Dilated cardiomyopathy

Introduction to dilated cardiomyopathy Dilated cardiomyopathy is a common type of primary cardiomyopathy. It is characterized by a significant enlargement of the left ventricle (most) or the right ventricle, and is accompanied by varying degrees of cardiac hypertrophy, ventricular systolic dysfunction, heart enlargement, heart strength Failure, arrhythmia, embolism is a basic feature. It used to be called congestive cardiomyopathy. The disease is often accompanied by arrhythmia, the condition is progressively aggravated, death can occur at any stage of the disease, and about 20% of DCM patients have a family history of cardiomyopathy. basic knowledge The proportion of illness: the incidence rate is about 0.005% - 0.006% Susceptible people: good for people aged 30-50 Mode of infection: non-infectious Complications: sudden death, heart failure, pleural effusion, ascites, arrhythmia, atrial fibrillation

Cause of dilated cardiomyopathy

Virus infection (30%)

The persistence of viral RNA in the body after viral infection is a risk factor for viral myocarditis to progress to dilated cardiomyopathy. Mouse animal experiments have shown that Coxsackie virus can dissolve cardiomyocytes, and enterovirus protease can cause myocardial cytoskeleton destruction. This change is recognized as a major feature of dilated cardiomyopathy. Viral damage to cardiomyocytes can occur during periods of high viral titer (Coxsack B1, B4 virus infection) or virus (Coxsack B3 virus) At the beginning of the immune response after infection, the damage of the virus to the myocardial tissue can be directly damaged or damaged by the immune mechanism. When the viral RNA persists in the myocardium, the T lymphocytes can infiltrate the myocardial tissue.

Studies have shown that low-level expression of viral genes can cause chronic progressive myocardial damage. When viral RNA persists in the myocardium for more than 90 days, the myocardium may present pathological changes similar to dilated cardiomyopathy.

When the body's defense ability is reduced, the body can be in a state of chronic virus carrying. In this chronic process, the virus can exist in the spleen, liver, pancreas and whole body lymph nodes. The harm is not the direct invasion of the myocardium, but the immunity of the body. The reaction; while the persistent presence of viral RNA can still replicate, producing a large amount of viral RNA that is non-invasive but antigenic, induces the body's immune response, causing myocardial damage.

Autoimmune response (25%)

It is currently speculated that immune-mediated myocardial damage is an important mechanism for the pathogenesis of DCM.

1 humoral immunity: a variety of anti-myocardial autoantibodies can be detected in serum samples from patients with dilated cardiomyopathy, including anti-mitochondrial ADP/ATP carrier antibodies, anti-1-adrenergic receptor antibodies, and anti-M2 cholinergic receptors. Antibodies, anti-heat shock protein antibodies, anti-myosin heavy chain antibodies, branched chain alpha ketoacid dehydrogenase (BCKD) complex antibodies and laminin antibodies, etc. Autoantibodies play an important role in the pathogenesis of this disease.

A. Anti-mitochondrial ADP/ATP vector (ANT) antibody: Studies have found that ANT and pathogen proteins share a common antigenic determinant, such as ANT amino acid sequence 27-36 and Coxsackie B3 virus arginine sequence 1218-1228, Autoantibody production is caused by cross-reaction, and studies have suggested that viral infection causes mitochondrial isolation of antigen release, or changes in myocardial antigen properties, or activation of autoreactive T lymphocytes by bypass, thereby inducing autoimmune responses against mitochondria.

Anti-ANT antibody can inhibit ATP/ADP transport of myocardial mitochondria, leading to myocardial cell energy metabolism disorder and impairing myocardial function. ANT and calcanin may also have the same antigenic determinant. Anti-ANT antibody can interact with calcium channel protein on myocardial cell membrane. The combination inhibits calcium channel inactivation, promotes calcium influx, and overloads intracellular calcium, leading to degeneration and necrosis of cardiomyocytes. In other words, calcium overload caused by anti-ANT antibody activation of Ica is one of the causes of myocardial damage in DCM patients.

B. Anti-1-receptor antibody: -receptor G protein-coupled membrane receptor, when -receptor is activated by binding to neurohumoral transmitter, when the physiological effect is produced, the receptor is invaginated, and Lysosomal fusion, proteolytic enzymes to degrade, lysosomes can bind to nuclear receptors containing major histocompatibility complex (MHC) molecules on the surface, if the receptor peptide produced after degradation can form with MHC molecules a complex that can be transported to the surface of the membrane, presented to the helper T lymphocyte (TH) receptor, activates TH, and activates TH to interact with B lymphocytes to produce antibodies specific for the self-receptor polypeptide molecule. Under normal circumstances, cardiomyocytes do not express MHC-like molecules, and only when they have immunological activity, they express MHC-like molecules. Viral infection can induce cardiomyocytes to express MHC-like molecules, making cardiomyocytes become antigen-presenting cells, and viruses and The -receptor molecule has a common antigenic determinant that can cause anti-beta receptor antibody production through a mimetic mechanism.

Anti-1 receptor antibodies activate Ca2 channels of receptors, increase Ca2 influx in cardiomyocytes, cause calcium overload, cause myocardial cell damage, and anti-1 receptor antibodies increase cAMP-dependent protein kinase (PK) activity in cardiomyocytes By binding to the receptor, the ratio of cytoplasmic to plasmid PK activity is significantly increased, resulting in cytoplasmic and plasmid cAMP-dependent PK activation, achieving positive degeneration, and some authors believe that anti-1-receptor antibodies can affect cardiomyocytes. The transmission of information causes the metabolism of cardiomyocytes regulated by the receptor to be disordered, and the number of -receptors in the cardiomyocytes is down-regulated to induce myocardial damage.

C. Anti-myosin antibody: It is currently believed that there are two mechanisms that cause an immune response in patients with dilated cardiomyopathy, producing anti-myosin antibodies: a. viral infection or other causes of myocardial tissue necrosis leading to myosin release and Exposure, triggering the body's autoimmunity; b. Viral molecules have similar antigenic determinants to myosin.

D. Anti-M2 cholinergic receptor antibody: M2 cholinergic receptor is a protein located on the membrane of cardiomyocytes, which belongs to the G protein-coupled membrane receptor, and synergizes with -receptor to regulate myocardial adenylate cyclase. The activity and ion channels regulate cardiac function, while the anti-M2 cholinergic receptor antibody has a cholinergic-like effect, which can reduce the increase of cyclic adenosine monophosphate (cAMP) concentration caused by isoproterenol in guinea pig ventricular muscle. Slows the contraction frequency of ventricular myocytes, slows the maximum rate of increase in ventricular pressure, and slows heart rate. This inhibition by anti-M2 cholinergic receptor antibodies can be offset by the cholinergic antagonist atropine or by neutralizing antibodies. The production of the antibody may be caused by the activation of an autoimmune reaction by causing the M2 cholinergic receptor to become an autoantigen after viral infection.

E. Other antibodies: In addition to the above several anti-myocardial autoantibodies, anti-mitochondrial M7 antibodies, anti-BCKD complex antibodies, anti-actin antibodies, anti-muscle ATPase antibodies, etc. are also present in the serum of patients with dilated cardiomyopathy. .

Although approximately 30% to 40% of patients with dilated cardiomyopathy have organ and disease-specific autoantibodies in their serum, some patients do not develop anti-autoantibodies, which may be related to several factors: a. dilated cardiomyopathy Is a multifactorial disease, lack of autoantibodies to cause damage caused by cellular immunity or caused by other factors; b. autoantibodies of the heart may be early signs of the disease, disappear with the prolongation of the disease; c. different expansion Different types of autoantibodies can occur in patients with cardiomyopathy, and negative results can be produced due to different detection methods and types of detection; d. The production of autoantibodies is related to human leukocyte antigens.

2 Cellular immunity: In dilated cardiomyopathy, cell-mediated abnormal immune responses appear to impair lymphocyte function, alter the proportion of lymphocyte subsets and activate the immune cytokine system, and peripheral blood T cells in patients with dilated cardiomyopathy ( CD3), inhibitory/cytotoxic T cells (CD8) were significantly reduced, and there was no significant change in helper/inducible T cells (CD4). Studies have shown that cytotoxic T lymphocytes have the effect of lysing virally infected cardiomyocytes in vitro, virus After infection, a polypeptide called T cell receptor can be present on the membrane of cardiomyocytes. T lymphocytes recognize and bind to this receptor, which can cause myocardial cell damage. Application of anti-T cell receptor antibody can damage myocardial cells. In addition, natural killer cells can secrete a perforin, which causes the cardiomyocytes to form a pore-like lesion.

The role of 3 cytokines: the level of inflammatory factors in serum of DCM patients was significantly increased, the ratio of tumor necrosis factor (TNF) / interleukin (IL)-10 was positively correlated with plasma adrenaline levels; serum TNF receptor (sTNFR) levels and Left ventricular size was correlated; interleukin content was positively correlated with myocardial weight and degree of myocardial fibrosis. Interferon gamma and TNF- induced intercellular adhesion molecule-1 (ICAM-1) on the surface of cardiomyocytes, the latter in the myocardium The role of cells and lymphocytes is linked.

Genetics (25%)

The family genetic predisposition of dilated cardiomyopathy is inferior to hypertrophic cardiomyopathy, but genetic factors still play a role. The family chain of dilated cardiomyopathy is more common than usual, and 20% of patients have first-degree relatives. Evidence for dilated cardiomyopathy suggests that family inheritance is relatively common.

Typical familial cardiomyopathy is neuromuscular disease, such as Duchenne muscular dystrophy, Becker chronic progressive muscular dystrophy associated with X-linked inheritance, both of which are dystrophin genes (a cytoskeletal protein) mutation. Recently, the absence of a cardiac catalyzed region associated with the dystrophin gene has been confirmed in a family with cardiomyopathy associated with X-linked inheritance but no skeletal muscle disease. It has been reported that mitochondria exist in familial cardiomyopathy. Abnormalities, such as Kearns-Sagre syndrome: cardiomyopathy, ophthalmoplegia, retinopathy, and cerebellar ataxia, in addition to muscle protein and metabolic abnormalities, genetic factors also affect the triggering of anti-myocardial immune responses, members of the same family in the virus Heart failure after infection or pregnancy, most familial cases are autosomal dominant, but the disease is genetically heterogeneous, has been reported autosomal recessive 49 and X-linked inheritance The promoter region of a type of familial X-linked dilated cardiomyopathy gene and the first outer code encoding dystrophin The latter protein is one of the components that make up the myocyte cytoskeleton. It is speculated that the deficiency of cardiac dystrophin caused by the above gene changes is the cause of dilated cardiomyopathy. In addition, mitochondria have also been reported. Mutations in DNA are still unknown as to whether the genetic susceptibility of dilated cardiomyopathy in patients without a significant family chain is present.

A number of chromosomal loci associated with dominant inheritance of familial cardiomyopathy have been identified, including chromosome 1 (q32, p1-q1), chromosome 2 (q31), chromosome 5 (q33-34), chromosome 6. (q12-16), chromosome 9 (q13-22), chromosome 14 (q11), chromosome 15 (q14, q22), and the dominant site of DCM patients with mitral valve prolapse is located at 10 Chromosome (q21-23).

Pathogenesis

Recent studies have shown that most dilated cardiomyopathy is associated with viral infection and autoimmune response. It has been found that viral myocarditis can evolve into dilated cardiomyopathy, which can be found in endocardial biopsy specimens of patients with myocarditis and dilated cardiomyopathy. Enterovirus genes, serum of patients with dilated cardiomyopathy can detect a variety of anti-myocardial autoantibodies, such as anti-ADP/ATP carrier antibodies, anti-1 adrenergic receptor antibodies, anti-M2 cholinergic receptor antibodies and anti-muscle Globulin heavy chain antibodies, etc., can also detect enterovirus gene fragments, viral infection and immune response damage theory is the main pathogenesis of current dilated cardiomyopathy, in addition, genetic factors may also play a role.

Dilated cardiomyopathy is the final result of myocardial damage caused by long-term effects of various factors (the main cause of DCM, infection or non-infectious myocarditis, alcoholism, metabolism, etc. may be related to the onset of dilated cardiomyopathy, short-lived Myocardial injury (such as exposure to toxic substances) may be fatal to some cardiomyocytes, but the residual cardiomyocytes will increase the load and compensatory hypertrophy. This compensatory change can still be early. Maintains the overall function of the heart, but will eventually manifest as myocardial contraction and diastolic dysfunction. Myocarditis has both irreversible cardiomyocyte death and reversible myocardial inhibition mediated by cytokines, although certain factors (such as alcohol) are Does not directly damage the cardiomyocytes, but can cause severe cardiac dysfunction if long-term effects, in addition, many injuries will also affect the heart's fibrous stent system, affecting myocardial compliance, and thus participate in the occurrence and development of ventricular enlargement.

Dilated cardiomyopathy prevention

1. Correct the cause and cause: If the lack of nutrition should be corrected, it is necessary to stop drinking after long-term drinking. If the drink relapses after treatment recovery, it is more difficult to treat. Perinatal cardiomyopathy should be contraceptive or sterilized to avoid recurrence. Seen in the epidemic area of Keshan disease can be treated with selenium salt, upper respiratory tract infection is a common cause of cardiac dysfunction induced by dilated cardiomyopathy, especially in the easy infection season (winter and spring), timely application of antibiotics, use transfer factor as appropriate, Globulin to improve the body's immunity and prevent respiratory infections.

2. Pay attention to rest: Rest can reduce the burden on the heart, promote myocardial recovery, limit or avoid physical and mental work according to the patient's heart function, it is appropriate to not have symptoms, but does not advocate complete rest, heart failure and obvious heart Expander, must stay in bed, take a longer rest, improve myocardial metabolism, avoid hypoxia, avoid fatigue, infection, toxins, alcohol, high blood pressure and other possible predisposing factors, Keshan disease may lack trace elements in drinking water and food Selenium or other substances are related, so selenium should be added.

3. Publicity and education: Fully understand the symptoms of patients, analyze their pathophysiological changes and heart function status. In the case of congestive heart failure, in addition to reasonable restrictions on activities, the sodium salt intake should be strictly limited. Generally, the salt is controlled below 5g/d. If the condition is severe, it is controlled below 1g/d. It is necessary to give the patient a knowledge of the drug and understand the overall condition of the patient, and regularly adjust the treatment plan. It is reported that there is a disease in the education and care group. The rate was significantly lower than the non-educational care group.

4. Factors that may cause cardiomyopathy should be avoided: active prevention and treatment of digestive and respiratory viral infections to prevent myocarditis, prevention and treatment of protozoa such as type 3 protozoa, and prevention of various infections, thereby avoiding myocardial damage caused by infection. Antigen-antibody reaction, avoiding coronary artery spasm, myocardial ischemia caused by obstruction, so that the myocardium does not show scattered and focal necrosis and fibrosis.

Dilated cardiomyopathy complications Complications sudden cardiac failure pleural effusion ascites arrhythmia atrial fibrillation

The duration of this type varies, the short ones die within 1 year after the onset, and the elders can survive for more than 20 years. All patients with enlarged heart, persistent heart failure or arrhythmia have poor prognosis, patients with liver and impaired renal function. The prognosis is also extremely poor, and many patients may have sudden death.

1, heart failure

Patients with dilated cardiomyopathy due to myocardial lesions, enlarged heart, left ventricular dilatation or biventricular dilatation, causing left ventricular systolic dysfunction, systolic heart failure, with progression of the disease, right heart failure or total heart failure, dilated myocardial Echocardiographic features of patients with heart failure:

1 left ventricular enlargement, due to extensive myocardial lesions, the four heart chambers have different degrees of expansion, the left ventricle is expanded into a spherical pattern, the ventricular swells forward, and the anterior wall of the aorta moves forward, while the nipple The position is displaced to the posterior side, not at the same level as the posterior wall of the aorta. The M-type shows that the anterior wall of the aorta continues to the interventricular septum, and the interventricular septum bulges forward while the posterior wall of the aorta continues with the anterior mitral valve. The position of the anterior lobe of the mitral valve is displaced backwards, and the two form a "bell" shape, and the left ventricular outflow tract is widened.

2 mitral valve changes, due to weakened myocardial contractility, left ventricular diastolic pressure is higher, mitral valve flow is reduced, mitral valve motion amplitude is reduced, and the enlarged left ventricular cavity is "large heart cavity small opening" change,

3 The ventricular wall motion was weakened, and the left ventricular wall was generally thinned with a diffuse reduction in the consistency of the activity.

2, pleural effusion

This disease is the most common cause of congestive heart failure. Edema is an important sign of right heart failure. It often starts from the low drooping part and gradually rises. In severe cases, pleural effusion and ascites may occur. When the patient is admitted to the hospital, there is a small amount of pleural effusion. The reason may be for:

1 total heart failure caused by the pleural wall to the venous return disorder, and caused the pleural visceral venous return disorder, so that the body and pulmonary venous pressure increased significantly, causing pleural effusion.

2 Chronic congestive heart failure causes long-term blood stasis in the liver, hypoxia, hepatocyte necrosis, atrophy and disappearance in the central area of the hepatic lobules, eventually leading to liver dysfunction; gastrointestinal tract bleeding during heart failure, making its digestive function low, so that Insufficient caloric and protein intake, both factors can lead to hypoproteinemia, lower plasma osmotic pressure, and water leaking into the chest to form pleural effusion.

3, arrhythmia

Dilated cardiomyopathy is prone to arrhythmia due to poor cardiac function, mainly due to atrial muscle damage, altered electrophysiological physiology, increased excitability of ectopic rhythm points and reentry movement, and affects myocardial contractile function, making the atria and Venous congestion! Atrial enlargement, increased intraventricular pressure, more damage to the atrial muscle, atrial arrhythmia increased, when the atrial enlargement significantly, the intraventricular pressure increased significantly, the atrial muscles undergo extensive degeneration and necrosis, resulting in atrial electrical Inconsistent activities, resulting in tortuous and complex circular motion, thus forming atrial fibrillation, diverse and variable arrhythmia and high incidence of its prominent features, early ventricular, early atrial and conduction block (atrioventricular block and bundle conduction resistance) Hysteresis is the most common arrhythmia, tachycardia, atrial fibrillation (20%), bradycardia is common, severe ventricular tachycardia can occur, and even ventricular fibrillation or arrest can cause death.

4, sudden cardiac death

It is the most serious complication of dilated cardiomyopathy, and it is also the main cause of death of dilated cardiomyopathy. The incidence of sudden cardiac death can be as high as 30% or more.

5, arterial embolism

The disease is complicated by thrombosis and embolic complications. Most studies and observations have found that the main part of thrombosis in dilated cardiomyopathy is the left ventricular apex and two auricles. The thrombus falls off to form an embolus, which causes embolism and embolism complications to the lungs. Brain, spleen and kidney embolism are more common.

Symptoms of Dilated Cardiomyopathy Common Symptoms Weak Hypertension Abdominal Discomfort Difficulty Heart Expansion Shoulder Arrhythmia Heart Failure Tide Breathing Ascites

First, symptoms and signs

The disease is slow onset, can occur at any age, more common in 30 to 50 years old, some patients have a history of primary hypertension, the onset is slow, the initial examination revealed a heart enlargement, cardiac function compensation without conscious discomfort After a period of time, the symptoms gradually appear. This period can sometimes reach more than 10 years. The main performances are as follows:

Symptom

(1) Congestive heart failure: the most prominent manifestation of this disease, of which air urgency and edema are the most common, which is mainly due to decreased ventricular contractility, decreased compliance and fluid retention, resulting in insufficient cardiac output and/or The ventricular filling pressure is excessively increased, and symptoms of left ventricular dysfunction may occur. Common symptoms include progressive fatigue or progressive labor endurance, labor dyspnea, sitting breathing, and paroxysmal nocturnal dyspnea. Performance, symptoms of right heart failure at the same time in the late stage of the disease: such as large liver, upper abdominal discomfort and peripheral edema.

(2) arrhythmia: a variety of rapid or slow arrhythmia can occur, even the first clinical manifestations of the disease; severe arrhythmia is a common cause of sudden death of the disease.

(3) embolism: heart, brain, kidney or pulmonary embolism can occur. The thrombus originates from the enlarged ventricle or atrium. Especially when accompanied by atrial fibrillation, peripheral blood vessel embolism is the first symptom of the disease.

(4) Chest pain: Although the main coronary artery is normal, there are still about one-third of patients with chest pain, which may be related to pulmonary hypertension, pericardial involvement, microvascular myocardial ischemia and other unknown factors.

2. Signs

(1) The apex beats are obviously shifted to the left side, but the left ventricle may not appear when it is enlarged backwards; the apex beats are often diffuse; the right ventricular pulsation can be reached under the xiphoid or the left sternal border during deep inhalation.

(2) It is often heard that the third and fourth heart sounds are "running horses", but no gallbladder can not exclude heart failure, and the third heart sound enhancement reflects the excessive load on the ventricular volume.

(3) There is obvious mitral regurgitation murmur when the heart function is decompensated. The murmur is most clear under the armpit. It can often be relieved after the heart function is improved. Sometimes it can be associated with the tricuspid regurgitation murmur of the sternum. Overlapping, but the latter generally occurs later in heart failure.

(4) Patients with alternating pulse and tidal breathing with obvious heart failure, pulmonary hypertension increased significantly, and transient, moderately adjusted pulmonary murmurs were heard early in diastole.

(5) When the right heart is insufficiency, cyanosis, jugular vein engorgement, hepatomegaly, lower extremity edema, and a few chest and ascites can be seen.

Diagnosis can be based on clinical manifestations, adjuvant examinations, and exclusion of other common heart conditions such as rheumatic, coronary atherosclerosis, congenital, hypertensive or pulmonary heart disease, and pericardial disease or acute myocarditis. , can refer to the following diagnostic criteria:

1 The onset is slow, with congestive heart failure as the main performance;

2 heart expansion, galloping, can appear a variety of arrhythmia;

3X line inspection shows that the heart shadow is enlarged;

4 ECG shows cardiac hypertrophy, myocardial damage, arrhythmia;

5 echocardiography shows that the intraventricular diameter is enlarged, the wall motion is weakened, and the left ventricular ejection fraction is reduced to less than 50%;

6 exclude other heart diseases.

Examination of dilated cardiomyopathy

The methods of examination that contribute to this disease are:

Laboratory inspection

1. Serological examination may have an increase in erythrocyte sedimentation rate, abnormal globulin, and occasionally enhanced myocardial enzyme activity, considering that DCM can be evolved from myocarditis.

2. Anti-myocardial antibody and virus detection is very necessary, and it is possible to detect a variety of anti-myocardial autoantibodies; continuous measurement of viral titers may contribute to the diagnosis of viral myocarditis.

3. Peripheral blood eosinophils should be further examined for the presence of systemic allergic disease, as these diseases can cause allergic myocarditis.

Auxiliary inspection

1. ECG often shows left atrial and / or left ventricular enlargement, but R wave abnormal increase is less common; there may be QRS wave low voltage, more common RV6> RV5; chest lead often see pathological Q wave, many Patients may have non-specific QRS wave broadening; about 1/4 of patients may have atrial fibrillation, and about 20% of patients may have left bundle branch block; except for Chagas disease, right bundle branch block is less common, PR Prolongation is also quite common and is associated with a reduction in survival in some patients. Severe blockade may indicate giant cell myocarditis or sarcoidosis, non-specific ST-segment depression and T-wave changes are common.

2. Chest X-ray examination of the heart enlargement to prominent performance, with the left ventricle enlarged main, accompanied by right ventricular enlargement, may also have left atrium and right atrium enlargement, because the sensitivity of the chest radiograph reflecting right ventricular enlargement is greater than the left ventricle expansion High, and right heart failure often indicates a poor prognosis, so the chest radiograph has a certain significance for prognosis. Kerer B line can be seen in pulmonary venous hypertension, and heart beat is weakened under fluoroscopy when there is pericardial effusion.

3. Echocardiography can determine whether there is left, right ventricular enlargement and decreased myocardial contractility, and it is helpful to identify other types of cardiomyopathy as well as valvular disease, congenital heart disease, etc., and its characteristic changes are left and right ventricular cavity. Increased and left ventricular posterior wall motion weakened, the interventricular septum can be contradictory, the thickness of the interventricular septum and ventricular free wall is thin, but it can also be normal, the short axis shortening rate is significantly reduced, visible functional mitral regurgitation, followed by Functional mitral regurgitation in DCM usually has no abnormal changes in the valve or chordae, and diffuse wall motion in DCM is also different from local ventricular dyskinesia in coronary heart disease, left ventricular enlargement, left ventricular outflow The dilation of the tract, the interval between the ventricular septum and the posterior wall of the left ventricle was weakened, and the sum of the amplitudes of the two strokes was <13 mm.

4. Cardiac catheterization In most patients with heart failure with heart enlargement, careful consideration should be given to coronary angiography in order to exclude coronary atherosclerosis or deformity. When there is a compensatory hemodynamic change in heart failure Right heart catheter measurement of cardiac output and ventricular filling pressure is helpful for clinical judgment and guidance of treatment.

5. Endocardial biopsy The absolute indication of endomyocardial biopsy is the monitoring of heart transplant rejection and anthracycline antibiotic myocardial toxicity. The following two groups of dilated cardiomyopathy may consider myocardial biopsy: 1 symptom appears in 3 months or less; 2 unexplained myocardial disease, lymphocyte infiltration as a histological manifestation in the first group of patients with a positive rate of 5% to 20%, less than 10% of the second group of patients, due to The significance of the above-mentioned histological changes is not known. If there are other diagnoses based on this diagnosis, it is necessary to consider the significance of definite diagnosis for treatment or prognosis when deciding on endocardial biopsy. How large, with the new biochemical technology to replace the existing staining and further development of the microscope, the application of myocardial biopsy will be more extensive.

6. Isotope examination: Isotope myocardial perfusion and visualization, mainly manifested by enlarged heart chamber, especially bilateral ventricular enlargement, myocardial development is said to be diffuse sparse.

Diagnostic identification of dilated cardiomyopathy

diagnosis

1. The clinical manifestations are heart enlargement, ventricular systolic function with or without congestive heart failure, often arrhythmia, complications such as embolism and sudden death.

2. Heart enlargement X-ray examination heart-thorax ratio>0.5, echocardiography shows heart enlargement, especially left ventricular enlargement, left ventricular end diastolic diameter 2.7cm/m2, heart can be spherical.

3. Ventricular systolic function was reduced by echocardiography. The wall motion was diffusely weakened and the ejection fraction was less than normal.

4. Other specific (secondary) cardiomyopathy and endemic cardiomyopathy (Keshan disease) must be excluded, including ischemic cardiomyopathy, peripartum cardiomyopathy, alcoholic cardiomyopathy, metabolic and endocrine diseases such as Hyperthyroidism, hypothyroidism, amyloidosis, diabetes, etc., cardiomyopathy caused by genetic familial neuromuscular disorders, systemic diseases such as systemic lupus erythematosus, rheumatoid arthritis, etc. Cardiomyopathy, toxic cardiomyopathy, etc. can diagnose idiopathic dilated cardiomyopathy.

Conditional patients can detect anti-cardiomyocyte peptide antibodies in patients' serum, such as anti-myocardial mitochondrial ADP/ATP carrier antibody, anti-myosin antibody, anti-1-receptor antibody, anti-M2 cholinergic receptor antibody, as an auxiliary for this disease. Diagnosis, clinically difficult to distinguish with coronary heart disease need to be coronary angiography.

Endomyocardial biopsy: pathological examination is not specific for the diagnosis of this disease, but it is helpful for differential diagnosis of specific cardiomyopathy and acute myocarditis. Endocardial biopsy specimens are used for polymerase chain reaction (PCR) or in situ hybridization. To facilitate the diagnosis of the cause of the infection; or to carry out genetic analysis of specific cell abnormalities.

In recent years, endocardial myocardial biopsy has been performed clinically. Specimens obtained from cardiac catheters with biopsy forceps for pathological and viral examinations can be used to find evidence of myocardial inflammation, but the current diagnostic criteria for histopathology and There are still some problems to be solved in removing artifacts.

Differential diagnosis

DCM lacks specific diagnostic indicators, and the establishment of the diagnosis often excludes other organic heart disease and needs to be identified with the following types of heart disease.

(1) Rheumatic heart disease Cardiomyopathy may also have systolic murmurs in the mitral or tricuspid valve area, but generally do not have diastolic murmurs. The former heart murmur is louder in heart failure, and after heart failure control, the murmur is reduced or Disappeared, while the latter in the heart failure control, the noise is obvious, and often accompanied by mitral stenosis and / or aortic valve murmur, in the continuous auscultation follow-up to help differential diagnosis, echocardiography can show significant pathology of the valve Sexual changes, but no cardiomyopathy, but the obvious expansion of the atrioventricular ring.

(B) the pericardial effusion cardiomyopathy when the heart is enlarged, the heart beat is weakened, and it must be distinguished from the pericardial effusion. When the pericardial effusion is left, the left outer rim is percussed as a real sound, the apex beats disappear, the heart sound is far away, and the left sound is in the real world. Hearing on the inside, echocardiography can clearly see the pericardial effusion area and determine the amount of fluid accumulation, make a definite diagnosis, DCM in the heart failure even if there is pericardial effusion, the amount is very small, and has a large heart chamber II The characteristics of the small cusp opening, the apical beat of the cardiomyopathy shifts to the left and the left, which is consistent with the left outer edge of the heart sounding boundary. The apical beat of the pericardial effusion is often not obvious or is located inside the left outer edge of the heart sounding boundary. Pleural or tricuspid systolic murmur, ventricular hypertrophy on the electrocardiogram, abnormal Q wave, various complex arrhythmias, all indicate cardiomyopathy, it is not difficult to distinguish between the two by ultrasound, and the amount of liquid flat or dark area in the pericardium Pericardial effusion, heart enlargement is cardiomyopathy, must pay attention to cardiomyopathy can also have a small amount of pericardial effusion, but not enough to cause cardiac tamponade, nor affect the heart's signs and heart function, only the discovery of ultrasound Shrinkage time Period when cardiomyopathy obvious abnormalities, pericardial disease is normal.

(3) Hypertensive heart disease Cardiomyopathy may have temporary hypertension, but the diastolic blood pressure does not exceed 14.67 kPa (110 mmHg), and occurs in acute heart failure, blood pressure declines after heart failure improves, and hypertensive heart disease Different, fundus, urine, normal kidney function.

(4) Patients with middle-aged coronary heart disease, if there is heart enlargement, arrhythmia or heart failure without other reasons, coronary heart disease and cardiomyopathy must be considered, and there are risk factors such as hypertension, hyperlipidemia or diabetes. Segmental abnormalities are conducive to the diagnosis of coronary heart disease, a small number of patients with severe coronary heart disease, multiple small infarcts in the myocardium or extensive fibrosis due to chronic ischemia, the heart chambers are enlarged, sometimes difficult to distinguish from DCM, the following Several points are helpful for differential diagnosis: 1DCM patients are younger and have no typical symptoms of angina; 2 patients with coronary heart disease have abnormal Q-wave and ST-T changes consistent with coronary blood supply, while DCM ST-T changes Widely, even Q waves are atypical, and there is no corresponding relationship with coronary blood supply distribution; 3 echocardiography, coronary heart disease mostly left ventricular involvement, necrotic myocardial no contraction function or opposite pulsation, segment Sexual distribution, DCM, all rooms are enlarged, myocardial exercise is generally weakened; 4 selective coronary angiography can exclude or affirm the diagnosis of coronary heart disease; 5 myocardial nucleus examination, in recent years For coronary artery disease, long-term extensive ischemia and fibrosis of the heart, the development of cardiac insufficiency is called "ischemic cardiomyopathy". If there is no angina or myocardial infarction in the past, it is difficult to distinguish it from cardiomyopathy, and then Cardiomyopathy can also have pathological Q waves and angina pectoris. At this time, coronary angiography is required for identification.

(5) Most of the congenital heart disease has obvious signs, it is not difficult to distinguish, the tricuspid valve is deformed with tricuspid valve murmur, and there may be galloping, heartbeat weakening, right heart enlargement and failure, and cardiomyopathy The difference, but the symptoms of this disease appear in the early years, the left ventricle is not large, the purpura is relatively, echocardiography can confirm the diagnosis.

(6) Systemic diseases of secondary cardiomyopathy such as systemic lupus erythematosus, scleroderma, hemochromatosis, amyloidosis, glycogen accumulation, neuromuscular diseases, etc. What is important is the differentiation from myocarditis. Acute myocarditis often occurs at or after the virus infection. The difference is not very difficult. If there is no clear history of acute myocarditis in chronic myocarditis, it is difficult to distinguish it from cardiomyopathy. In fact, many dilated cardiomyopathy It is derived from the development of myocarditis, the so-called "myocarditis after cardiomyopathy".

(7) Myocarditis Viral or rheumatic myocarditis In a few serious cases, there may be obvious heart enlargement, galloping, systolic murmur, etc., similar to DCM. In general, this severe myocarditis is mostly in the acute phase, but Can also be extended to several weeks to 2,3 months, and DCM is mostly chronic, detailed inquiries about the history of upper respiratory tract infection, viral serum test has some help, some serological tests to determine rheumatism can provide some basis.

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