Names of diseases Chinese name: dilated cardiomyopathy Disease Introduction This type is characterized by left ventricular or biventricular or expanded calendar, accompanied by cardiac hypertrophy. Ventricular systolic dysfunction, with or without congestive heart failure. Ventricular or atrial arrhythmia common. Condition was progressively increased, can occur at any stage of the disease death. Symptom A detailed description of the symptoms All ages can be the disease, but mostly middle-aged. On_set_ and more slowly, the initial inspection found enlarged heart, heart decompensation without conscious discomfort. After a period of time symptoms appear gradually, over this period, sometimes up to 10 years. The main symptoms of congestive heart failure, with shortness of breath and swelling of the most common. Initially shortness of breath or tired after work, after mild activity or rest when there are shortness of breath, or paroxysmal nocturnal dyspnea. Because of low cardiac output, patients often feel weak. Examination see accelerated heart rate, lower left displaced apex beat, may have lifting of the pulse, the heart dullness extended to the left, you can often hear the third or fourth tone sound, rapid heart rate when gallop. Since the expansion of the heart chamber, may have relative systolic mitral or tricuspid insufficiency due to murmur, heart function after such improvements to reduce noise. Most normal blood pressure, lower blood pressure, but in advanced cases, a small pulse pressure, diastolic heart failure may be mildly elevated. Alternating pulse of left heart failure prompted. Pulse is often weak. Two veins at the base may have rales heart failure. Enlargement of the liver when right heart failure, lower limb edema appeared from the beginning, pleural effusion and ascites in patients with advanced uncommon. Various arrhythmias can occur, or key performance led to see, and a variety of arrhythmias in combination, constitute more complex rhythm that can occur repeatedly, sometimes very stubborn. Degree atrioventricular block, ventricular fibrillation, sinoatrial block or suspension may cause - Adams syndrome, became one cause of death. In addition, they can still have a brain, kidney, lung, etc. embolism. Etiology and pathogenesis So far the cause of the disease is unknown, the disease has been found with the following factors: 1 cause of infection in animal experiments Coxsackie virus, encephalomyocarditis virus not only can cause viral myocarditis, and can cause similar lesions dilated cardiomyopathy, acute viral myocarditis in patients on long-term clinical follow-up discoveries into dilated cardiomyopathy chances significantly greater than in the general population, the patients live specimen of myocardial inflammatory virus checking performance, many of the patients blood b Coxsackie virus neutralizing antibody titer higher than normal; using molecular biology techniques in recent years The patients with myocardial biopsy specimens were found to have intestinal virus or cytomegalovirus rna, above all illustrate the disease is closely related with viral myocarditis, an infection of the disease may persist. 2 gene and autoimmune disease and the findings related to histocompatibility antigens, compared to non-patients, the disease hlab27, hlaa2, hladr4, hladq4 you point increase, decrease hladrw6 sites, changes and hla autosomal recessive genetic, patients may explain part of this familial tendency. On the other hand, there can be changes in the immune response, increased susceptibility to viral infection, resulting in autoimmune heart myocardial injury. 3 cell-mediated immunity of the patients to reduce natural killer cell activity, weaken the body's defenses, inhibiting lymphocyte number and function of reducing t, thus cell-mediated immune response occurs, causing the blood vessels and myocardial injury. In summary see, now that the pathogenesis of this disease may be possible is to have a heart attack Coxsackie virus, proliferation and cause myocardial necrosis in the myocardium, the second phase of the virus can not be found in the heart, but there lymphocytosis, Such sensitized cells to cardiomyocytes, causing an immune response and cause myocardial necrosis, inflammatory cell infiltration in the late decreased or disappeared, becoming fibrosis, intertwined with myocardial hypertrophy or reduced form of dilated cardiomyopathy lesions. Virus infection, the immune response is the main doctrine, although the incidence say, but many did not understand the question, pending further study. Pathological changes Increased heart weight, about twice the normal. Expansion of the heart chamber, myocardial gray and relaxation. Although ventricular wall myocardial hypertrophy, but the expansion chamber and wall thickness remains near normal. Endocardial also be thickened. Heart chamber enclosing wall thrombosis uncommon. Myocardial fibrosis common, patchy wall at the inner edge, but also satisfying wall into a piece of damaged cardiac conduction system can pacing violations. Microscopic examination of heart disease, the lack of specificity of the discovery. You can see the myocardial fiber hypertrophy, nuclear condensation, deformation or disappeared, the formation of vacuoles in the cytoplasm. Fibrous tissue increased, due to an increase in collagen or between organizations, or because of focal myocardial fibers are replaced by fibrous tissue. Myocardial fibers can be divided cord-like fibrous tissue. Endocardial collagen and elastic fibers is also increased. Varying degrees of degeneration can be seen, the majority of myocardial cell lysis, especially prevalent in cases of long duration. Electron microscope examination showed myocardial mitochondrial swelling, cristae or disappeared; muscle serous space to expand, there is a fibrous material and granular lipofuscin; myofibrils can disappear. Cardiomyopathy the heart contractility. Slowed early left ventricular systolic left ventricular pressure and other content rate of increase, spurting speed slows down. At this time of accelerated heart rate, stroke volume decrease compensatory, cardiac output can still be maintained. After emptying the left ventricle endless, residual blood, diastolic pressure, the gradual development of left ventricular failure. Lasting left atrium, pulmonary artery pressures have increased, and finally right heart failure. A few cases of right ventricular lesions mainly the development of right heart failure. Ventricular dilation causes atrioventricular valve ring to expand, resulting in mitral or tricuspid regurgitation. Cardiac chamber dilatation, increased tension in the ventricular wall, increased oxygen consumption, cardiac hypertrophy, heart rate caused by the relative myocardial ischemia, and myocardial oxygen uptake capacity has reached the limit, which can cause angina. Pacing and cardiac conduction system disease involved can cause a variety of arrhythmias. Diagnosis 1980 World Health Organization indicate that the disease is unexplained left ventricular or bi-ventricular enlargement, ventricular systolic dysfunction, with or without congestive heart failure and arrhythmias, shall exclude the diagnosis of the disease can only be made after other causes. 1995 Symposium on Cardiovascular Diseases Society of Chinese organizations, proposed diagnostic reference standard of the disease are as follows: 1 Clinical manifestations of cardiac enlargement, reduce ventricular systolic function with or without congestive heart failure, arrhythmias often can be complications such as thrombosis and sudden death. 2 enlarged heart x-ray cardiothoracic ratio> 0.5, Echocardiography fully expanded, especially in the left ventricle was significantly enlarged, left ventricular end-diastolic internal diameter ≥ 2.7cm/m2, the heart can be presented ball. 3 ventricular systolic function by echocardiography reduce diffuse weakened wall motion detection, ejection fraction less than normal. 4 must rule out other specific (secondary) cardiomyopathy and endemic cardiomyopathy (Keshan disease), including ischemic heart disease, peripartum cardiomyopathy, alcoholic cardiomyopathy, metabolic and endocrine diseases such as hyperthyroidism, hypothyroidism, amyloidosis, diabetes-induced cardiomyopathy, genetic neuromuscular disorder caused by familial cardiomyopathy, systemic diseases such as systemic lupus erythematosus, rheumatoid arthritis, etc. due before the diagnosis of cardiac disease, toxic cardiomyopathy idiopathic dilated cardiomyopathy. Conditions can detect serum anti-peptide antibodies such as anti-myocardial myocardial mitochondrial adp / atp carrier antibody, anti-myosin antibody, anti-β1-receptor antibodies, anti-m2 cholinergic receptor antibodies, as auxiliary of the disease diagnosis. Identification of clinically difficult and coronary heart disease as those who need coronary angiography. Endomyocardial biopsy: pathological diagnosis of the disease non-specific, but contribute to the differential diagnosis and specific cardiomyopathy and acute myocarditis. Endomyocardial biopsies heart polymerase chain reaction (pcr) or in situ hybridization, diagnosis of the cause of infection to help; specific cells or abnormal gene analysis. (A) rheumatic heart disease cardiomyopathy, mitral or tricuspid area also has a systolic murmur, but generally not associated with diastolic murmur, and louder when heart failure, after failure to control reduce or disappear, rheumatic heart disease is to the contrary. How often cardiomyopathy heart chamber while expanding, as rheumatic heart disease in the left atrium, left or right ventricular-based. Ultrasound helps distinguish. (B) pericardial effusion cardiomyopathy enlarged heart, heart weakened, and pericardial effusion required difference. When cardiomyopathy displaced apex beat to the left, in line with the outer edge of the left heart dullness, pericardial effusion apex beat is often not obvious or inside the outer edge of the left heart dullness. Mitral or tricuspid systolic murmur, ventricular hypertrophy on electrocardiogram, abnormal q waves, a variety of complex arrhythmias, cardiomyopathy both directions. Ultrasound is not difficult to distinguish between the two, a lot of the pericardial fluid level segment or dark areas described pericardial effusion, cardiac enlargement, compared with cardiomyopathy. There must also be noted that when a small amount of pericardial effusion, cardiac disease, but only enough to cause cardiac tamponade, signs still will not affect the heart and heart function, only the ultrasound findings. Systolic time when obvious abnormalities cardiomyopathy, pericardial disease is normal. (C) hypertensive heart disease cardiomyopathy may have a temporary high blood pressure, diastolic blood pressure, but no more than 14.67kpa (110mmhg), and appeared in acute heart failure, after failure to improve blood pressure. Hypertensive heart disease is different eyes, urine, kidney function was normal. (Four) than middle-aged patients with coronary heart disease, if enlarged heart, heart failure, arrhythmias, or other causes must be considered without coronary heart disease and cardiomyopathy. There are risk factors for high blood pressure, high cholesterol or diabetes, segmental wall motion abnormalities were conducive to the diagnosis of coronary heart disease. In recent years, a wide range of long coronary lesions caused by ischemia and cardiac fibrosis, cardiac dysfunction in the development of the situation as "ischemic heart disease", if the past is no angina or myocardial infarction, and cardiomyopathy quite difficult to distinguish, Furthermore cardiomyopathy may spread angina pathologic q, then the identification required by coronary angiography. (E) the majority of congenital heart disease has obvious signs, difficult to distinguish. Ebstein malformation murmur tricuspid area, and may have gallop, heart weakened and enlarged right heart failure, cardiomyopathy, the difference shall be, but the disease symptoms in the early years, not the left ventricle, compared with cyanosis forward. Echocardiography can confirm the diagnosis. (F) secondary to cardiomyopathy systemic diseases such as performance has its primary disease systemic lupus erythematosus, scleroderma, hemochromatosis, amyloidosis, glycogen storage disease, neuromuscular diseases can be funded difference. More important is to distinguish and myocarditis. Acute myocarditis, viral infection often occurs in the time or shortly after, the difference is not very difficult. Chronic myocarditis Without a clear history of acute myocarditis and cardiomyopathy is difficult to distinguish, in fact, a lot of dilated cardiomyopathy is evolved from myocarditis, the so-called "post-myocarditis cardiomyopathy." In recent years, carried out in clinical endomyocardial biopsy forceps biopsies obtained from the heart with a catheter specimens for pathological examination with a virus, you can find any evidence of myocardial inflammation, but the diagnostic criteria for pathological and histological removal of artifacts and some aspects of the problem to be solved. x-ray examination showed enlarged heart shadow, the late appearance such as spherical, indicating that the heart chamber were increased, the shape resembling pericardial effusion. Small number of patients with left ventricle, left atrium or right ventricle mainly looks like mitral valve disease. Fluoroscopy see weaker than normal heart beat. Aortic generally do not expand. Patients often have larger duration and pulmonary edema pulmonary congestion, lungs costophrenic corner may have spaced lines, pulmonary vein and pulmonary artery shadow can be expanded; pleural effusion uncommon. ECG in patients with symptomatic almost not normal, asymptomatic ECG changes have been many changes in cardiac hypertrophy, myocardial damage and arrhythmias based. Left ventricular hypertrophy is more common, often associated with myocardial strain, often late right ventricular hypertrophy; may also have left or right atrial hypertrophy. Myocardial damage common to st segment depression, t-wave flat or biphasic or inverted as the main performance, sometimes t wave was ischemic change. A few patients pathologic q waves, like myocardial infarction, more than the front part of the interval (v1, v2 lead), the interval may result in fibrosis. Common intraventricular conduction block, left, right bundle branch or branches of left bundle branch block can occur. Arrhythmia common, however, especially late in ectopic rhythm and conduction block based. Ectopic rhythm can be derived from the atrium, atrioventricular junction, or ventricles, the premature evolved into tachycardia, as well as flutter or fibrillation, may also have sinus disease, atrioventricular junction escape or escape the law, or ventricular arrhythmia itself and so on. One to three degree atrioventricular block can occur. Echocardiography can be seen early in the disease mildly enlarged heart chambers, particularly the left ventricle wall motion weakened, late of the heart chamber are expanding, septal and left ventricular posterior wall movement is weakened. Anterior mitral 叶双峰 may disappear after leaves are different to the activities. Number ratio of left ventricular spurting often reduced to 50% or less, also reduces the number of myocardial shortening ratio. There may be a small amount of pericardial effusion. Radionuclide ventriculography can also be displayed enlarged heart chamber wall motion and decreased left ventricular ejection fraction decreased more significantly after exercise. Early systolic time period can not normal left ventricular spurting time (lvet) shortened spurting early (pep) extend, pep / lvet increases. Early check near normal cardiac catheterization, left ventricular end-diastolic pressure may be slightly higher. When heart failure is reduced cardiac index, arteriovenous oxygen difference is large, pulmonary and atrial pressure increased. Cardiovascular angiography showed enlarged heart chambers, wall motion weakened. Treatment Because of unknown etiology, prevention more difficult. Note that the change in the viral infection and early treatment of heart, there are practical significance. The main treatment for clinical manifestations 1 rest and avoid fatigue must be very stressed, if enlarged heart, heart dysfunction should be noted, should be long-term rest, to prevent disease progression. 2 heart failure and general failure by the same principles of treatment, the use of cardiac drugs, diuretics and vasodilators, due to myocardial damage is more extensive and detailed to yellow class, diuretics beneficial at low glomerular filtration, hydrochlorothiazide may failure, this time, required loop diuretics, such as: furosemide. Vasodilators, such as: angiotensin-converting enzyme inhibitors are also useful to start with small doses when required, taking care to avoid hypotension. In recent years with the discovery of the disease when there is failure β-blockers effective mechanism may be chronic heart failure adrenergic nerve hyperexcitability, β receptor density reduction in the extent of the disease in more than myocardial infarction, β receptor density down, after the extent of the disease in more than myocardial infarction, with the β-adrenergic receptor blockers nerve hyperexcitability harmful effects are removed, myocardial β receptor density increases, better known β1 , starting with a small agent, and then slowly increase the dose, can prolong the life of such treatment. 3 arrhythmia, especially in the symptoms required antiarrhythmic drug therapy or electrical methods for rapid ventricular arrhythmia with a high degree atrioventricular block and there is the risk of sudden death by treatment should be positive. 4 can be used for the prevention of thromboembolic complications in oral anticoagulant or antiplatelet drugs. 5. Improve myocardial metabolism of drugs such as vitamin c, adenosine triphosphate, coenzyme a, cyclic adenosine monophosphate, coenzyme q10, etc. can be used as adjuvant therapy. 6 long-term heart failure, medical therapy should be considered for a heart transplant, after active infection control, improve immune suppression, correct rejection, 1-year survival rate of up to 85% after. Prognosis This type of course of varying lengths, the shorter one year after the on_set_ of death, the elderly can survive for more than 20 years. Where a significant enlargement of the heart, heart failure or arrhythmias stubborn persistence of poor prognosis. Many patients may have sudden death. Prevention of common sense: For the diagnosis of dilated cardiomyopathy patients should maintain good mood, avoid fatigue, nutritional supplement, attention to the prevention of respiratory tract infection, abstain from alcohol, regularly to the hospital, to protect or improve heart function and improve quality of life. Such as palpitation, shortness of breath, chest discomfort, fatigue and other symptoms, should go to the hospital. Female patients should not become pregnant. Heart failure occurs when the function, should be a longer time to rest, low-salt diet. Such as severe breathing difficulties, when supine increased sweating, possibly severe heart failure, the patient should be sitting or semi-lying position, to call for help or emergency medical center in the most secure, stable, fast traffic Tools taken to a nearby hospital.
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Names of diseases
Chinese name: dilated cardiomyopathy Pinyin: kuò zhāng xíng xīn jī bìng English: Dilated Cardiomyopathy Abbreviation: DCM Treatment department: Department of Cardiology
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Disease Introduction
This type is characterized by the left or right ventricle or bilateral ventricular enlargement, accompanied by cardiac hypertrophy. Ventricular systolic dysfunction, with or without congestive heart failure. Ventricular or atrial arrhythmia common. Condition was progressively increased, can occur at any stage of the disease death.
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Etiology
So far the cause of the disease is unknown, the disease has been found with the following factors: 1 cause of infection in animal experiments Coxsackie virus, encephalomyocarditis virus not only can cause viral myocarditis, and can cause similar lesions dilated cardiomyopathy, acute viral myocarditis in patients on long-term clinical follow-up discoveries into dilated cardiomyopathy chances significantly greater than in the general population, the patients live specimen of myocardial inflammatory virus checking performance, many of the patients blood Coxsackie B virus neutralizing antibody titer higher than normal; using molecular biology techniques in recent years The patients with myocardial biopsy specimens were found to have enterovirus RNA or CMV, above all indicating that the disease is closely related with viral myocarditis, an infection of the disease may persist. 2 gene and autoimmune disease and the findings related to histocompatibility antigens, compared to non-patients, the disease HLAB27, HLAA2, HLADR4, HLADQ4 you point increase, decrease HLADRw6 sites, changes with the HLA autosomal recessive genetic, patients may explain part of this familial tendency. On the other hand, there can be changes in the immune response, increased susceptibility to viral infection, resulting in autoimmune heart myocardial injury. 3 cell-mediated immunity in the patients reduce the activity of natural killer cells, weakening the body's defenses, suppressor T lymphocyte function to reduce the number and thus cell-mediated immune response occurs, causing the blood vessels and myocardial injury. In summary see, now that the pathogenesis of this disease may be possible is to have a heart attack Coxsackie virus, proliferation and cause myocardial necrosis in the myocardium, the second phase of the virus can not be found in the heart, but there lymphocytosis, Such sensitized cells to cardiomyocytes, causing an immune response and cause myocardial necrosis, inflammatory cell infiltration in the late decreased or disappeared, becoming fibrosis, intertwined with myocardial hypertrophy or reduced form of dilated cardiomyopathy lesions. Virus infection, the immune response is the main doctrine, although the incidence say, but many did not understand the question, pending further study.
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Pathological changes
Increased heart weight, about twice the normal. Expansion of the heart chamber, myocardial gray and relaxation. Although ventricular wall myocardial hypertrophy, but the expansion chamber and wall thickness remains near normal. Endocardial also be thickened. Heart chamber enclosing wall thrombosis uncommon. Myocardial fibrosis common, patchy wall at the inner edge, but also satisfying wall into a piece of damaged cardiac conduction system can pacing violations. Microscopic examination of heart disease, the lack of specificity of the discovery. You can see the myocardial fiber hypertrophy, nuclear condensation, deformation or disappeared, the formation of vacuoles in the cytoplasm. Fibrous tissue increased, due to an increase in collagen or between organizations, or because of focal myocardial fibers are replaced by fibrous tissue. Myocardial fibers can be divided cord-like fibrous tissue. Endocardial collagen and elastic fibers is also increased. Varying degrees of degeneration can be seen, the majority of myocardial cell lysis, especially prevalent in cases of long duration. Electron microscope examination showed myocardial mitochondrial swelling, cristae or disappeared; muscle serous space to expand, there is a fibrous material and granular lipofuscin; myofibrils can disappear. Cardiomyopathy the heart contractility. Slowed early left ventricular systolic left ventricular pressure and other content rate of increase, spurting speed slows down. At this time of accelerated heart rate, stroke volume decrease compensatory, cardiac output can still be maintained. After emptying the left ventricle endless, residual blood, diastolic pressure, the gradual development of left ventricular failure. Lasting left atrium, pulmonary artery pressures have increased, and finally right heart failure. A few cases of right ventricular lesions mainly the development of right heart failure. Ventricular dilation causes atrioventricular valve ring to expand, resulting in mitral or tricuspid regurgitation. Cardiac chamber dilatation, increased tension in the ventricular wall, increased oxygen consumption, cardiac hypertrophy, heart rate caused by the relative myocardial ischemia, and myocardial oxygen uptake capacity has reached the limit, which can cause angina. Pacing and cardiac conduction system disease involved can cause a variety of arrhythmias.
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Clinical manifestations
All ages can be the disease, but mostly middle-aged. On_set_ and more slowly, the initial inspection found enlarged heart, heart decompensation without conscious discomfort. After a period of time symptoms appear gradually, over this period, sometimes up to 10 years. The main symptoms of congestive heart failure, with shortness of breath and swelling of the most common. Initially shortness of breath or tired after work, after mild activity or rest when there are shortness of breath, or paroxysmal nocturnal dyspnea. Because of low cardiac output, patients often feel weak. Examination see accelerated heart rate, lower left displaced apex beat, may have lifting of the pulse, the heart dullness extended to the left, you can often hear the third or fourth tone sound, rapid heart rate when gallop. Since the expansion of the heart chamber, may have relative systolic mitral or tricuspid insufficiency due to murmur, heart function after such improvements to reduce noise. Most normal blood pressure, lower blood pressure, but in advanced cases, a small pulse pressure, diastolic heart failure may be mildly elevated. Alternating pulse of left heart failure prompted. Pulse is often weak. Two veins at the base may have rales heart failure. Enlargement of the liver when right heart failure, lower limb edema appeared from the beginning, pleural effusion and ascites in patients with advanced uncommon. Various arrhythmias can occur, or key performance led to see, and a variety of arrhythmias in combination, constitute more complex rhythm that can occur repeatedly, sometimes very stubborn. Degree atrioventricular block, ventricular fibrillation, sinoatrial block or suspension may cause - Adams syndrome, became one cause of death. In addition, they can still have a brain, kidney, lung, etc. embolism.
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Disease diagnosis
1980 World Health Organization indicate that the disease is unexplained left ventricular or bi-ventricular enlargement, ventricular systolic dysfunction, with or without congestive heart failure and arrhythmias, shall exclude the diagnosis of the disease can only be made after other causes. 1995 Symposium on Cardiovascular Diseases Society of Chinese organizations, proposed diagnostic reference standard of the disease are as follows: 1 Clinical manifestations of cardiac enlargement, reduce ventricular systolic function with or without congestive heart failure, arrhythmias often can be complications such as thrombosis and sudden death. 2 enlarged heart X-ray examination cardiothoracic ratio> 0.5, Echocardiography fully expanded, especially in the left ventricle was significantly enlarged, left ventricular end-diastolic internal diameter ≥ 2.7cm/m2, the heart can be presented ball. 3 ventricular systolic function by echocardiography reduce diffuse weakened wall motion detection, ejection fraction less than normal. 4 must rule out other specific (secondary) cardiomyopathy and endemic cardiomyopathy (Keshan disease), including ischemic heart disease, peripartum cardiomyopathy, alcoholic cardiomyopathy, metabolic and endocrine diseases such as hyperthyroidism, hypothyroidism, amyloidosis, diabetes-induced cardiomyopathy, genetic neuromuscular disorder caused by familial cardiomyopathy, systemic diseases such as systemic lupus erythematosus, rheumatoid arthritis, etc. due before the diagnosis of cardiac disease, toxic cardiomyopathy idiopathic dilated cardiomyopathy. Conditions can detect serum anti-peptide antibodies such as anti-myocardial myocardial mitochondrial ADP / ATP carrier antibody, anti-myosin antibody, anti-β1-receptor antibodies, anti-M2 cholinergic receptor antibodies, as auxiliary of the disease diagnosis. Identification of clinically difficult and coronary heart disease as those who need coronary angiography. Endomyocardial biopsy: pathological diagnosis of the disease non-specific, but contribute to the differential diagnosis and specific cardiomyopathy and acute myocarditis. Endomyocardial biopsies heart polymerase chain reaction (PCR) or in situ hybridization, diagnosis of the cause of infection to help; specific cells or abnormal gene analysis. (A) rheumatic heart disease cardiomyopathy, mitral or tricuspid area also has a systolic murmur, but generally not associated with diastolic murmur, and louder when heart failure, after failure to control reduce or disappear, rheumatic heart disease is to the contrary. How often cardiomyopathy heart chamber while expanding, as rheumatic heart disease in the left atrium, left or right ventricular-based. Ultrasound helps distinguish. (B) pericardial effusion cardiomyopathy enlarged heart, heart weakened, and pericardial effusion required difference. When cardiomyopathy displaced apex beat to the left, in line with the outer edge of the left heart dullness, pericardial effusion apex beat is often not obvious or inside the outer edge of the left heart dullness. Mitral or tricuspid systolic murmur, ventricular hypertrophy on electrocardiogram, abnormal Q waves, a variety of complex arrhythmias, cardiomyopathy both directions. Ultrasound is not difficult to distinguish between the two, a lot of the pericardial fluid level segment or dark areas described pericardial effusion, cardiac enlargement, compared with cardiomyopathy. There must also be noted that when a small amount of pericardial effusion, cardiac disease, but only enough to cause cardiac tamponade, signs still will not affect the heart and heart function, only the ultrasound findings. Systolic time when obvious abnormalities cardiomyopathy, pericardial disease is normal. (C) hypertensive heart disease cardiomyopathy may have a temporary high blood pressure, diastolic blood pressure, but no more than 14.67kPa (110mmHg), and appeared in acute heart failure, after failure to improve blood pressure. Hypertensive heart disease is different eyes, urine, kidney function was normal. (Four) than middle-aged patients with coronary heart disease, if enlarged heart, heart failure, arrhythmias, or other causes must be considered without coronary heart disease and cardiomyopathy. There are risk factors for high blood pressure, high cholesterol or diabetes, segmental wall motion abnormalities were conducive to the diagnosis of coronary heart disease. In recent years, a wide range of long coronary lesions caused by ischemia and cardiac fibrosis, cardiac dysfunction in the development of the situation as "ischemic heart disease", if the past is no angina or myocardial infarction, and cardiomyopathy quite difficult to distinguish, Furthermore cardiomyopathy also pathologic Q wave and angina, when identification is required by coronary angiography. (E) the majority of congenital heart disease has obvious signs, difficult to distinguish. Ebstein malformation murmur tricuspid area, and may have gallop, heart weakened and enlarged right heart failure, cardiomyopathy, the difference shall be, but the disease symptoms in the early years, not the left ventricle, compared with cyanosis forward. Echocardiography can confirm the diagnosis. (F) secondary to cardiomyopathy systemic diseases such as performance has its primary disease systemic lupus erythematosus, scleroderma, hemochromatosis, amyloidosis, glycogen storage disease, neuromuscular diseases can be funded difference. More important is to distinguish and myocarditis. Acute myocarditis, viral infection often occurs in the time or shortly after, the difference is not very difficult. Chronic myocarditis Without a clear history of acute myocarditis and cardiomyopathy is difficult to distinguish, in fact, a lot of dilated cardiomyopathy is evolved from myocarditis, the so-called "post-myocarditis cardiomyopathy." In recent years, carried out in clinical endomyocardial biopsy forceps biopsies obtained from the heart with a catheter specimens for pathological examination with a virus, you can find any evidence of myocardial inflammation, but the diagnostic criteria for pathological and histological removal of artifacts and some aspects of the problem to be solved. X-ray examination showed enlarged heart shadow, the late appearance such as spherical, indicating that the heart chamber were increased, the shape resembling pericardial effusion. Small number of patients with left ventricle, left atrium or right ventricle mainly looks like mitral valve disease. Fluoroscopy see weaker than normal heart beat. Aortic generally do not expand. Patients often have larger duration and pulmonary edema pulmonary congestion, lungs costophrenic corner may have spaced lines, pulmonary vein and pulmonary artery shadow can be expanded; pleural effusion uncommon. ECG in patients with symptomatic almost not normal, asymptomatic ECG changes have been many changes in cardiac hypertrophy, myocardial damage and arrhythmias based. Left ventricular hypertrophy is more common, often associated with myocardial strain, often late right ventricular hypertrophy; may also have left or right atrial hypertrophy. Myocardial damage common to ST-segment depression, T wave flat or biphasic or inverted as the main performance, and sometimes showed ischemic changes in T wave. A few patients pathologic Q waves, like myocardial infarction, more than the front part of the space (V1, V2 lead), fibrosis may result interval. Common intraventricular conduction block, left, right bundle branch or branches of left bundle branch block can occur. Arrhythmia common, however, especially late in ectopic rhythm and conduction block based. Ectopic rhythm can be derived from the atrium, atrioventricular junction, or ventricles, the premature evolved into tachycardia, as well as flutter or fibrillation, may also have sinus disease, atrioventricular junction escape or escape the law, or ventricular arrhythmia itself and so on. One to three degree atrioventricular block can occur. Echocardiography can be seen early in the disease mildly enlarged heart chambers, particularly the left ventricle wall motion weakened, late of the heart chamber are expanding, septal and left ventricular posterior wall movement is weakened. Anterior mitral 叶双峰 may disappear after leaves are different to the activities. Number ratio of left ventricular spurting often reduced to 50% or less, also reduces the number of myocardial shortening ratio. There may be a small amount of pericardial effusion. Radionuclide ventriculography can also be displayed enlarged heart chamber wall motion and decreased left ventricular ejection fraction decreased more significantly after exercise. Early systolic time period can not normal left ventricular spurting time (LVET) shortens, spurting early (PEP) to extend, PEP / LVET increases. Early check near normal cardiac catheterization, left ventricular end-diastolic pressure may be slightly higher. When heart failure is reduced cardiac index, arteriovenous oxygen difference is large, pulmonary and atrial pressure increased. Cardiovascular angiography showed enlarged heart chambers, wall motion weakened.
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Treatment
Treatment principles: 1, the general treatment: rest, use of sedatives, heart failure low-salt diet, if necessary; 2, prevention and treatment of arrhythmias and heart failure; 3, there is a history of thrombosis for anticoagulant therapy; 4, how the amount of pleural effusion, pleural puncture fluid for; 5, may be considered in patients with severe heart surgery or artificial heart transplant, you can line CRT therapy; 6, symptomatic and supportive treatment. Because of unknown etiology, prevention more difficult. Note that the change in the viral infection and early treatment of heart, there are practical significance. The main treatment for clinical manifestations 1 rest and avoid fatigue must be very stressed, if enlarged heart, heart dysfunction should be noted, should be long-term rest, to prevent disease progression. 2 heart failure and general failure by the same principles of treatment, the use of cardiac drugs, diuretics and vasodilators, due to myocardial damage is more extensive and detailed to yellow class, diuretics beneficial at low glomerular filtration, hydrochlorothiazide may failure, this time, required loop diuretics, such as: furosemide. Vasodilators, such as: angiotensin-converting enzyme inhibitors are also useful to start with small doses when required, taking care to avoid hypotension. In recent years with the discovery of the disease when there is failure β-blockers effective mechanism may be chronic heart failure adrenergic nerve hyperexcitability, β receptor density reduction in the extent of the disease in more than myocardial infarction, β receptor density down, after the extent of the disease in more than myocardial infarction, with the β-adrenergic receptor blockers nerve hyperexcitability harmful effects are removed, myocardial β receptor density increases, better known β1 , starting with a small agent, and then slowly increase the dose, can prolong the life of such treatment. 3 arrhythmia, especially in the symptoms required antiarrhythmic drug therapy or electrical methods for rapid ventricular arrhythmia with a high degree atrioventricular block and there is the risk of sudden death by treatment should be positive. 4 can be used for the prevention of thromboembolic complications in oral anticoagulant or antiplatelet drugs. 5. Improve myocardial metabolism of drugs such as vitamin C, adenosine triphosphate, coenzyme A, cyclic adenosine monophosphate, coenzyme Q10, etc. can be used as adjuvant therapy. 6 long-term heart failure, medical therapy should be considered for a heart transplant, after active infection control, improve immune suppression, correct rejection, 1-year survival rate of up to 85% after. Medication principles: 1, cardiomyopathy digitalis drugs sensitive to small dose should be applied, and pay attention to toxicity, or use of non-cardiac glycoside inotropic drugs; 2, diuretics should be noted that during the electrolyte balance; 3, there are drugs that inhibit heart rate or electrical cardioversion tachyarrhythmia when, at the same time should be alert to the presence of sick sinus syndrome may be; 4, for patients with chronic complete atrioventricular block, sick sinus syndrome can install a permanent artificial heart pacemaker; 5, during the application of anti-arrhythmic drugs, should be regularly reviewed electrocardiogram; 6, there is the use of anticoagulants during hemorrhage should be noted, periodic review of the clotting time, prothrombin time. Features therapy Treating patients with dilated cardiomyopathy from "toxic" Dilated cardiomyopathy is a worldwide difficult cases, the cause is unknown because there is no effective therapy. Although Western medicine for the treatment of heart failure has made considerable progress, but because of the limitations of the drug and its side effects, and dilated cardiomyopathy own complexity, symptoms of the disease after five years survival rate is only 40 percent, 10-year survival rate is only about 22%. To find an ideal method of treatment, Shijiazhuang Great Wall Hospital Integrative Medicine Research Group of Experts cardiomyopathy Division of academic leaders, graduated from the China Academy of Traditional Chinese Medicine graduate, under the leadership of Wang Renping chief physician, based on years of clinical experience in affirmed an effective role in Western medicine treatment of the disease, while re-examine and study the pathogenesis of the disease medicine, considered the heart qi, cult poison is a major violation of the pathogenesis of cardiac disease. Accordingly they creatively put forward the "righteous immunity doctrine," a mere change in the past with traditional Chinese medicine with western medicine and pure qi, blood, and water treatment programs, created a "Yiqitiaoxue free, detoxification Ning heart", "From poison theory cure "treatment rules, and _select_ion of relevant TCD, concentrated fry series herbs. Heart transplantation in the treatment of dilated cardiomyopathy Dilated cardiomyopathy patients often younger, in the absence of other diseases, heart transplantation prolong life, since cyclosporine (Cyclsporin) applied to the anti-rejection after heart transplantation, the prognosis is greatly improved. Operative mortality of 10% -25%. Successful transplant, 1, 3 and 5 year survival rate was 80%, 60% -70% and 52%. Inclusion criteria heart transplant Heart Center, University of Minnesota include: (1) LVEF <35%; (2) active medical therapy; (3) persistent symptoms, medical treatment can not be tolerated; (4) non-reversible disease factors, such as myocardial ischemia or mitral regurgitation, etc.; (5) Estimated 1-year survival rate <50%. In the post-transplant care in total found electrocardiogram QRS voltage (Ⅰ - Ⅲ, V1, V6 of QRS voltage algebra and) reducing more than 20%, or appear atrial / ventricular arrhythmias, or heart failure, elevated serum LDH , which should be endocardial biopsy after 4-6 weeks in a weekly routine. According to histopathological features of three: Ⅰ grade (mild): endocardial and interstitial edema with peripheral vascular mild lymphocytic infiltration. Ⅱ (moderate): more obvious inflammatory cell infiltration, myocardial degeneration seen cytolysis. Ⅲ grade (severe): A large number of lymphocytes and addicted pyronine polymorphonuclear leukocyte infiltration, interstitial hemorrhage visible. Myocardial biopsy confirmed the presence of post-transplant rejection, can be used cyclosporine, prednisone and azathioprine and other immunosuppressive therapy line.
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Prognostic measures
This type of course of varying lengths, the shorter one year after the on_set_ of death, the elderly can survive for more than 20 years. Where a significant enlargement of the heart, heart failure or arrhythmias stubborn persistence of poor prognosis. Many patients may have sudden death.
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Prevention of common sense
For the diagnosis of dilated cardiomyopathy patients should maintain good mood, avoid fatigue, nutritional supplement, attention to the prevention of respiratory tract infection, abstain from alcohol, regularly to the hospital, to protect or improve heart function and improve quality of life. Such as palpitation, shortness of breath, chest discomfort, fatigue and other symptoms, should go to the hospital. Female patients should not become pregnant. Heart failure occurs when the function, should be a longer time to rest, low-salt diet. Such as severe breathing difficulties, when supine increased sweating, possibly severe heart failure, the patient should be sitting or semi-lying position, to call for help or emergency medical center in the most secure, stable, fast traffic Tools taken to a nearby hospital. Upper respiratory tract infections are the most common cause of dilated cardiomyopathy induced exacerbations, thus preventing the flu is particularly important especially cold. Lianriyinyu, somatosensory clammy, but also need timely weatherization. Usually have to do any work, adequate rest can reduce the burden on the heart, promote myocardial recovery. Long-term alcohol drinkers are required, such as recovery after treatment and then drinking, relapse after treatment is more difficult. When congestive heart failure, in addition to reasonable restrictions activities, but also severely restricted sodium intake. Standard low-salt diet is to control the amount of salt in the daily five grams or less, serious illness control in one gram a day or less. The disease of unknown cause, including effective control of the activities of heart failure and arrhythmias, remission (no active shortness of breath) in order to improve the patient's quality of life and survival-oriented, can be wing Pill, musele binding β-affected blockers, ACEI or ARB and myocardial nutritional medicine for treatment.
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Disease Encyclopedia
Disease name: dilated cardiomyopathy English name: Drug therapy: rest; avoid fatigue; cardiac drugs; diuretics; vasodilators; antiarrhythmic drugs; anticoagulants; antiplatelet drugs; improve myocardial metabolism; vitamin C; adenosine triphosphate; coenzyme A; cyclic adenosine monophosphate ; heart transplantation Clinical manifestations Auxiliary examination [prognosis] [Overview] This type is characterized by left ventricular or biventricular or expanded calendar, accompanied by cardiac hypertrophy. Ventricular systolic dysfunction, with or without congestive heart failure. Ventricular or atrial arrhythmia common. Condition was progressively increased, can occur at any stage of the disease death. [Diagnosis] 1980 World Health Organization indicate that the disease is unexplained left ventricular or bi-ventricular enlargement, ventricular systolic dysfunction, with or without congestive heart failure and arrhythmias, shall exclude the diagnosis of the disease can only be made after other causes. 1995 Symposium on Cardiovascular Diseases Society of Chinese organizations, proposed diagnostic reference standard of the disease as follows: 1 clinical manifestations of heart enlargement, reduce ventricular systolic function with or without congestive heart failure, arrhythmia often can occur embolism and sudden death and other complications. 2 enlarged heart X-ray examination cardiothoracic ratio> 0.5, Echocardiography fully expanded, especially in the left ventricle was significantly enlarged, left ventricular end-diastolic internal diameter ≥ 2.7cm/m2, the heart can be presented ball. 3 ventricular systolic function by echocardiography reduce diffuse weakened wall motion detection, ejection fraction less than normal. 4 must rule out other specific (secondary) cardiomyopathy and endemic cardiomyopathy (Keshan disease), including ischemic heart disease, peripartum cardiomyopathy, alcoholic cardiomyopathy, metabolic and endocrine diseases such as hyperthyroidism, hypothyroidism, amyloidosis, diabetes-induced cardiomyopathy, genetic neuromuscular disorder caused by familial cardiomyopathy, systemic diseases such as systemic lupus erythematosus, rheumatoid arthritis, etc. due before the diagnosis of cardiac disease, toxic cardiomyopathy idiopathic dilated cardiomyopathy. Conditions can detect serum anti-peptide antibodies such as anti-myocardial myocardial mitochondrial ADP / ATP carrier antibody, anti-myosin antibody, anti-β1-receptor antibodies, anti-M2 cholinergic receptor antibodies, as auxiliary of the disease diagnosis. Identification of clinically difficult and coronary heart disease as those who need coronary angiography. Endomyocardial biopsy: pathological diagnosis of the disease non-specific, but contribute to the differential diagnosis and specific cardiomyopathy and acute myocarditis. Endomyocardial biopsies heart polymerase chain reaction (PCR) or in situ hybridization, diagnosis of the cause of infection to help; specific cells or abnormal gene analysis. (A) rheumatic heart disease cardiomyopathy, mitral or tricuspid area also has a systolic murmur, but generally not associated with diastolic murmur, and louder when heart failure, after failure to control reduce or disappear, rheumatic heart disease is to the contrary. How often cardiomyopathy heart chamber while expanding, as rheumatic heart disease in the left atrium, left or right ventricular-based. Ultrasound helps distinguish. (B) pericardial effusion cardiomyopathy enlarged heart, heart weakened, and pericardial effusion required difference. When cardiomyopathy displaced apex beat to the left, in line with the outer edge of the left heart dullness, pericardial effusion apex beat is often not obvious or inside the outer edge of the left heart dullness. Mitral or tricuspid systolic murmur, ventricular hypertrophy on electrocardiogram, abnormal Q waves, a variety of complex arrhythmias, cardiomyopathy both directions. Ultrasound is not difficult to distinguish between the two, a lot of the pericardial fluid level segment or dark areas described pericardial effusion, cardiac enlargement, compared with cardiomyopathy. There must also be noted that when a small amount of pericardial effusion, cardiac disease, but only enough to cause cardiac tamponade, signs still will not affect the heart and heart function, only the ultrasound findings. Systolic time when obvious abnormalities cardiomyopathy, pericardial disease is normal. (C) hypertensive heart disease cardiomyopathy may have a temporary high blood pressure, diastolic blood pressure, but no more than 14.67kPa (110mmHg), and appeared in acute heart failure, after failure to improve blood pressure. Hypertensive heart disease is different eyes, urine, kidney function was normal. (Four) than middle-aged patients with coronary heart disease, if enlarged heart, heart failure, arrhythmias, or other causes must be considered without coronary heart disease and cardiomyopathy. There are risk factors for high blood pressure, high cholesterol or diabetes, segmental wall motion abnormalities were conducive to the diagnosis of coronary heart disease. In recent years, a wide range of long coronary lesions caused by ischemia and cardiac fibrosis, cardiac dysfunction in the development of the situation as "ischemic heart disease", if the past is no angina or myocardial infarction, and cardiomyopathy quite difficult to distinguish, Furthermore cardiomyopathy also pathologic Q wave angina, identification is required at this time
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Wikipedia Encyclopedia
Dilated cardiomyopathy Also known as "congestive cardiomyopathy." A clinical type of cardiomyopathy. The cause is unknown, but it can be inferred or with some acquired diseases such as viruses, bacteria-induced myocarditis, drug toxicity, metabolic disorders caused by a variety of myocardial injury. Its characteristics are: enlargement of the heart, especially in left ventricular enlargement, left ventricular dilatation and systolic volume increased left ventricular systolic pump failure, left ventricular systolic dysfunction. Slow on_set_, clinical manifestations of dyspnea, edema, hepatomegaly and other manifestations of heart failure. Others still have arrhythmia, thrombosis, and even sudden death. Physical enlargement of the heart, can be heard the third and fourth heart sound gallop. X-ray, echocardiography and other help to diagnose the disease. Treatment to correct heart failure, supplemented by symptomatic treatment. Significantly enlarged heart, heart failure or arrhythmias refractory persistent poor prognosis.
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Containing Phrases
Afflux nature Expand model myocardosis
Afflux nature myocardosis Expand model myocardosis