
Desmocollins are a family of proteins that are involved in the formation and maintenance of desmosomes, which are specialized cell-cell junctions found in many tissues throughout the body. Desmosomes are important for maintaining the structural integrity of tissues, particularly in areas that experience mechanical stress, such as the skin and heart. Desmocollins are encoded by a group of genes located on chromosome 12, and there are several different isoforms of the protein that have been identified. These proteins are characterized by the presence of a conserved central domain that is responsible for binding to other desmosomal proteins, as well as a number of other domains that are involved in regulating the activity of the protein. Desmocollins play a critical role in the formation and maintenance of desmosomes, and mutations in the genes encoding these proteins have been linked to a number of inherited disorders that affect the skin, hair, and other tissues. These disorders, which include epidermolysis bullosa simplex and junctional epidermolysis bullosa, are characterized by fragile skin that is prone to blistering and other injuries.
LIM domain proteins are a family of proteins that contain two zinc finger motifs, known as LIM domains, which are responsible for mediating protein-protein interactions. These proteins are involved in a variety of cellular processes, including cytoskeletal organization, cell adhesion, and signal transduction. They are found in a wide range of organisms, including humans, and have been implicated in a number of diseases, including cancer, cardiovascular disease, and neurological disorders.
Metoprolol is a medication that belongs to a class of drugs called beta blockers. It is primarily used to treat high blood pressure, angina (chest pain), and certain types of heart rhythm disorders. Metoprolol works by blocking the effects of adrenaline (a hormone that can cause the heart to beat faster and harder) on the heart, which helps to lower blood pressure and reduce the workload on the heart. It can also be used to prevent migraines and to treat anxiety and panic disorders. Metoprolol is available in both immediate-release and extended-release forms, and it is usually taken by mouth.
Desmoplakins are a group of proteins that are found in the desmosomes of epithelial cells. Desmosomes are specialized cell junctions that provide mechanical strength and stability to tissues, particularly in the skin and other epithelial tissues. Desmoplakins are important components of the desmosomal complex, which also includes cadherins, plakoglobins, and plakophilins. They are large, heavily glycosylated proteins that are synthesized in the endoplasmic reticulum and transported to the Golgi apparatus, where they are modified and packaged for transport to the cell membrane. Desmoplakins play a critical role in maintaining the structural integrity of epithelial tissues and are involved in a number of cellular processes, including cell adhesion, migration, and signaling. Mutations in desmoplakin genes have been associated with a number of human diseases, including epidermolysis bullosa simplex, a genetic disorder characterized by fragile skin that is prone to blistering.
Noonan syndrome is a genetic disorder that affects many parts of the body, including the face, heart, and skeletal system. It is caused by mutations in the PTPN11 gene, which is responsible for producing a protein that helps regulate cell growth and development. People with Noonan syndrome may have distinctive facial features, such as a prominent forehead, upturned nose, and short stature. They may also have heart defects, such as a hole in the heart or an abnormality in the valves, and skeletal abnormalities, such as scoliosis or a curved spine. Other symptoms may include learning difficulties, developmental delays, and an increased risk of certain types of cancer. Noonan syndrome is usually diagnosed through a combination of physical examination, medical history, and genetic testing. There is no cure for Noonan syndrome, but treatment is available to manage the symptoms and improve quality of life.
Receptors, Adrenergic, beta-1 (β1-adrenergic receptors) are a type of protein found on the surface of cells in the body that bind to and respond to the hormone adrenaline (also known as epinephrine). These receptors are primarily located in the heart, lungs, and blood vessels, and play a key role in the body's "fight or flight" response to stress or danger. When adrenaline binds to β1-adrenergic receptors, it triggers a series of chemical reactions within the cell that can have a number of effects on the body. For example, it can cause the heart to beat faster and harder, which can increase blood flow to the muscles and prepare the body for physical activity. It can also cause blood vessels to constrict, which can raise blood pressure and help to direct blood flow to the most important organs. β1-adrenergic receptors are also involved in a number of other physiological processes, including the regulation of glucose metabolism and the control of inflammation. They are an important target for medications used to treat a variety of conditions, including heart disease, high blood pressure, and asthma.
Muscle proteins are proteins that are found in muscle tissue. They are responsible for the structure, function, and repair of muscle fibers. There are two main types of muscle proteins: contractile proteins and regulatory proteins. Contractile proteins are responsible for the contraction of muscle fibers. The most important contractile protein is actin, which is found in the cytoplasm of muscle fibers. Actin interacts with another protein called myosin, which is found in the sarcomeres (the functional units of muscle fibers). When myosin binds to actin, it causes the muscle fiber to contract. Regulatory proteins are responsible for controlling the contraction of muscle fibers. They include troponin and tropomyosin, which regulate the interaction between actin and myosin. Calcium ions also play a role in regulating muscle contraction by binding to troponin and causing it to change shape, allowing myosin to bind to actin. Muscle proteins are important for maintaining muscle strength and function. They are also involved in muscle growth and repair, and can be affected by various medical conditions and diseases, such as muscular dystrophy, sarcopenia, and cancer.
Carbazoles are a class of organic compounds that contain a six-membered aromatic ring with two nitrogen atoms. They are structurally similar to benzene, but with two nitrogen atoms replacing two carbon atoms. In the medical field, carbazoles have been studied for their potential use as anti-cancer agents. Some carbazole derivatives have been shown to selectively target and kill cancer cells, while sparing healthy cells. They are also being investigated for their potential use in the treatment of other diseases, such as Alzheimer's and Parkinson's. Carbazoles have also been used as fluorescent dyes in biological imaging and as photoactive materials in optoelectronic devices.
Dobutamine is a medication that is used to increase the strength of the heart's contractions and to increase the heart's rate. It is a synthetic form of dopamine, a hormone that is naturally produced by the body to help regulate blood pressure and heart function. Dobutamine is typically used to treat heart failure, a condition in which the heart is unable to pump blood effectively throughout the body. It is also sometimes used to treat low blood pressure (hypotension) and to increase blood flow to the heart muscle after a heart attack. Dobutamine is usually given intravenously, and the dosage is adjusted based on the patient's response and any side effects that may occur.
Ventricular premature complexes (VPCs) are abnormal heartbeats that originate from the ventricles, which are the lower chambers of the heart. They are also known as ventricular extra beats or ventricular premature contractions (VPCs). VPCs are a common type of arrhythmia, which is an irregular heartbeat. VPCs can occur spontaneously or in response to certain triggers, such as stress, caffeine, or alcohol. They are usually harmless and do not cause any symptoms in most people. However, in some cases, VPCs can be a sign of an underlying heart condition, such as heart disease or heart failure. VPCs can be detected through an electrocardiogram (ECG), which is a test that records the electrical activity of the heart. Treatment for VPCs may not be necessary if they are not causing any symptoms or if they are a result of a temporary trigger. However, if VPCs are frequent or are causing symptoms, treatment may include medications or other interventions to help regulate the heartbeat.
Cardiac output (CO) is the amount of blood pumped by the heart per minute, typically measured in liters per minute (L/min). Low cardiac output refers to a condition where the heart is not pumping enough blood to meet the body's needs. This can be caused by a variety of factors, including heart failure, low blood volume, severe anemia, and certain medications. Symptoms of low cardiac output may include shortness of breath, fatigue, dizziness, and decreased urine output. Treatment for low cardiac output depends on the underlying cause and may include medications, fluid replacement, or surgery.
Doxorubicin is an anthracycline chemotherapy drug that is used to treat a variety of cancers, including breast cancer, ovarian cancer, and leukemia. It works by interfering with the production of DNA and RNA, which are essential for the growth and division of cancer cells. Doxorubicin is usually administered intravenously, and its side effects can include nausea, vomiting, hair loss, and damage to the heart and kidneys. It is a powerful drug that can be effective against many types of cancer, but it can also have serious side effects, so it is typically used in combination with other treatments or in low doses.
Diabetes Mellitus, Experimental refers to a type of diabetes that is studied in laboratory animals, such as mice or rats, to better understand the disease and develop potential treatments. This type of diabetes is typically induced by injecting the animals with chemicals or viruses that mimic the effects of diabetes in humans. The experimental diabetes in animals is used to study the pathophysiology of diabetes, test new drugs or therapies, and investigate the underlying mechanisms of the disease. The results of these studies can then be used to inform the development of new treatments for diabetes in humans.
Friedreich ataxia is a rare genetic disorder that affects the nervous system, causing progressive damage to the spinal cord and brainstem. It is caused by a mutation in the FXN gene, which leads to a deficiency in the production of a protein called frataxin. This deficiency disrupts the normal functioning of mitochondria, the energy-producing structures within cells, leading to damage and death of nerve cells. The symptoms of Friedreich ataxia typically begin in childhood or adolescence and include difficulty with, balance, and speech, as well as muscle weakness and sensory loss. The disease is usually progressive, and symptoms can worsen over time. There is currently no cure for Friedreich ataxia, but treatments can help manage symptoms and improve quality of life.
Muscular dystrophies are a group of genetic disorders that cause progressive muscle weakness and wasting. These disorders are caused by mutations in genes that are responsible for producing proteins that are essential for maintaining the structure and function of muscle fibers. There are many different types of muscular dystrophies, each with its own specific genetic cause and pattern of inheritance. Some of the most common types of muscular dystrophy include Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD), facioscapulohumeral muscular dystrophy (FSHD), and myotonic dystrophy (DM). The symptoms of muscular dystrophy can vary widely depending on the type and severity of the disorder. Common symptoms include muscle weakness, difficulty with movement, muscle stiffness, and fatigue. In some cases, muscular dystrophy can also affect other organs, such as the heart and lungs. There is currently no cure for muscular dystrophy, but there are treatments available that can help manage symptoms and slow the progression of the disease. These may include physical therapy, medications, and assistive devices such as braces or wheelchairs.
Amyloidosis is a rare disorder characterized by the abnormal accumulation of a protein called amyloid in various tissues and organs of the body. Amyloid is a protein that is normally produced by cells in the body and broken down naturally. However, in amyloidosis, the amyloid protein is produced in excess or is not broken down properly, leading to the formation of abnormal deposits in tissues and organs. The accumulation of amyloid can cause damage to the affected organs and tissues, leading to a range of symptoms and complications depending on the location and severity of the deposits. Common symptoms of amyloidosis include fatigue, weakness, weight loss, swelling in the legs and abdomen, and difficulty breathing. There are several types of amyloidosis, including primary amyloidosis, secondary amyloidosis, and familial amyloidosis. Primary amyloidosis is the most common form and is usually caused by abnormal production of the amyloid protein in the body. Secondary amyloidosis is caused by another underlying medical condition, such as chronic inflammatory diseases or cancer. Familial amyloidosis is an inherited form of the disease that is caused by mutations in certain genes. Treatment for amyloidosis depends on the type and severity of the disease, as well as the underlying cause. Treatment options may include medications to manage symptoms, chemotherapy, radiation therapy, stem cell transplantation, and supportive care to manage complications.
Mitochondrial myopathies are a group of inherited disorders that affect the mitochondria, which are the energy-producing structures within cells. These disorders can cause muscle weakness, fatigue, and other symptoms, and can affect various organs in the body. Mitochondrial myopathies are caused by mutations in genes that are involved in the production or function of mitochondrial proteins. These mutations can lead to a decrease in the production of energy within the mitochondria, which can cause muscle weakness and other symptoms. There are many different types of mitochondrial myopathies, and they can range in severity from mild to severe. Some people with mitochondrial myopathies may have only mild symptoms, while others may have more severe symptoms that can affect their ability to perform daily activities. Treatment for mitochondrial myopathies may involve medications to manage symptoms, physical therapy to improve muscle strength and function, and other supportive therapies. In some cases, a liver transplant or other type of organ transplantation may be necessary to treat complications of the disorder.
Sarcoplasmic Reticulum Calcium-Transporting ATPases (SERCA) are a family of proteins that play a crucial role in regulating intracellular calcium levels in muscle cells. They are responsible for pumping calcium ions from the cytosol back into the sarcoplasmic reticulum, a specialized organelle within muscle cells that stores calcium ions. This process is essential for muscle contraction and relaxation. There are several types of SERCA proteins, including SERCA1, SERCA2a, and SERCA2b, which are found in different types of muscle cells. SERCA1 is primarily found in cardiac muscle cells, while SERCA2a and SERCA2b are found in skeletal and smooth muscle cells, respectively. Defects in SERCA proteins can lead to a variety of medical conditions, including heart failure, arrhythmias, and muscle disorders. For example, mutations in the SERCA2a gene can cause a condition called dilated cardiomyopathy, which is characterized by the enlargement and weakening of the heart muscle. Similarly, mutations in the SERCA1 gene can cause a condition called atrial fibrillation, which is a type of irregular heartbeat.
Disease progression refers to the worsening or progression of a disease over time. It is a natural course of events that occurs in many chronic illnesses, such as cancer, heart disease, and diabetes. Disease progression can be measured in various ways, such as changes in symptoms, physical examination findings, laboratory test results, or imaging studies. In some cases, disease progression can be slowed or stopped through medical treatment, such as medications, surgery, or radiation therapy. However, in other cases, disease progression may be inevitable, and the focus of treatment may shift from trying to cure the disease to managing symptoms and improving quality of life. Understanding disease progression is important for healthcare providers to develop effective treatment plans and to communicate with patients about their condition and prognosis. It can also help patients and their families make informed decisions about their care and treatment options.
Ventricular fibrillation (VF) is a type of abnormal heart rhythm that occurs when the lower chambers of the heart (ventricles) quiver instead of contracting normally. This quivering causes the heart to be unable to pump blood effectively, leading to a lack of oxygen to the body's vital organs and potentially causing sudden cardiac arrest. VF is a medical emergency that requires immediate treatment with defibrillation, a procedure that uses an electric shock to restore the heart's normal rhythm. Without prompt treatment, VF can be fatal.
A heart aneurysm is a bulge or balloon-like enlargement of a weakened portion of the wall of a blood vessel in the heart. It occurs when a section of the wall becomes thin and weak, causing it to balloon outwards. Aneurysms can occur in any blood vessel in the body, but they are most commonly found in the aorta, which is the largest artery in the body and carries blood from the heart to the rest of the body. Heart aneurysms can be caused by a variety of factors, including high blood pressure, atherosclerosis (the buildup of plaque in the arteries), infections, and injuries. They can also be caused by genetic factors, such as Marfan syndrome or Ehlers-Danlos syndrome. Heart aneurysms can be asymptomatic, meaning that they do not cause any noticeable symptoms. However, if an aneurysm becomes large enough, it can cause symptoms such as chest pain, shortness of breath, and palpitations. In some cases, an aneurysm can rupture, which is a life-threatening emergency that requires immediate medical attention. Treatment for heart aneurysms depends on the size and location of the aneurysm, as well as the underlying cause. Small aneurysms may be monitored with regular imaging tests, while larger aneurysms may require surgery or other interventions to prevent rupture. Medications may also be prescribed to manage symptoms or lower the risk of complications.
Atrial Natriuretic Factor (ANF) is a hormone that is produced by the heart's atria in response to increased pressure within the atria. ANF is released into the bloodstream and acts as a natural diuretic, helping to regulate blood pressure and fluid balance in the body. ANF works by relaxing blood vessels, which reduces blood pressure and allows the kidneys to excrete more sodium and water. This helps to reduce the volume of fluid in the body and lower blood pressure. ANF also inhibits the release of aldosterone, a hormone that regulates the balance of sodium and potassium in the body. In addition to its role in regulating blood pressure and fluid balance, ANF has been shown to have other effects on the body, including reducing the workload on the heart and improving heart function. ANF is also involved in the regulation of the renin-angiotensin-aldosterone system, which plays a key role in blood pressure regulation. Abnormal levels of ANF can be associated with a variety of medical conditions, including heart failure, hypertension, and kidney disease.
Gadolinium DTPA, also known as gadopentetate dimeglumine, is a contrast agent used in magnetic resonance imaging (MRI) to enhance the visibility of certain structures within the body. It is a paramagnetic substance that increases the relaxation time of water molecules in the tissue surrounding the targeted area, making it easier for the MRI machine to detect and visualize the area of interest. Gadolinium DTPA is commonly used to diagnose a variety of medical conditions, including brain and spinal cord disorders, cardiovascular diseases, and certain types of cancer. It is typically administered intravenously and can cause side effects such as nausea, headache, and allergic reactions in some patients. However, the benefits of using gadolinium DTPA in MRI imaging generally outweigh the risks, and it is considered a safe and effective diagnostic tool when used appropriately.
Barth syndrome is a rare genetic disorder that affects the body's ability to produce energy. It is caused by mutations in the TAZ gene, which is located on the X chromosome. The disorder is characterized by symptoms such as short stature, delayed puberty, heart problems, skeletal abnormalities, and muscle weakness. Barth syndrome is also associated with an increased risk of sudden cardiac death, particularly in young males. Treatment for Barth syndrome typically involves managing the symptoms and providing supportive care. There is currently no cure for the disorder.
Atrioventricular (AV) block is a type of heart rhythm disorder that occurs when the electrical signals that regulate the heartbeat are delayed or blocked as they travel from the atria (upper chambers) to the ventricles (lower chambers) of the heart. This can cause the heart to beat too slowly or irregularly, which can lead to symptoms such as dizziness, fainting, and shortness of breath. There are three main types of AV block: first-degree, second-degree, and third-degree. First-degree AV block is the mildest form and is characterized by a delay in the electrical signal between the atria and ventricles. Second-degree AV block is more severe and is characterized by a partial blockage of the electrical signal, which can result in a slower heart rate. Third-degree AV block is the most severe form and is characterized by a complete blockage of the electrical signal, which can result in a very slow or irregular heart rate. AV block can be caused by a variety of factors, including damage to the heart muscle, certain medications, and underlying heart conditions such as coronary artery disease or heart failure. Treatment for AV block depends on the severity of the condition and may include medications, a pacemaker, or surgery.
Calcium is a chemical element with the symbol Ca and atomic number 20. It is a vital mineral for the human body and is essential for many bodily functions, including bone health, muscle function, nerve transmission, and blood clotting. In the medical field, calcium is often used to diagnose and treat conditions related to calcium deficiency or excess. For example, low levels of calcium in the blood (hypocalcemia) can cause muscle cramps, numbness, and tingling, while high levels (hypercalcemia) can lead to kidney stones, bone loss, and other complications. Calcium supplements are often prescribed to people who are at risk of developing calcium deficiency, such as older adults, vegetarians, and people with certain medical conditions. However, it is important to note that excessive calcium intake can also be harmful, and it is important to follow recommended dosages and consult with a healthcare provider before taking any supplements.
In the medical field, carrier proteins are proteins that transport molecules across cell membranes or within cells. These proteins bind to specific molecules, such as hormones, nutrients, or waste products, and facilitate their movement across the membrane or within the cell. Carrier proteins play a crucial role in maintaining the proper balance of molecules within cells and between cells. They are involved in a wide range of physiological processes, including nutrient absorption, hormone regulation, and waste elimination. There are several types of carrier proteins, including facilitated diffusion carriers, active transport carriers, and ion channels. Each type of carrier protein has a specific function and mechanism of action. Understanding the role of carrier proteins in the body is important for diagnosing and treating various medical conditions, such as genetic disorders, metabolic disorders, and neurological disorders.
Muscular diseases are a group of disorders that affect the muscles and muscle tissue. These diseases can cause weakness, pain, and stiffness in the muscles, and can affect the ability to move and perform daily activities. Some common muscular diseases include muscular dystrophy, myositis, and myopathy. These diseases can be caused by a variety of factors, including genetic mutations, infections, and autoimmune disorders. Treatment for muscular diseases may include medications, physical therapy, and in some cases, surgery.
Gamma catenin, also known as gamma-catenin or plakoglobin, is a protein that plays a role in cell adhesion and signaling pathways in the mammalian body. It is a member of the catenin family of proteins, which are involved in the formation and maintenance of cell-cell adhesion complexes called adherens junctions. Gamma catenin is a multifunctional protein that interacts with other proteins, including alpha-catenin, beta-catenin, and cadherins, to form a complex that links the cadherin-catenin complex to the actin cytoskeleton. This complex is essential for the stability and function of adherens junctions, which are important for maintaining tissue integrity and regulating cell-cell communication. In addition to its role in cell adhesion, gamma catenin has also been implicated in a variety of cellular processes, including cell proliferation, differentiation, and migration. It has been implicated in the development and progression of several diseases, including cancer, and is a target for therapeutic intervention in some cases.
Gadolinium is a chemical element that is commonly used in the medical field as a contrast agent for magnetic resonance imaging (MRI) scans. It is a paramagnetic metal that enhances the visibility of certain structures in the body on MRI images. When gadolinium is administered to a patient, it binds to proteins in the body and becomes concentrated in areas with high blood flow, such as blood vessels and tumors. This increased concentration of gadolinium in these areas makes them more visible on MRI images, allowing doctors to better diagnose and monitor a variety of medical conditions, including cancer, cardiovascular disease, and neurological disorders. Gadolinium-based contrast agents are generally considered safe and effective when used as directed. However, in some cases, patients may experience adverse reactions to gadolinium, such as allergic reactions or nephrogenic systemic fibrosis (NSF), a rare but serious condition that can cause skin thickening and scarring. As a result, healthcare providers must carefully weigh the benefits and risks of gadolinium use on a case-by-case basis.
In the medical field, a syndrome is a set of symptoms and signs that occur together and suggest the presence of a particular disease or condition. A syndrome is often defined by a specific pattern of symptoms that are not caused by a single underlying disease, but rather by a combination of factors, such as genetic, environmental, or hormonal. For example, Down syndrome is a genetic disorder that is characterized by a specific set of physical and intellectual characteristics, such as a flattened facial profile, short stature, and intellectual disability. Similarly, the flu syndrome is a set of symptoms that occur together, such as fever, cough, sore throat, and body aches, that suggest the presence of an influenza virus infection. Diagnosing a syndrome involves identifying the specific set of symptoms and signs that are present, as well as ruling out other possible causes of those symptoms. Once a syndrome is diagnosed, it can help guide treatment and management of the underlying condition.
Fabry disease is a rare genetic disorder that affects the body's ability to break down a protein called globotriaosylceramide (Gb3). This leads to the accumulation of Gb3 in various organs and tissues, including the kidneys, heart, and nervous system. The disease is caused by mutations in the GLA gene, which provides instructions for making an enzyme called alpha-galactosidase A (α-Gal A). Without enough α-Gal A, Gb3 builds up in cells and can damage them over time. The symptoms of Fabry disease can vary widely and may not appear until adulthood. Common symptoms include pain in the hands and feet, skin rashes, numbness or tingling in the hands and feet, and gastrointestinal problems. In severe cases, the disease can lead to heart problems, kidney failure, and stroke. There is no cure for Fabry disease, but treatments are available to manage symptoms and slow the progression of the disease. These may include enzyme replacement therapy, which involves regular infusions of a synthetic version of α-Gal A, and medications to manage symptoms such as pain and high blood pressure.
LEOPARD Syndrome is a rare genetic disorder that is characterized by a distinctive pattern of birthmarks on the skin, heart defects, and other abnormalities. The acronym LEOPARD stands for the following symptoms: - L: Lentigines (birthmarks on the skin) - E: Ears (abnormalities of the ears) - O: Ocular hypertelorism (widely spaced eyes) - P: Pulmonic stenosis (narrowing of the pulmonary valve in the heart) - A: Aortic stenosis (narrowing of the aortic valve in the heart) - R: Retardo (growth retardation) - D: Diabetes mellitus (type 2 diabetes) Other symptoms of LEOPARD Syndrome may include intellectual disability, hearing loss, and thyroid disorders. The syndrome is caused by mutations in the PTPN11 gene, which is located on chromosome 12. It is inherited in an autosomal dominant pattern, meaning that a person only needs to inherit one copy of the mutated gene from one parent to develop the syndrome.
In the medical field, a chronic disease is a long-term health condition that persists for an extended period, typically for more than three months. Chronic diseases are often progressive, meaning that they tend to worsen over time, and they can have a significant impact on a person's quality of life. Chronic diseases can affect any part of the body and can be caused by a variety of factors, including genetics, lifestyle, and environmental factors. Some examples of chronic diseases include heart disease, diabetes, cancer, chronic obstructive pulmonary disease (COPD), and arthritis. Chronic diseases often require ongoing medical management, including medication, lifestyle changes, and regular monitoring to prevent complications and manage symptoms. Treatment for chronic diseases may also involve rehabilitation, physical therapy, and other supportive care.
Amiodarone is a medication that is used to treat a variety of heart rhythm disorders, including atrial fibrillation, ventricular tachycardia, and ventricular fibrillation. It is a type of antiarrhythmic drug that works by slowing down the electrical activity in the heart and allowing it to beat more regularly. Amiodarone is available in both oral and intravenous forms and is typically used as a long-term treatment for heart rhythm disorders. It is also sometimes used to treat other conditions, such as thyrotoxicosis (overactive thyroid) and pneumonia. However, amiodarone can have serious side effects, including lung problems, liver damage, and thyroid disorders, and it should only be used under the supervision of a healthcare professional.
Ethanol, also known as ethyl alcohol, is a type of alcohol that is commonly used in the medical field as a disinfectant and antiseptic. It is a clear, colorless liquid that is flammable and has a distinctive odor. Ethanol is effective at killing a wide range of microorganisms, including bacteria, viruses, and fungi, and is often used to clean surfaces and equipment in healthcare settings to prevent the spread of infection. In addition to its use as a disinfectant, ethanol is also used as a solvent for medications and other substances, and as a fuel for medical devices such as inhalers and nebulizers. It is also used as a preservative in some medications and vaccines to prevent the growth of microorganisms. Ethanol can be toxic if consumed in large amounts, and can cause a range of symptoms including dizziness, nausea, vomiting, and even death. It is important to use ethanol and other disinfectants and antiseptics safely and according to the instructions provided, to avoid accidental exposure or injury.
Endocardial fibroelastosis (EFE) is a rare heart condition that occurs in infants and young children. It is characterized by the abnormal accumulation of fibrous and elastic tissue in the inner lining of the heart's heart chambers (endocardium). This buildup of tissue can obstruct blood flow through the heart and lead to heart failure. EFE is usually diagnosed in infants and young children, and it is more common in boys than girls. The exact cause of EFE is not known, but it is thought to be related to a viral infection or exposure to certain medications during pregnancy. Other risk factors for EFE include prematurity, low birth weight, and a family history of heart disease. Treatment for EFE typically involves medications to manage symptoms and improve heart function. In some cases, surgery may be necessary to remove the excess tissue and improve blood flow through the heart. The prognosis for children with EFE depends on the severity of their condition and how well they respond to treatment. Some children with EFE may recover fully, while others may require ongoing medical care.
Alpha-crystallin B chain is a protein that is encoded by theCRYAB gene in humans. It is a component of the alpha-crystallin family of proteins, which are found in the lens of the eye and play a role in maintaining the transparency and shape of the lens. The alpha-crystallin B chain is a small, heat-stable protein that is thought to help stabilize the alpha-crystallin complex and protect it from denaturation. Mutations in the CRYAB gene have been associated with several eye disorders, including cataracts and glaucoma.
Premature cardiac complexes, also known as premature beats or PVCs, are extra heartbeats that occur before the normal heartbeat. They are a common type of arrhythmia, which is an abnormal heart rhythm. PVCs can be caused by a variety of factors, including stress, anxiety, caffeine, alcohol, certain medications, and heart disease. They are usually not a serious problem, but in some cases, they can be a sign of an underlying heart condition and may require medical treatment.
Myocardial stunning is a reversible condition in which the heart muscle becomes temporarily weakened or dysfunctional after a period of stress or injury. This can occur in response to a variety of factors, including ischemia (reduced blood flow to the heart), myocardial infarction (heart attack), or severe arrhythmias (irregular heartbeats). During myocardial stunning, the heart muscle may not contract as effectively as it normally would, even though there is no permanent damage to the cells. This can lead to symptoms such as chest pain, shortness of breath, and fatigue. The condition is typically reversible with appropriate treatment, although in some cases it may lead to more serious complications such as heart failure. Myocardial stunning is an important consideration in the diagnosis and management of heart disease, as it can affect the effectiveness of treatments and the long-term prognosis for patients. It is often diagnosed using imaging techniques such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment may involve medications to improve blood flow to the heart, lifestyle changes to reduce stress and improve overall heart health, or in some cases, surgery or other invasive procedures.
Hypertrophy refers to the enlargement or thickening of a tissue or organ due to an increase in the size of its cells. In the medical field, hypertrophy can occur in various organs and tissues, including the heart, skeletal muscles, liver, and kidneys. In the context of the heart, hypertrophy is often associated with an increase in the size of the heart muscle in response to increased workload or pressure on the heart. This can occur in conditions such as hypertension, aortic stenosis, or chronic obstructive pulmonary disease (COPD). Hypertrophy of the heart muscle can lead to a decrease in the heart's ability to pump blood efficiently, which can result in heart failure. In skeletal muscles, hypertrophy is often associated with increased physical activity or resistance training, which can lead to an increase in muscle size and strength. This is a normal response to exercise and is not typically associated with any health problems. Overall, hypertrophy can be a normal response to increased workload or physical activity, but it can also be a sign of an underlying health condition that requires medical attention.
Receptors, Adrenergic, beta (β-adrenergic receptors) are a type of protein found on the surface of cells in the body that bind to and respond to signaling molecules called catecholamines, including adrenaline (epinephrine) and noradrenaline (norepinephrine). These receptors are part of the adrenergic signaling system, which plays a critical role in regulating a wide range of physiological processes, including heart rate, blood pressure, metabolism, and immune function. There are three main types of β-adrenergic receptors: β1, β2, and β3. Each type of receptor is found in different tissues and has different functions. For example, β1 receptors are primarily found in the heart and are responsible for increasing heart rate and contractility. β2 receptors are found in the lungs, blood vessels, and muscles, and are involved in relaxing smooth muscle and increasing blood flow. β3 receptors are found in adipose tissue and are involved in regulating metabolism. Activation of β-adrenergic receptors can have a variety of effects on the body, depending on the specific receptor subtype and the tissue it is found in. For example, activation of β2 receptors in the lungs can cause bronchodilation, which can help to open up airways and improve breathing in people with asthma or other respiratory conditions. Activation of β1 receptors in the heart can increase heart rate and contractility, which can help to improve blood flow and oxygen delivery to the body's tissues. Activation of β3 receptors in adipose tissue can increase metabolism and help to promote weight loss. β-adrenergic receptors are important therapeutic targets for a variety of medical conditions, including heart disease, asthma, and diabetes. Drugs that target these receptors, such as beta blockers and beta agonists, are commonly used to treat these conditions.
Desmosomal cadherins are a type of cadherin protein that play a crucial role in the formation and maintenance of desmosomes, which are specialized cell-cell adhesion structures found in many tissues throughout the body. Desmosomes are particularly important in tissues that experience mechanical stress, such as the skin, heart, and muscles. Desmosomal cadherins are encoded by a family of genes that include desmogleins, desmocollins, and desmoplakin. These proteins form homotypic or heterotypic complexes at the cell surface, which link adjacent cells together and provide a strong, stable bond that is resistant to mechanical forces. Mutations in genes encoding desmosomal cadherins can lead to a group of inherited disorders known as desmosomal diseases, which are characterized by abnormal desmosome function and can result in a range of clinical manifestations, including skin fragility, cardiac arrhythmias, and neurological problems.
Mitochondrial diseases are a group of genetic disorders that affect the function of mitochondria, which are the energy-producing structures in cells. These diseases are caused by mutations in genes that are located in the mitochondria or in the nuclear genome and affect the function of mitochondria. Mitochondrial diseases can affect any organ in the body, but they are most commonly associated with muscle weakness, fatigue, and problems with energy production. Other symptoms may include hearing loss, vision problems, developmental delays, and neurological disorders. There are over 700 known mitochondrial diseases, and they can range from mild to severe. Some people with mitochondrial diseases may have only mild symptoms, while others may have life-threatening complications. Treatment for mitochondrial diseases depends on the specific type and severity of the disorder. In some cases, medications or dietary changes may be used to manage symptoms. In more severe cases, supportive care such as respiratory support or physical therapy may be necessary.
Enterovirus infections are a group of viral infections caused by enteroviruses, which are a type of RNA virus that primarily affect the gastrointestinal tract and nervous system. These viruses are highly contagious and can be transmitted through contact with contaminated surfaces, bodily fluids, or respiratory droplets. Enterovirus infections can cause a range of symptoms, depending on the specific virus and the severity of the infection. Common symptoms include fever, headache, nausea, vomiting, diarrhea, and rash. In some cases, enterovirus infections can lead to more serious complications, such as meningitis, encephalitis, and paralysis. There is no specific treatment for enterovirus infections, as the viruses cannot be killed by antibiotics. Treatment typically involves managing symptoms and providing supportive care, such as fluids and pain relief. In severe cases, hospitalization may be necessary. Prevention of enterovirus infections involves practicing good hygiene, such as washing hands frequently and avoiding contact with infected individuals or surfaces. Vaccines are not currently available for all types of enteroviruses, but some vaccines are in development.
Thallium radioisotopes are radioactive isotopes of the element thallium that are used in medical imaging procedures, particularly in nuclear medicine. Thallium-201 (Tl-201) is the most commonly used thallium radioisotope in medical imaging, and it is used primarily for myocardial perfusion imaging (MPI) to evaluate blood flow to the heart muscle. During an MPI procedure, a small amount of Tl-201 is injected into the patient's bloodstream, and a gamma camera is used to detect the gamma rays emitted by the Tl-201 as it is taken up by the heart muscle. The gamma camera creates images of the heart that can reveal areas of reduced blood flow, which may indicate the presence of coronary artery disease or other heart conditions. Thallium radioisotopes are also used in other medical imaging procedures, such as bone scans and brain scans, but Tl-201 is the most commonly used thallium radioisotope in nuclear medicine.
Genetic predisposition to disease refers to the tendency of an individual to develop a particular disease or condition due to their genetic makeup. It means that certain genes or combinations of genes increase the risk of developing a particular disease or condition. Genetic predisposition to disease is not the same as having the disease itself. It simply means that an individual has a higher likelihood of developing the disease compared to someone without the same genetic predisposition. Genetic predisposition to disease can be inherited from parents or can occur due to spontaneous mutations in genes. Some examples of genetic predisposition to disease include hereditary breast and ovarian cancer, Huntington's disease, cystic fibrosis, and sickle cell anemia. Understanding genetic predisposition to disease is important in medical practice because it can help identify individuals who are at high risk of developing a particular disease and allow for early intervention and prevention strategies to be implemented.
Adenine nucleotide translocator 1 (ANT1) is a protein that plays a role in the transport of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) across the inner mitochondrial membrane. It is a member of the ANT family of proteins, which are involved in the regulation of energy metabolism in cells. ANT1 is encoded by the ANTX1 gene and is found in many tissues throughout the body, including the heart, skeletal muscle, and brain. In the medical field, ANT1 is of interest because it has been implicated in a number of diseases, including heart failure, diabetes, and cancer.
Troponin C is a regulatory protein that plays a crucial role in the contraction of muscle fibers. It is a component of the troponin complex, which is responsible for regulating the interaction between actin and myosin filaments in muscle cells. In a resting muscle, troponin C blocks the binding of calcium ions to troponin I, which prevents the activation of the myosin heads and thus prevents muscle contraction. When a muscle is stimulated to contract, calcium ions are released from the sarcoplasmic reticulum and bind to troponin C, causing a conformational change in the troponin complex that exposes the binding sites on actin for myosin heads to attach and generate force. Troponin C is a sensitive marker of myocardial injury and is commonly used in clinical practice to diagnose and monitor patients with acute myocardial infarction (heart attack). Levels of troponin C in the blood can rise within hours of a heart attack and remain elevated for several days, making it a valuable tool for detecting and monitoring the progression of the disease.
Troponin is a protein that plays a crucial role in muscle contraction. It is found in cardiac and skeletal muscles and is released into the bloodstream when muscle cells are damaged or die. In the medical field, the measurement of troponin levels in the blood is commonly used as a diagnostic tool for myocardial infarction (heart attack) and other heart-related conditions. High levels of troponin in the blood are a strong indicator of heart muscle damage and can help doctors determine the severity of the condition and guide treatment decisions.
DNA, Mitochondrial refers to the genetic material found within the mitochondria, which are small organelles found in the cells of most eukaryotic organisms. Mitochondrial DNA (mtDNA) is a small circular molecule that is separate from the nuclear DNA found in the cell nucleus. Mitochondrial DNA is maternally inherited, meaning that a person inherits their mtDNA from their mother. Unlike nuclear DNA, which is diploid (contains two copies of each gene), mtDNA is haploid (contains only one copy of each gene). Mutations in mitochondrial DNA can lead to a variety of inherited disorders, including mitochondrial disorders, which are a group of conditions that affect the mitochondria and can cause a range of symptoms, including muscle weakness, fatigue, and neurological problems.
Congenital heart defects (CHDs) are structural abnormalities in the heart that are present at birth. These defects can affect the heart's structure, function, or both, and can range from minor to severe. CHDs are the most common type of birth defect and affect approximately 1 in 100 live births. CHDs can occur in any part of the heart, including the valves, arteries, veins, and chambers. Some common types of CHDs include: - Atrial septal defect (ASD): A hole in the wall between the two upper chambers of the heart. - Ventricular septal defect (VSD): A hole in the wall between the two lower chambers of the heart. - Patent ductus arteriosus (PDA): A blood vessel that remains open between the pulmonary artery and the aorta. - Coarctation of the aorta: A narrowing of the aorta, the main artery that carries blood from the heart to the rest of the body. - Tetralogy of Fallot: A combination of four heart defects that affect the flow of blood through the heart. CHDs can cause a range of symptoms, including shortness of breath, fatigue, chest pain, and heart palpitations. Treatment for CHDs depends on the type and severity of the defect, and may include medications, surgery, or other interventions. Early diagnosis and treatment are important for improving outcomes and reducing the risk of complications.
In the medical field, a cicatrix is a scar that forms after the healing of a wound or injury. It is typically a raised, thickened area of skin that is usually pale or lighter in color than the surrounding skin. Cicatrices can be caused by a variety of factors, including surgery, burns, acne, and skin infections. They can range in size and appearance, and may be permanent or fade over time. In some cases, cicatrices may cause discomfort or interfere with the function of the affected area. Treatment options for cicatrices may include topical creams, laser therapy, or surgical procedures.
Myocardial infarction (MI), also known as a heart attack, is a medical condition that occurs when blood flow to a part of the heart muscle is blocked, usually by a blood clot. This lack of blood flow can cause damage to the heart muscle, which can lead to serious complications and even death if not treated promptly. The most common cause of a heart attack is atherosclerosis, a condition in which plaque builds up in the arteries that supply blood to the heart. When a plaque ruptures or becomes unstable, it can form a blood clot that blocks the flow of blood to the heart muscle. Other causes of heart attacks include coronary artery spasms, blood clots that travel to the heart from other parts of the body, and certain medical conditions such as Kawasaki disease. Symptoms of a heart attack may include chest pain or discomfort, shortness of breath, nausea or vomiting, lightheadedness or dizziness, and pain or discomfort in the arms, back, neck, jaw, or stomach. If you suspect that you or someone else is having a heart attack, it is important to call emergency services immediately. Early treatment with medications and possibly surgery can help to reduce the risk of serious complications and improve the chances of a full recovery.
Autoantibodies are antibodies that are produced by the immune system against the body's own cells, tissues, or organs. In other words, they are antibodies that mistakenly target and attack the body's own components instead of foreign invaders like viruses or bacteria. Autoantibodies can be present in people with various medical conditions, including autoimmune diseases such as rheumatoid arthritis, lupus, and multiple sclerosis. They can also be found in people with certain infections, cancer, and other diseases. Autoantibodies can cause damage to the body's own cells, tissues, or organs, leading to inflammation, tissue destruction, and other symptoms. They can also interfere with the normal functioning of the body's systems, such as the nervous system, digestive system, and cardiovascular system. Diagnosis of autoantibodies is typically done through blood tests, which can detect the presence of specific autoantibodies in the blood. Treatment for autoimmune diseases that involve autoantibodies may include medications to suppress the immune system, such as corticosteroids or immunosuppressants, as well as other therapies to manage symptoms and prevent complications.
Calcium-binding proteins are a class of proteins that have a high affinity for calcium ions. They play important roles in a variety of cellular processes, including signal transduction, gene expression, and cell motility. Calcium-binding proteins are found in many different types of cells and tissues, and they can be classified into several different families based on their structure and function. Some examples of calcium-binding proteins include calmodulin, troponin, and parvalbumin. These proteins are often regulated by changes in intracellular calcium levels, and they play important roles in the regulation of many different physiological processes.
Chagas disease, also known as American trypanosomiasis, is a tropical parasitic disease caused by the protozoan parasite Trypanosoma cruzi. It is primarily transmitted to humans through the feces of infected triatomine bugs, also known as "kissing bugs," which bite humans while they sleep. Chagas disease can cause a range of symptoms, including fever, fatigue, swelling of the abdomen, and heart problems. In some cases, the disease can be asymptomatic for years or even decades, but it can eventually lead to serious complications such as heart failure, arrhythmias, and digestive problems. Chagas disease is most prevalent in Latin America, particularly in rural areas, but it can also occur in other parts of the world where the triatomine bugs are present. It is estimated that there are around 6-7 million people worldwide who are infected with T. cruzi, and around 30,000-40,000 new cases are diagnosed each year.
Dilated cardiomyopathy with ataxia syndrome
List of OMIM disorder codes
Dogue de Bordeaux
English Cocker Spaniel
Ayodele Olajide Falase
Myocardial infarction diagnosis
Dilated cardiomyopathy: MedlinePlus Medical Encyclopedia
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Idiopathic dilated cardiomyopathy3
- Dilated cardiomyopathy is a condition strongly related to heart attacks, in which the ventricles are enlarged, resulting in a thinning of cardiac walls, and insufficient pumping of blood. (cyberessays.com)
- Variations in the sequence of the cardiac troponin I (TNNI3) gene were examined in 235 patients with dilated cardiomyopathy. (dcmproject.com)
- Familial dilated cardiomyopathy is a primary myocardial disease that can lead to the development of congestive heart failure and sudden cardiac death. (slovgen.sk)
- Circulating cardiac MicroRNAs safeguard against dilated cardiomyopathy. (bvsalud.org)
- Variant Creutzfeldt-Jakob disease, caused by transmission of bovine spongiform encephalopathy to humans, may manifest with cardiac symptoms from prion-amyloid cardiomyopathy. (cdc.gov)
- Dilated cardiomyopathy is 1 of the 3 traditional classes of cardiomyopathy, along with hypertrophic and restrictive cardiomyopathy. (medscape.com)
- Hypertrophic cardiomyopathy is a hereditary condition where the heart fails to pump properly because the heart muscles (myocardium) have thickened (hypertrophied) and become stiff. (news-medical.net)
- Hypertrophic cardiomyopathy can affect people at any age and is equally common among men and women. (news-medical.net)
- Few people with hypertrophic cardiomyopathy develop symptoms and many find that their quality of life is not compromised. (news-medical.net)
- Hypertrophic cardiomyopathy is caused by one or more gene mutations within the proteins of heart muscle cells. (news-medical.net)
- The thickened ventricles may eventually obstruct blood flow from the heart and the disease is sometimes referred to as obstructive hypertrophic cardiomyopathy. (news-medical.net)
- This is sometimes referred to as non-obstructive hypertrophic cardiomyopathy. (news-medical.net)
- The condition is usually inherited and there is a 50% chance that each child born to a parent with hypertrophic cardiomyopathy will inherit the mutation for the disease. (news-medical.net)
- This complication affects only a small proportion of people with hypertrophic cardiomyopathy. (news-medical.net)
- Research is being conducted in many breeds, not only to look at the genetics of cardiomyopathy, but also the pathophysiology associated with the disease in each breed, and this has led to a number of different treatment recommendations that are specific to one or several individual breeds. (orivet.com)
- Most important are hypertension, stroke, cardiomyopathies and coronary heart disease. (who.int)
- A splice site mutation in a gene encoding for PDK4 a mitochondrial protein, is associated with the development of dilated cardiomyopathy in the Doberman pinscher. (orivet.com)
- Evidence for autosomal recessive inheritance of infantile dilated cardiomyopathy: studies from the Eastern Province of Saudi Arabia. (dcmproject.com)
- While a routine physical examination can suggest to your Phoenix vet that your pup may have an enlarged heart, a final diagnosis will require further testing to determine if the above symptoms are a result of dilated cardiomyopathy. (phoenixvrec.com)
- Therefore, the aim of this study was to test the diagnostic accuracy of ECVCCT in patients with a recent diagnosis of dilated cardiomyopathy, having ECVCMR as the reference technique. (cardiologicomonzino.it)
- Echocardiography was diagnostic of dilated cardiomyopathy. (who.int)
- Dilated cardiomyopathy is a progressive disease of heart muscle that is characterized by ventricular chamber enlargement and contractile dysfunction. (medscape.com)
- Characterized by ventricular dilatation, systolic dysfunction, and progressive heart failure, dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy in patients. (ca.gov)
- Dilated cardiomyopathy is myocardial dysfunction causing heart failure in which ventricular dilation and systolic dysfunction predominate. (msdmanuals.com)
- There has been a lot of buzz about the US Food and Drug Administration (FDA) statements alerting pet owners about a possible link between dilated cardiomyopathy (DCM), a type of heart disease, in dogs eating diets containing peas, lentils, potatoes and other legume seeds as main ingredients. (petcurean.com)
- An enlarged heart in dogs (or Dilated Cardiomyopathy) is a serious condition which describes the expansion of the lower chambers of the heart (ventricles) or, less commonly, its upper chamber (atria). (phoenixvrec.com)
- Symptoms of dilated cardiomyopathy in dogs can range from mild to severe as the condition progresses. (phoenixvrec.com)
- We sort through the confusion and share expert information about dilated cardiomyopathy in dogs. (myollie.com)
- What Is Dilated Cardiomyopathy in Dogs? (myollie.com)
- Dilated cardiomyopathy (DCM) is one of the more common acquired heart diseases in dogs. (vin.com)
- While accumulating clinical trials have focused on the impact of cell therapy in patients with acute myocardial infarction (MI) and ischemic cardiomyopathy, there are fewer efforts to examine cell-based therapy in patients with non-ischemic cardiomyopathy (NICM). (emmes.com)
- Treatment of dilated cardiomyopathy is essentially the same as treatment of chronic heart failure (CHF). (medscape.com)
- However, the classification of cardiomyopathies continues to evolve, based on the rapid evolution of molecular genetics as well as the introduction of recently described diseases. (medscape.com)
- The most important cardiovascular diseases (CVDs) in the African Region are those related to atherosclerosis, cardiomyopathies and rheumatic heart disease. (who.int)
- Breeds such as Doberman Pinschers and Great Danes do not have taurine-deficient cardiomyopathy. (vin.com)
- Cardiomyopathy is fairly common in the dog, with certain breeds showing a distinct disposition to develop the disease. (orivet.com)
- Cardiomyopathy is disease in which the heart muscle becomes weakened, stretched, or has another structural problem. (medlineplus.gov)
- We have been receiving questions lately regarding items in the news about certain hypoallergenic, novel protein dog foods and a form of heart disease called dilated cardiomyopathy (DCM). (hartfieldanimalhospital.com)
- There has recently been a fair bit of talk about the link between pet foods and dilated cardiomyopathy (DCM). (annarboranimalhospital.com)
- Some cats may develop taurine-deficient DCM, although this has become rare as taurine is now added to virtually all quality cat foods (see Feline Cardiomyopathy ). (vin.com)
- Boxers get a specific type of cardiomyopathy called arrhythmogenic right ventricular cardiomyopathy (ARVC). (vin.com)
- Clinical signs of cardiomyopathy are commonly seen around the ages of 3 - 6 years of age. (orivet.com)
- The high demand for the leading drugs for the treatment of dilated cardiomyopathy from developed regions such as Europe and North America is a reason for the large market shares of these classes of drugs. (cyberessays.com)
- Dilated cardiomyopathy is a condition in which the heart muscle becomes weakened and enlarged. (medlineplus.gov)
- Dilated cardiomyopathy (DCM) has become a household topic among dog owners in recent years as connections continue to emerge between this degenerative heart condition and nutrition. (myollie.com)
- Overview of Dilated Cardiomyopath. (msdmanuals.com)
- Dilated cardiomyopathy is the most common form, but it may be the result of different underlying conditions. (medlineplus.gov)
- There is no cure for cardiomyopathy, and medication is used to control signs and improve quality of life for as long as possible. (orivet.com)
- Because of this, it is very important to bring your four legged companion in for regular routine exams to provide as many opportunities as possible for your Phoenix vet to uncover early signs of dilated cardiomyopathy. (phoenixvrec.com)
- Dilated cardiomyopathy may be diagnosed on a routine screening test or as a result of a dog having exhibited illness signs. (myollie.com)
- One of the major reasons of dilated cardiomyopathy is genetic. (cyberessays.com)
- What are Dilated Cardiomyopathy risk factors? (myollie.com)
- Note the thickened, dilated left ventricle with subendocardial fibrosis manifested as increased whiteness of the endocardium. (cdc.gov)
- Occult cardiomyopathy can result in sudden death, due to a sudden onset of a fatal arrhythmia. (orivet.com)
- The dilated heart wall cannot contract hard enough to pump blood properly. (news-medical.net)