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About DCM (dilated cardiomyopathy, DCM) based on the characteristics of left ventricular (majority) or significant expansion of the right ventricle
Dilated cardiomyopathy, and are associated with different degrees of cardiac hypertrophy, left ventricular systolic dysfunction in cardiac enlargement, heart failure, arrhythmia, embolism as the basic features. In the past been referred to as congestive cardiomyopathy. The disease is often accompanied by arrhythmia, mortality is higher. About 20% of DCM patients determined to family history of myopathy. Slow onset of any age may be the disease, more common 30 to 50 years of age, history of essential hypertension in some patients. Characteristics of dilated cardiomyopathy (dilated cardiomyopathy, DCM) based on the characteristics of left ventricular (majority) or right ventricle has expanded significantly, and are associated with different degrees of cardiac hypertrophy, left ventricular systolic dysfunction in cardiac enla


rgement, heart failure, heart rhythm disorders, embolization as the basic features. In the past been referred to as congestive cardiomyopathy. The disease is often accompanied by arrhythmia, mortality is higher. About 20% of DCM patients determined to family history of myopathy. The diagnosis of dilated cardiomyopathy rate gradually increased, it is estimated that the annual diagnosis rate of about 8 / 10 million, prevalence rate is about 37/10 million, half of them were aged under 55 years of age, about 1 / 3 of cardiac function grade ~ (New York Heart Association classification standards). However, some patients with undiagnosed light could cause actual prevalence rate higher. Cause of dilated cardiomyopathy caused by long-term effect of several factors the end result of myocardial damage. Infection or non-infectious myocarditis, alcoholism, metabolic and other factors may be related to the pathogenesis of dilated cardiomyopathy. Short-term primary myocardial injury (such as exposure to toxic substances) for some myocardial cells may be lethal, but the remnants of the myocardial cells will thus increase the load, the occurrence of compensatory hypertrophy. Such compensatory changes in the early still capable of maintaining the overall function of the heart, but eventually will be reflected in myocardial systolic and diastolic dysfunction. Myocarditis both irreversible myocardial cell death, but also by the cytokine-mediated reversible myocardial depression. Some factors (such as alcohol) although
Edema does not directly damage cardiac cells, but can cause serious long-term effects such as cardiac dysfunction. In addition, many injuries also involving cardiac fiber stent system of myocardial compliance and thereby participate in the occurrence of ventricular enlargement and development. Pathophysiological mechanism of disease has shown that most patients with dilated cardiomyopathy and viral infection and autoimmune response. Has been found that viral myocarditis can evolve into dilated cardiomyopathy, myocarditis and in dilated cardiomyopathy patients with endomyocardial biopsy specimens can be found in the intestinal virus, in patients with dilated cardiomyopathy can be detected in a variety of anti-serum cardiac autoantibodies, such as anti-ADP / ATP carrier antibodies, anti 1 adrenergic receptor antibodies, anti-M
Gene 2 receptor antibody and anti-cholinergic myosin heavy chain antibody, also can detect intestinal virus gene fragment. Viral infection and immune response to injury theory is dilated cardiomyopathy incidence of major theories. In addition, genetic factors may also play a role. Persistent infection with virus persistence in vivo after infection of the virus RNA is a viral myocarditis progress to dilated cardiomyopathy as a risk factor. Animal experiments in mice showed that myocardial cells can be dissolved Coxsackie virus, enterovirus can cause myocardial cytoskeletal protein damage, and that change is recognized as a dilated main features. The virus can damage the cardiac muscle cells occurs in a period of high viral titer (Coxsackie B1, B4 virus infection), may also occur in the virus (Coxsackie B3 virus) immune response after infection at the beginning. Myocardial tissue damage viruses can directly damage the immune system can also be caused by injury. When the virus persists in the myocardium when the RNA, T lymphocytes can infiltrate myocardium. Studies have shown that low levels of viral gene expression can lead to chronic progressive myocardial injury, as the persistence of the virus RNA in the myocardium more than 90 days, the heart can present as dilated cardiomyopathy similar to the pathological changes. When the body's defense capability is lowered, the body can be presented with chronic virus carrier state. In this chronic process, the virus can exist in the spleen, liver, pancreas and systemic lymph nodes. The harm is not a direct attack on the heart, but rather stimulate the body's immune response; the same time persistent viral RNA replication can produce non-invasive but has a large number of antigenic virus RNA, induced the immune response induced myocardial injury . Autoimmunity is currently speculated that immune-mediated myocardial damage is an important mechanism for the pathogenesis of DCM. humoral immunity: in patients with dilated cardiomyopathy can be detected in serum samples of a variety of anti-myocardial autoantibodies, including anti-mitochondrial ADP / ATP carrier antibodies, anti 1-adrenergic receptor antibodies, anti-M2 cholinergic receptor antibody, heat shock protein antibody, anti-myosin heavy chain antibodies, anti- -keto acid dehydrogenase, branched chain (branched chain alpha ketoacid dehydrogenase, BCKD) complex antibody and anti-laminin (laminin) antibodies, which autoantibodies in the pathogenesis of this disease may play an important role. A. anti-mitochondrial ADP / ATP carrier (ANT) antibody: The study found, ANT and pathogens share common protein epitopes, such as ANT amino acid sequence of 27 to 36 and Coxsackie B3 virus 1218 ~ 1228 Arg sequence is similar to cross-reaction caused by autoantibodies. Also been suggested that a virus antigen in the release of mitochondrial isolation, or the nature of changes in cardiac antigens, or through the bypass activation of autoreactive T lymphocytes, and induce an autoimmune response against the mitochondria. Anti-ANT antibodies can inhibit myocardial mitochondrial ATP / ADP transporter, resulting in myocardial energy metabolism, damage myocardial function. ANT with calcium channel proteins may also have the same epitope. Anti-ANT antibody and cardiac calcium channels on the cell membrane protein binding, inhibition of calcium channel inactivation, promoting calcium influx, intracellular calcium overload, leading to myocardial cell degeneration and necrosis. In other words, anti-ANT antibody activated Ica DCM induced calcium overload is one of the causes of myocardial injury. B. anti- 1-receptor antibody: -receptor is a G protein-coupled membrane receptor, when the -receptor binding after activation of neurohumoral transmitters, have physiological effects at the same time, receptor retraction, and the solution enzyme body harmony, proteolytic enzymes to degrade. Lysosomes with the surface containing the major histocompatibility complex (MHC) class I molecules of the nuclear receptor binding, if the degradation of the receptor peptides can be produced with the MHC molecules form a complex, the complex can be transported to the membrane surface , Auxiliary presented to T lymphocytes (TH) receptor, activation of TH. TH and B lymphocytes activated interaction, resulting in peptide receptor molecules for their own specific antibodies. Normally, myocardial cells do not express MHC class I molecules, only when the immune activity with the expression of MHC class I molecules only. Virus infection induces the expression of MHC class I molecules myocardial cells, cardiac cells to become antigen presenting cells. In addition, the virus and the molecular structure of -receptor, the common epitopes, can be caused by simulating the mechanism of anti- -receptor antibody. Antibodies against 1 receptor can activate the receptor Ca2 channel, increased Ca2 influx of myocardial cells, leading to calcium overload, causing myocardial injury. Meanwhile, anti 1 receptor antibody increased myocardial cAMP-dependent protein kinase (PK) activity and -receptor combination with the cytoplasm and the plasmid significantly improved the ratio of PK activity, leading to cytoplasmic and plasmid cAM
PK P dependent activation of heart disease, to achieve positive chronotropic denaturation. Also of the that anti- 1-receptor antibody can affect the myocardial cell communication, so that receptor regulation of cardiac cell metabolism disorder, the number of myocardial -receptor down, induced myocardial damage. C. anti-myosin antibodies: Currently, there are two mechanisms that cause dilated cardiomyopathy patients immune response occurs, resulting in anti-myosin antibodies: a. HIV infection or other causes of myocardial tissue necrosis causes release of myosin and exposure triggers the body's own immune; b. myosin molecules and viruses have similar epitopes. D. anti-M2 cholinergic receptor antibodies: M2 cholinergic receptors are located in the heart of a membrane protein, is a G protein-coupled membrane receptor, in conjunction with the regulation of myocardial -receptor adenylate cyclase activity and ion channels, regulation of cardiac function. The anti-M2 cholinergic receptor antibodies has to be cholinergic-like effects, can reduce isoproterenol in guinea pig ventricular muscle caused by the cyclic adenosine monophosphate (cAMP) concentration, slow down the contraction frequency of ventricular cells, slow down the increase in the maximum speed of ventricular pressure, heart rate. That the anti-M2 cholinergic receptor antibodies may be caused by inhibition of cholinergic antagonist atropine or neutralizing antibodies offset. The antibodies may be due to virus infection to become the M2 acetylcholine receptor autoantibodies, autoimmune response caused by excitation. E. Other antibodies: in addition to several anti-myocardial autoantibodies above, but in the serum of patients with dilated cardiomyopathy, there are still anti-mitochondrial antibodies M7, anti-BCKD complex antibodies, anti-actin antibody, anti-SR antibodies ATP enzyme . Although about 30% to 40% of patients with dilated cardiomyopathy have serum autoantibodies specific organs and diseases, but there are still some patients do not appear anti-self antibodies, which may be several factors: a. Dilated cardiomyopathy is a multifactorial disease, the lack of antibodies that cause damage to cellular immune-based or by other factors; b. heart disease, autoantibodies may be early signs disappear with the extension of the course; c. the expansion of different cardiomyopathy patients with autoantibodies may appear different due to different types of testing methods and testing, can produce negative results; d. autoantibodies and human leukocyte antigen related. cellular immunity: in dilated cardiomyopathy, the abnormal cell-mediated immune response manifested as lymphocyte function damage, change the ratio of lymphocyte subsets and activation of immune cell factor system. Dilated cardiomyopathy patients with peripheral blood T cells (CD3), suppressor / cytotoxic T cells (CD8) significantly reduced adjuvant / induction of T cells (CD4) did not change. Studies have shown that cytotoxic T lymphocytes in vitro dissolution of infected cardiac cells. Viral infection, myocardial cell membrane can present a peptide known as T cell receptor, T cell receptor recognition and binding, and this can cause myocardial cell injury; using anti-T cell receptor antibody can cardiomyocytes Damage reduced. In addition, natural killer cells can still secrete a perforin (perforin), to form a hole-like injury of myocardial cells. the role of cytokines: DCM serum levels of inflammatory factors were significantly higher tumor necrosis factor (TNF) / interleukin (IL) -10 ratio was positively correlated with plasma epinephrine levels; serum TNF receptor (sTNFR) levels and related to left ventricular size; interleukin increased content and ventricular mass and myocardial fibrosis was positively correlated. IFN- and TNF- can induce myocardial cell surface expression of intercellular adhesion molecule -1 (ICAM-1), the latter in the coupling of myocardial cells and lymphocytes play a role. Genetic familial dilated cardiomyopathy genetic predisposition hypertrophic cardiomyopathy is less than, but still plays a role of genetic factors, familial dilated cardiomyopathy chain more common than usually realized. 20% of their first-degree relatives of patients also showed evidence of dilated cardiomyopathy, suggesting that family history is relatively common. Typical family of neuromuscular diseases as heart disease, such as Duchenne muscular dystrophy, and X-linked genetic-related chronic progressive Becker muscular dystrophy, both of which are dystrophin gene (a cytoskeletal protein) mutations To. Recently, a suffering with X-linked hereditary cardiomyopathy but no skeletal muscle disease and the family confirmed the dystrophin gene in the heart of the catalytic domain of the missing. It has been reported that there is familial cardiomyopathy, mitochondrial disorders such as Kearns-Sagre syndrome: cardiomyopathy, ophthalmoplegia, retinopathy, and cerebellar ataxia. In addition to muscle proteins and metabolic abnormalities, the genetic factors also affect the immune response triggered by myocardial. Family members have the same viral infection or pregnancy after reports of heart failure. Most familial cases are autosomal dominant, but the disease is of great genetic heterogeneity has been reported that there were 49 autosomal recessive and X-linked inheritance are. There is a type of familial X-linked dilated cardiomyopathy Department gene promoter region and encoding dystrophin (dystrophin) missing the first exon due to the latter constitute the muscle proteins are components of the cytoskeleton one. Inferred from the genetic changes caused by the lack of cardiac dystrophin but the cause of dilated cardiomyopathy. In addition, there are also those who reported a mutation in mitochondrial DNA. The patient had no family, whether linked to dilated cardiomyopathy have a genetic predisposition is still unknown. Has been found that many with autosomal dominant familial cardiomyopathy associated with chromosomal loci, including chromosome 1 (q32, p1-q1), 2 chromosome (q31), 5 chromosome (q33-34), 6 chromosome (q12-16), 9 chromosome (q13-22), 14 chromosome (q11), 15 chromosome (q14, q22), and found that patients with DCM associated with mitral valve prolapse in 10 dominant loci chromosome (q21-23). 2. Pathology and pathophysiology of DCM, usually twice the normal enlargement of the heart, and there is a certain degree of cardiac hypertrophy and heart dilation of universality, which are the expansion of the atrioventricular cavity, mitral and tricuspid valve ring by large, occasionally the edge of the valve leaflets thickened, due to both myocardial and endocardial fibrosis, it is the heart of the appearance of pale color, the heart cavity thrombus. Light microscope, the muscle fibers often significantly thicker, degeneration, necrosis and fibrosis. Electron microscope, the cardiac muscle cells to reduce the original fiber content of mitochondria increased, increased, crest or ruptured, sarcoplasmic reticulum, glycogen increased. Histochemical examination, succinate dehydrogenase, glycogen phosphonate different levels of enzymes and reduced calcium-dependent ATP enzyme, maleate dehydrogenase, glutamate dehydrogenase and 5 - nucleotidase decreased, LDH and LDH5 increased, probably related to hemodynamic decompensation. DCM patients have cardiomyopathy, the systolic dysfunction, reduced cardiac output, heart residual blood volume increased, left ventricular end diastolic pressure and heart cavity passive expansion, pulmonary congestion and systemic circulation, resulting in the performance of refractory heart failure. Extreme expansion of the chambers of the heart, atrioventricular valve with increasing the circumferential diameter of atrioventricular valve regurgitation and produce the corresponding systolic murmur. Life time, the left atrium, pulmonary artery pressures have increased, last seen right heart failure, ventricular cavity to expand, the heart wall tension increases, oxygen consumption increased, cardiac hypertrophy, heart rate, the relative speed leading to myocardial ischemia, and myocardial oxygen uptake capacity has reached limit, thus angina. Cardiac pacemaker and conduction system disease involving the time can cause a variety of arrhythmias. DCM developed to the stage of congestive heart failure, excessive neuroendocrine activation, including the sympathetic nervous system (SNS), renin - angiotensin system (RAS) and vasopressin, thereby contributing to worsening heart failure, endogenous atrial natriuretic peptide also activation, but not enough to offset the role of SNS and RAS. In DCM the initial myocardial damage, circulatory endocrine rapid activation, but to obtain compensation of cardiovascular, endocrine cycle returned to normal or only slightly elevated, but the compensation is the cost of the expense of effective blood flow come until Finally, enter into decompensation, recycling and re-activate the endocrine, many sub-clinical pathophysiology, including cardiovascular remodeling under way, and myocardial tissue in an autocrine and paracrine then play an important role. Therefore, Packar activation of the neuroendocrine system that lead to heart failure aggravated sexual reasons. Summary of the slow onset of phases may, at any age, disease, but the more common 30 to 50 years of age, earlier onset of hereditary DCM. DCM course of the disease can be divided into three stages: asymptomatic can be a normal physical examination, X-ray examination the heart slightly expanded non-specific changes in ECG, echocardiography, left ventricular end diastolic diameter 5 ~ 6.5cm, ejection fraction 40% 50%. Mainly for symptoms of extreme fatigue, hair force, shortness of breath, palpitations and other symptoms, early diastolic gallop, echocardiography, left ventricular end-diastolic diameter 6.5 ~ 7.5cm, ejection fraction between 20% to 40% . Advanced disease hepatomegaly, edema, ascites and other manifestations of congestive heart failure may be relatively stable for several years to ten years of repeated failure, but also progressive increase in the short term death. Most patients with a variety of arrhythmias, some patients with thromboembolism or sudden death. The main signs is the heart enlargement, gallop, pulmonary and systemic congestion levy. Patients with congestive heart failure symptoms the most prominent performance-oriented. Its occurrence was mainly due to decreased ventricular contractility, compliance, and reduce fluid retention and lead to insufficient cardiac output (or) increased ventricular filling pressure due to excessive. There may be symptoms of left ventricular dysfunction, common to progressive weakness or decreased endurance of labor, exertional dyspnea, orthopnea and paroxysmal nocturnal dyspnea and other manifestations of left heart failure, which can occur with advanced disease the right heart failure symptoms: such as the liver large, upper abdominal discomfort, and peripheral edema. A variety of arrhythmias can occur quickly or slowly arrhythmia, or even first clinical disease-oriented performance; serious arrhythmia is a common cause of sudden death caused the disease. Embolism can occur in heart, brain, kidney, or pulmonary embolism. Thrombosis or atrial from ventricular enlargement, especially when associated with atrial fibrillation. Even as the blood clots around the first symptom of the disease. Although chest pain and normal coronary artery, but there are still about 1 / 3 of patients with chest pain, its occurrence may be related to pulmonary hypertension, pericardial involvement, microvascular myocardial ischemia, and other unknown factors. Signs (1) The apex beat was often shifted to the left, but the left ventricle significantly increases do not appear backward; apex beat often diffuse; deep breathing or chest under the xiphoid touched the left edge of the right ventricle can be beat. (2) can often hear the third and fourth heart sounds, "gallop", but no other than heart failure can not gallop. The third heart sound enhancement reflects ventricular volume overload. (3) cardiac decompensation occurs when significant mitral regurgitation murmur. Most clearly in the armpit of the noise, improved heart function often reduce, and sometimes with parasternal murmur of tricuspid regurgitation overlap, but the latter usually occurs late in heart failure. (4) can occur when heart failure was alternately pulse and tidal breathing. Pulmonary arterial pressure was significantly higher in patients can be heard in early diastole is short, in the tone of the pulmonary regurgitation murmur. (5) visible when right ventricular failure, cyanosis, jugular vein distention, hepatomegaly, lower extremity edema, a small number of chest, ascites. Check the common method 1. Electrocardiogram (ECG): QRS low voltage, we can see various types of ventricular and atrial arrhythmia, ST-T changes and pathological Q waves. 2.X-ray: increased heart shadow, cardiothoracic r 0.6, pulmonary congestion symptoms, sometimes with pleural effusion. 3. Echocardiography: often show the following characteristics: "a great": heart cavity to expand, particularly as a significant left ventricular dilatation, left ventricular diastolic diameter 50 ~ 55mm, = 2.7cm / m ^ 2; "two thin": wall, septal thinning, <7 ~ 11mm; "three weak": wall, septal motion universal decline; "little four": the small valve port open range. Determination of left ventricular ejection fraction and may (LVEF) and diastolic function, pulmonary hypertension, can also be displayed containing chambers of the heart thrombus. 4. Radionuclide imaging: radionuclide cardiac blood pool imaging shows enlarged weakened wall motion in general, the overall ejection fraction decreased and the phase of partial ejection fraction, myocardial perfusion imaging will see more changes in the segmental spend porphyritic or segmental reduction; myocardial metabolic imaging very few metabolic defects, most uneven performance of metabolic and perfusion / metabolism match abnormal myocardial segments accounted for the majority. 5. Magnetic resonance imaging (MRI): visible involvement enlarged heart, atrial ventricular function decreased accordingly. Another magnetic resonance spectroscopy (MRS) can measure myocardial metabolism dysfunction. 6. Electron beam CT: an accurate measurement of the heart meridian, quantitative analysis of cardiac function, and ventricular septal movement observed, and the coronary artery scan to identify ischemic cardiomyopathy. 7. Cardiac catheterization and angiography: left ventricular end diastolic pressure, left atrial pressure and pulmonary capillary Lease pressure and cardiac output and stroke volume decreased ejection fraction reduction. Left ventricular angiography shows left ventricular cavity to expand, the left ventricular wall motion decreases. Often normal coronary angiography. 8. Endomyocardial biopsy: a lack of specificity. In recent years, carried out in clinical endomyocardial biopsy, the biopsy forceps with a cardiac catheterization to obtain samples for pathology and virus checking, you can find any evidence of myocarditis, but the diagnosis of histological criteria and artifact removal and some aspects of the problem to be solved. 9. Serology: recent years have reported that serum antibodies against cardiac peptides, such as myocardial mitochondrial ADP / ATP carrier antibodies, anti-myosin antibodies, anti-B1 receptor antibodies, anti-M2 cholinergic receptor antibodies, but also help aid diagnosis as DCM, and with the severity of DCM heart failure. Laboratory 1. Serological tests may have increased erythrocyte sedimentation rate, immunoglobulin abnormalities, occasional enzyme activity increased. Myocarditis and DCM may be taken into account evolved. 2. Anti-myocardial antibodies and virus detection is necessary, it may detect a variety of anti-myocardial autoantibodies; contribute to the continuous determination of virus titer viral diagnosis. 3. Eosinophils in peripheral blood should be further increased to check for the existence of systemic allergic diseases, as these diseases can cause allergic myocarditis. Other auxiliary examinati. Electrocardiogram usually shows left atrial and (or) left ventricle increased, but less common abnormal increase of R wave; can have low-voltage QRS wave, common RV5; precordial often see pathological Q wave, Many patients experience non-specific QRS wave can be widened; about 1 / 4 of patients may have atrial fibrillation, approximately 20% of patients may present with left bundle branch block; addition to Chagas disease outside the right bundle branch block is rare. PR interval prolongation is also very common and some patients with shortened survival time. Severe conduction block suggests the likelihood of giant cell myocarditis or sarcoidosis. Non-specific ST segment depression and T wave changes in common. 2. Chest X-ray film multi-center increases, but some patients with left ventricular heart before shadow has been a marked increase of backward increased. Expansion of the chest X-ray reflection of the sensitivity of right ventricular to left ventricular dilatation is higher than that, and right heart failure often indicates a poor prognosis, so the chest of some significance for prognosis. Pulmonary hypertension may have Kerley B lines. Pericardial effusion with heart beat less visible under fluoroscopy. 3. Echocardiography to determine whether the left and right ventricular enlargement and reduced myocardial contractility, and help with other types of heart disease and valvular disease, congenital heart disease, etc. were identified. The characteristic changes for the left and right ventricular cavity enlargement and left ventricular posterior wall motion decreases, ventricular septal contradiction can be presented, and ventricular septal free wall thickness thinning, but also normal, fractional shortening was significantly reduced, visible functional mitral regurgitation. DCM secondary to functional mitral regurgitation is usually no valvular abnormality or tendons, and diffuse wall motion when DCM is also different from coronary heart disease decreased regional wall movement disorders. 4. Cardiac catheterization in most patients with heart failure with cardiac enlargement in order to exclude coronary atherosclerosis and coronary angiography, or abnormal when the need to consider carefully. The presence of decompensated heart failure, hemodynamic changes and right heart catheterization and cardiac output measured ventricular filling pressure in clinical diagnosis and help guide treatment. 5. Endomyocardial biopsy endomyocardial biopsy is an absolute indication for heart transplant rejection and anthracycline cardiac toxicity monitoring. The following 2 groups of dilated cardiomyopathy myocardial biopsy may be considered the line: the onset of symptoms at 3 months or 6 months; unexplained cardiac disease. The lymphocyte infiltration in the histological features of patients in group 1 positive rate of 5% to 20% in group 2 patients less than 10%. As the significance of the histological changes is not certain, there is thus confirmed, also come to the other diagnosis. Patients in deciding on endomyocardial biopsy, the diagnosis must take into account the prognosis of the significance of treatment or how much. As new technologies replace the existing biochemical staining and further development of the microscope, myocardial biopsy applications will be more extensive. Diagnosis of the World Health Organization in 1980, the disease is unexplained left ventricle or double ventricular enlargement, ventricular systolic dysfunction, with or without congestive heart failure and arrhythmias, should be made only after excluding other reasons for the diagnosis of the disease . Society of Cardiology in 1995, organizing seminars, proposed reference standard for the diagnosis of this disease are as follows: 1. Clinical manifestations of heart enlargement, reduced left ventricular systolic function with or without congestive heart failure, often arrhythmia, can occur complications such as embolism and sudden death. 2. Cardiomegaly X-ray cardiothoracic r 0.5, Echocardiography heart to expand, especially as a significant left ventricular dilatation, left ventricular end diastolic diameter 2.7cm/m2, the heart can be presented ball. 3. Ventricular systolic function detected by echocardiography to reduce diffuse decreased wall motion, ejection fraction less than normal. 4. To the exclusion of other specific (secondary) heart disease and endemic cardiomyopathy (Keshan disease), including ischemic cardiomyopathy, peripartum cardiomyopathy, alcoholic cardiomyopathy, metabolic and endocrine diseases such as thyroid hyperactivity, hypothyroidism, amyloidosis, diabetes-induced cardiomyopathy, familial genetic neuromuscular disorder caused by cardiac disease, systemic diseases such as systemic lupus erythematosus, rheumatoid arthritis due to cardiomyopathy, toxic cardiomyopathy, etc. before diagnosis of idiopathic dilated cardiomyopathy. Differential diagnosis of rheumatic heart disease patients with mitral or tricuspid valve area can also systolic murmur, but generally not associated with diastolic murmur, and in heart failure
Rheumatic valvular heart disease, than sound, reduce or disappear after controlling for heart failure, rheumatic heart disease is the opposite. How often cardiomyopathy heart chamber while expanding, as rheumatic heart disease with left atrial and left ventricular or right ventricular-based. Ultrasound helps to distinguish. When pericardial effusion cardiac enlargement cardiomyopathy, heart weakened, and the pericardial effusion to be different. Cardiomyopathy when the apex beat displaced to the lower left, with the outer edge of the left heart dullness consistent with pericardial effusion often not obvious or when the apex beat in the heart of the left edge of the inside of the dullness. Systolic murmur of mitral or tricuspid valve area, left ventricular hypertrophy on ECG, abnormal Q wave, a variety of complex arrhythmias, were instructed cardiomyopathy. Ultrasound is not difficult to distinguish between the two, flat section of intrapericardial large amounts of liquid or dark areas that pericardial effusion, cardiac enlargement, compared with cardiomyopathy. Must be noted that cardiomyopathy may also be a small amount of pericardial effusion, but only enough to cause cardiac tamponade, that does not affect the heart of the signs and cardiac function, but only the ultrasound findings. Systolic time was clearly abnormal in cardiomyopathy, pericardial disease were normal. Hypertensive heart disease cardiomyopathy may have temporary high blood pressure, but diastolic pressure does not exceed more than 14.67kPa (110mmHg), and when seen in acute heart failure, heart failure, improves blood pressure. Hypertensive heart disease with different eyes, urine routine, renal function was normal. Middle-aged patients with coronary heart disease, if enlarged heart, arrhythmia or heart failure without the need to consider other causes coronary heart disease and heart disease. Have high blood pressure, high cholesterol or diabetes risk factors, abnormal segmental wall activity was beneficial diagnosing coronary artery disease. In recent years, the long-term coronary heart disease caused by extensive fibrosis, ischemia, cardiac insufficiency the development of the situation as "ischemic cardiomyopathy", if the past no angina or myocardial infarction, and heart disease quite difficult to distinguish, Furthermore pathologic Q cardiomyopathy may also affect angina, identification must depend on coronary angiography at this time. Most congenital heart disease has obvious signs, is not difficult to distinguish. Ebstein tricuspid valve area deformity noise, and a gallop, heart weakened, right heart failure to expand and to be different with cardiomyopathy, but the disease symptoms in the early years, left ventricular little more cyanotic forward. Echocardiography can confirm the diagnosis. Secondary cardiomyopathy systemic diseases such as systemic lupus erythematosus, scleroderma, hemochromatosis, amyloidosis, glycogen storage disease, neuromuscular disease, have their primary disease, the performance difference can be funded. More important is the distinction between myocarditis. Acute myocarditis often occurs in viral infection or shortly after that time, the difference is not very difficult. Chronic myocarditis without a clear history of acute myocarditis and cardiomyopathy is difficult to distinguish, in fact, many of dilated cardiomyopathy from myocarditis developed from the so-called "post-myocarditis cardiomyopathy." Complications of the disease often occurs with heart failure, arrhythmia, sudden cardiac death and embolism.
Heart failure 1. Heart failure patients with dilated cardiomyopathy as cardiomyopathy, cardiac enlargement, left ventricular dilation or double ventricular dilatation, caused by left ventricular systolic dysfunction, systolic heart failure occurs. As the illness progresses, the occurrence of right heart failure or total failure. 2. Arrhythmia disease complicated by cardiac arrhythmia, various volatile high incidence of arrhythmia and its prominent features. PVCs, atrial premature beats and conduction block (atrioventricular block and bundle branch block) is the most common arrhythmia, tachycardia, atrial fibrillation (20%), bradycardia common, serious ventricular may occur tachycardia, or ventricular fibrillation or cardiac arrest, can cause death. 3. Sudden cardiac death is a dilated cardiomyopathy most serious complication of dilated cardiomyopathy leading cause of death. The incidence of sudden cardiac death can be as much as 30%. 4. Artery embolization disease complicated by thrombosis and embolism. Most studies and observed the formation of dilated left ventricular thrombus is a major part of the apex and the two atrial appendage, thrombus formation of emboli shedding, resulting in thrombosis. Embolism to the lung, brain, spleen and kidney embolism common. Guangxi Nanning Epidemiology (1978) 6 counties sampling 66,632 cases, aged 7 to 93 years of age. By history taking, physical examination, screening of suspicious persons, the line of X ray and ECG examination, determined to check the suspected myopathy underwent ultrasound examination. Diagnostic criteria as following: the performance of cardiac enlargement; heart failure; ECG ST-T changes and no history of myocardial infarction Q wave abnormalities; severe arrhythmia; circulation pulmonary embolism and history. Have more than one person, the exclusion of other organic heart disease, can be diagnosed as idiopathic dilated cardiomyopathy. The results showed that: diagnosed with idiopathic dilated cardiomyopathy, a total of 56 patients, the prevalence was 84.0/10 million. This study used cross-section of the population survey, therefore, can only estimate the prevalence of heart disease. Results of the study there were two obvious shortcomings: suspects only by ultrasound, can not detect early, asymptomatic cases; ECG changes in diagnostic criteria, lack of specificity of the history of arrhythmia and thrombosis. But because it is based on population surveys, age range, therefore, the results of this study widely cited in the literature. Nanjing Population idiopathic dilated cardiomyopathy incidence survey (1985 ~ 1989), 14 urban hospitals based on clinical and ultrasound data, according to WHO (1980) diagnostic criteria and classification, 5 years, 60 years of age were found to expand Type heart
134 cases of cardiac myopathy chart, the annual incidence rate was 1.3/10 million people, age-standardized rate was 1.1/10 million. This report can not be found in the future treatment of asymptomatic cases and cases of dissemination in small hospitals. In order to rule out coronary heart disease, only the analysis of the data below the age of 60. Therefore, the incidence rate is clearly underestimated. On the other hand, can not be excluded under the age of 60 ischemic heart disease in men may be. Summary of reasons for the treatment of the disease is unknown because, in addition to heart transplantation, but there is no complete cure. Goal of treatment is to control heart failure and arrhythmias, alleviate immune-mediated myocardial damage, improve the patient's quality of life and survival. The treatment of heart failure limit physical activity, low-salt diet, most patients can be used digitalis preparations, but prone to digitalis toxicity, dosage should be small, the usual dose of digoxin was 0.125mg / d. According to the patient's hemodynamic status and diuretic use discretion vasodilators. Almost all patients can make use of angiotensin-converting enzyme inhibitors (ACEI), ACEI can not only improve the hemodynamic abnormalities of heart failure, heart failure can also block the abnormal activation of the neuroendocrine system, inhibition of myocardial remodeling to improve prognosis. Progressed very quickly in recent years, ACEI drugs, commonly used drugs have captopril 12.5 ~ 25mg / d, enalapril 2.5 ~ 10mg / d. Myocardial protection (1) -receptor blockers: DCM patients with anti- 1-adrenergic receptor agonist antibody with -like activity, anti 1-receptor antibodies may be through receptor gated channels, causing cell calcium overload, leading to myocardial cell damage, and blockers can block the effect. In addition, blockers can significantly reduce the DCM patients with TNF , IL-10 and sTNFR levels, suggesting that blockers have a role in immune regulation. Long-term treatment of blockers can be prevented dilated cardiomyopathy in patients with disease progression and improve clinical symptoms and left ventricular function, reduce mortality and improve prognosis. DCM patients because there are anti- 1 receptor antibody, and its mediated myocardial damage occurred early in the disease, so
DCM patients with cardiac enlargement in the early application of blockers will get better results. Commonly used drugs metoprolol, bisoprolol, carvedilol, etc., the application should start small dose, no adverse reactions and then gradually increase the dose, such as metoprolol 6.25mg, 2 times / d, gradually increasing to 12.5 ~ 50mg, 2 times / d; Bisoprolol 1.25mg / d, gradually increased to 5 ~ 10mg / d; the initial dose of carvedilol was 3.125mg, 2 times / d, gradually increased to 25 ~ 50mg, 2 times / d. (2) calcium antagonist: DCM in the presence of serum anti-ADP / ATP carrier antibodies by increasing the myocardial cell membrane calcium current and cytosolic free calcium concentration induced myocardial injury, application of calcium antagonists can prevent the occurrence of this effect. 1996 Figulla et al reported that diltiazem treatment of dilated cardiomyopathy, multicenter trial (Diltiazem in Dilated Cardiomyopathy, DiDi), which showed that the treatment in heart failure based on the Canadian site of diltiazem therapy can significantly improve patients with dilated heart index and exercise tolerance. DCM diltiazem intervention (Intervention Study of Diltiazem in DilatedCardiomyopathy, ISDDC) can improve the display of diltiazem in patients with early stage DCM left ventricular end diastolic diameter and ejection fraction, significantly improved cardiac function. Prognostic analysis showed that, due to worsening heart failure requiring hospital treatment reduced mortality. ISDDC tests show that diltiazem treatment of DCM is safe and effective treatment for early DCM, its main pharmacological mechanism is considered to be antibody-mediated intervention in myocardial damage, protect the myocardium. Recent, randomized double-blind clinical trials suggest PRAISE new calcium antagonist amlodipine (amlodipine) can prolong survival in patients with DCM, severe heart failure patients does not increase cardiovascular morbidity and mortality. Animal experiments showed that amlodipine can cause dose-dependent increase of NOx production, but also increase the large coronary artery and aortic production of nitride, the latter reflecting nitric oxide (NO) synthesis increase; local vascular release of NO may be to vasodilation. Some scholars believe that amlodipine treatment may be due to the mechanism of heart failure, the drug can reduce the IL-6 and other cytokines induced, especially in early treatment for DCM. (3) immune adsorption therapy: Since about 70% DCM can be detected in serum antibodies against 1 receptor, in vitro studies have shown that the antibody-mediated chronic stimulation of 1 receptors, leading to heart damage and disease continued to progress. Foreign reports, the application of immunoglobulin assay in the blood of patients clear the DCM IgG, IgM, IgA, IgE and anti- 1 receptor antibodies, and to correct basic treatment of heart failure after 1 year follow-up, DCM patients with left ventricular ejection fraction, left ventricular end diastolic diameter and cardiac function were significantly improved. (4) Ig: immunoglobulin inflammatory factors and by regulating the balance between anti-inflammatory factors, resulting in good anti-inflammatory effects and improve cardiac function. Studies have shown that a newly diagnosed dilated cardiomyopathy (time to onset of symptoms within 6 months) intravenous immunoglobulin 2g/kg, 6 months and 12 months after the LVEF increased. Prevent complications of thrombosis and embolism in patients with atrial fibrillation for, in addition to a contraindication, but might consider using a small dose of anticoagulants or thrombolytic agents (such as urokinase, streptokinase, A & P for the enzymes) treatment. Warfarin, aspirin, ticlopidine (Ticlid), low molecular weight heparin with long-term use of films such as the role of preventing thrombosis. For a line of patients with atrial fibrillation cardioversion transesophageal ultrasound to check the exclusion of intracardiac thrombus or effective anticoagulant treatment for at least 4 weeks before attempting cardioversion. When an anti-arrhythmic treatment of symptomatic arrhythmias or cause ventricular hemodynamic deterioration frequent episodes of premature contractions should be actively given antiarrhythmic drugs such as amiodarone, propafenone and so on. Immunomodulatory effects of astragalus root, can be used for the treatment of this disease. Other (1) thyroid hormone: studies have reported that most adult patients with DCM associated with subclinical disease, the use of thyroid powder (100 g / d), the visible left ventricular ejection fraction, left ventricular inotropic effect can be improved , resting peripheral resistance decreased and cardiac output increase. Thyroid powder also increase -receptor density, thus improving the DCM patients with -receptor down. Currently, thyroid powder is still in the clinical trial stage, the need for further research and clinical validation. (2) growth hormone: growth hormone (GH) regulation of not only involved in the process of human growth, but also involved in heart development and myocardial thickening of the regulation. GH deficiency can reduce left ventricular mass, reduced left ventricular ejection fraction; chronic GH deficiency can cause dilated cardiomyopathy, and even heart failure. Studies have shown that DCM patients with left ventricular mass change associated with changes in plasma concentrations of IGF. Based on the lack of GH for GH in patients with left ventricular mass to increase and improve cardiac function, suggesting that GH can be used for the treatment of DCM. GH for the treatment of DCM are also currently in clinical trial stage, the effect remains to be seen. 7. Interventional therapy (1) biventricular pacing: In recent years, biventricular pacing for refractory heart failure treatment has achieved encouraging results. Although biventricular pacing in heart failure and myocardial disease due to primary disease does not work (such as myocardial ischemia and myocardial strain), but corrects abnormal heart function. Biventricular pacing, biventricular restore electrical and mechanical activities of the synchronization, so that was narrow QRS wave, ventricular mechanical delay shortened ventricular filling time was increased, decreased mitral regurgitation, the effort level of grade ~ heart failure patients improved to varying degrees, the heart narrow, so as to improve prognosis and prolong survival purposes. (2) automatically switch to cardiac rehabilitation - defibrillator (AICD): recovery of all patients from a cardiac arrest, ventricular tachycardia associated with recurrent or worsening heart failure and shock, and can not be anti-arrhythmia drug therapy control patients are to be implanted AICD. On with refractory paroxysmal ventricular tachycardia, ventricular fibrillation in patients with DCM AICD placement of the automatic stay can be sudden ventricular tachycardia and ventricular fibrillation, significantly prolong life, but can not terminate the development of the disease. (3) RF ablation: for patients with chronic atrial flutter patients, advocates implementation of radiofrequency ablation. Clinical studies found that with the disappearance of atrial flutter, heart function improved availability. Advances in surgical treatment (1) left ventricular volume reduction surgery: left ventricular volume reduction surgery was first reported by the Batista and so, they will expand the DCM patients with left ventricular free wall longitudinal resection. The results showed that patients with left ventricular volume reduction surgery, heart function improved. Left ventricular volume reduction surgery in patients with left ventricular DCM-based expansion, relaxation, and left ventricular cavity volume reduction surgery decreases and tends to be more oval, the local stress decreases the left ventricular wall, reduced ventricular stiffness, decreased left ventricular afterload (such as systolic wall stress), further reducing cardiac oxygen consumption, improve left ventricular pump function. (2) dynamic cardiomyoplasty: 1993 was first reported by Carpentier, etc., will be left with dilated cardiomyopathy latissimus dorsi muscle isolated parcels to expand the heart, started 2 weeks after DC stimulation of latissimus dorsi to increase left ventricular force of contraction. The s concluded 7 years of 52 patients who underwent heart angioplasty in patients with heart failure showed that the preoperative mortality rate 23% (12/52), postoperative mortality 20% (8 / 40), 7 years after the actual survival rate of 70.4 %. Follow-up was found to improve heart function in patients, LVEF increased. Cardiac catheterization showed pulmonary artery pressure, pulmonary capillary wedge pressure and left ventricular pressure did not change significantly. When the heart transplant taboo, this method can be used as alternative methods. The operation mechanism of action to improve the heart function is: skeletal muscle surrounding the heart, play a winding effect, in order to stop the reconstruction of cardiac failure; active muscle contraction, heart failure secondary enhanced contractility. (3) left ventricular assist device (LVAD): Cooley and other first proposed temporary mechanical circulatory support for advanced heart failure awaiting heart transplantation in patients with transitional period. The reported left ventricular assist device (LVAD) are both TCI and Navaco be buried LVAD. LVAD placement, including the body drive control unit and battery box in vitro. Department placed in the abdominal cavity driven by the inflow tube and outflow pipes are connected through the diaphragm and the proximal ascending aorta, left ventricular. Percutaneous leads connect the drive and control of the Department of the Ministry and the battery compartment. Driven placement in the opposite direction within the Department of Driver 2 pieces, a bioprosthetic valve (porcine pericardium) and energy converters can be directly pumped into the left ventricle aortic blood. Control Division and the battery box in vitro can be hung on the belt or placed in the bag for easy carrying. LVAD can provide the maximum stroke volume 70ml, pump discharge amount of 10L/min. Frazier et al reported a multicenter clinical trial, 34 patients with advanced heart failure awaiting heart transplantation after LVAD patients with liver and renal function improved cardiac function, LVAD use of time and even more than 300 days; 65% of patients to undergo heart transplant. LVAD placement of the following complications may occur: bleeding, infection, right heart failure, hemolysis, peripheral organ dysfunction and thrombosis embolism. However, LVAD awaiting heart transplantation is still regarded as a treatment method for the transition period. (4) heart transplantation: 1967 Barnard completed the first heterotopic heart transplantation with 30 years of heart transplantation from experimental stage to clinical stage, the current applications are more widely in the international arena. Hosenpud et al reported that the international registration of heart transplantation (including 301 heart transplant centers) from 1982 to March 1998, the world total of 45,993 cases of heart transplantation, 1 year survival rate of 97%, 5-year survival rate of about 65%, half of the deaths time of 8.7 years, the annual mortality rate of about 4%. Over time, technological advances, the survival rate increases. Half the time of death from 1980 to 1985 was 5.3 years, from 1986 to 1990 was 8.8 years, 1991 to 1997 was 9.4 years. Heart transplantation is currently more mature, can improve patient survival and improve cardiac function, quality of life. Is the effective treatment of patients with advanced DCM methods. Heart transplantation following problems: the lack of donor; expensive; postoperative infection; after rejection. Heart transplantation in China started late, the relatively slow development. Shanghai Ruijin Hospital, 1978 first heart transplant patients survived 109 days. Zhen Hospital, Beijing 1992, Mudanjiang Cardiovascular Hospital, Second Affiliated Hospital of Harbin Medical University, has reported a successful heart transplant, who currently live more than 5 years. 1993, Fu Wai Hospital, Beijing reported that heart and lung transplantation. So far a limited number of cases of heart transplantation, compared with international standards, have significant gaps. (5) from skeletal muscle satellite cell transplantation: a recently developed for the treatment of dilated cardiomyopathy, myocardial infarction and other diseases, a new surgical approach. The basic principle is more differentiation of appliances, skeletal muscle stem cells by transplanting methods, to replace the function of low or no myocardial function. Differentiation of transplanted cells in the myocardium of mature cardiac myocyte contraction is similar to the structure, electrophysiological properties of striated muscle cells and cardiac function with enhanced effects. This method is experimental research stage, the clinical effects, especially long-term efficacy has not been reported. Prevention of sudden death 1. To correct heart failure, reduce wall tension. 2. To correct hypokalemia hypomagnesemia. 3. To improve the neurohormonal disorders, the choice of ACEI and metoprolol. 4. Avoid drug factors, such as digitalis, diuretics side effects. 5. Amiodarone can effectively control the arrhythmia. Prognosis of dilated cardiomyopathy course of varying lengths, faster development at 1 to 2 years who died, those who can survive up to 20 slow years, depending on the degree of cardiac enlargement, is associated with serious arrhythmias and refractory heart failure. Dilated cardiomyopathy reported in the literature of natural history, course and outcome, subject to patient selection, the use of diagnostic methods and standards, when the patients were enrolled and follow-up time of the impact of various factors, survival or mortality vary. The results of many studies indicate that dilated cardiomyopathy with poor prognosis, high mortality. According to historical statistics, dilated 1-year survival rate of 58% to 63%, 5-year survival rate of 33% to 40%, 10-year survival rate of 20%; and 1 year mortality of 25% to 58%, 2 years 30% ~ 48% mortality, 5-year mortality of 50% to 80%, 10-year fatality rate was 70% and 92%. Dilated cardiomyopathy because of many factors, and their differences in treatment conditions, especially in the etiology of the disease and risk factors has not been elucidated, nor specific diagnostic criteria, survival and mortality can be understood on many different reports. Most patients with dilated cardiomyopathy who died of refractory heart failure, sudden death a few individual died of pulmonary embolism or other causes. Died of heart failure were more common heart failure, left heart failure, followed by right heart failure less. Most of sudden death and malignant ventricular arrhythmia episodes related. Some research results showed that the prognosis of dilated cardiomyopathy an improving trend. Di Lenarda and other research from 1978 to 1994, 235 cases of dilated cardiomyopathy morbidity and mortality, each designated as a 5-year research phase, to death or heart transplantation as the endpoint of the study. 2-year survival rate was found in 1978 to 1982 to make the diagnosis group ( group, a total of 26 patients) was 73.8%; in 1983 to 1987 group ( group, a total of 65 cases) 87.7% in 1988 to 1992 group ( group, a total of 144 patients) was 93.3%; 4-year survival rate in the three groups were 53.8%, 72.3% and 82.9%. This shows that dilated cardiomyopathy in 15 years the number of cases the disease gradually increased, and gradually reduce the number of death cases. Of analysis, subjects in the age of light, early diagnosis and in recent years by application of ACEI, blockers were increased, dilated cardiomyopathy is the reason for increased survival. Preventi. To correct the cause, and incentives such as nutritional deficiencies should be corrected, and long-term alcohol consumption to be alcohol, then alcohol treatment such as relapse after recovery is more difficult to treat. Perinatal cardiomyopathy should be persuaded to contraception or sterilization in order to avoid recurrence. Seen in Keshan disease endemic areas may be given selenium salt treatment. Upper respiratory tract infection induced dilated cardiomyopathy a common cause of heart failure, especially in susceptible season (winter and spring), timely application of antibiotics, appropriate use of transfer factor, gamma globulin, in order to improve immunity, prevention of respiratory tract infections. 2. Note that rest can reduce the burden on the heart and promote cardiac recovery. According to the patient's cardiac function, limit or avoid physical and mental work, appropriate to the symptoms do not occur, but does not advocate a complete rest. There was expansion of heart failure and heart are required to stay in bed, to rest a long time. 3. Public education and care to fully understand the symptoms, analyze the pathophysiological changes and cardiac function. Congestive heart failure, in addition to reasonable limits activities, should be severely restricted sodium intake. The standard low-salt diet, the general control of salt in the 5g / d less severe disease control in the 1g / d below. Spit to the patient medication knowledge and understanding of the overall condition of patients regularly adjust the treatment. According to reports, educational care group mortality was significantly lower than educational care group. Health Tips nutritional deficiencies should be corrected, and long-term alcohol consumption to be alcohol, then alcohol treatment such as relapse after recovery is more difficult to treat. Perinatal cardiomyopathy should be persuaded to contraception or sterilization in order to avoid recurrence. Seen in Keshan disease endemic areas may be given selenium salt treatment. Improve immunity, prevention of respiratory tract infections. Rest can reduce the burden on the heart and promote cardiac recovery. According to the patient's cardiac function, limit or avoid physical and mental work, appropriate to the symptoms do not occur, but does not advocate a complete rest. There was expansion of heart failure and heart are required to stay in bed, to rest a long time.


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