Dilated cardiomyopathy in the elderly

Introduction to elderly patients with dilated cardiomyopathy Dilated cardiomyopathy (DCM) is the main type of cardiomyopathy, accounting for 70% to 80% of cardiomyopathy. It has been called congestive cardiomyopathy. It is characterized by obvious enlargement of the left ventricle or right ventricle or enlargement of the biventricular. The main left ventricular enlargement. With heart enlargement, heart failure, arrhythmia, and embolism as the basic features. Although all age groups have onset, the hospitalization age is 20 to 49 years old, and about 20% of DCM patients have a family history of cardiomyopathy. basic knowledge The proportion of illness: the probability of illness in the elderly is 0.23% Susceptible people: the elderly Mode of infection: non-infectious Complications: arrhythmia pulmonary embolism

The cause of dilated cardiomyopathy in the elderly

Infection factor (30%):

It is an important cause of the disease and is considered to be a long-term result or sequela of viral myocarditis. About one-fifth of patients have severe influenza syndrome before DCM, and virus particles can be observed in myocardial biopsy specimens of some patients. And found that in this group of patients Coxsackie B3 virus antibody titer is significantly higher than healthy people, animal experiments found that viral myocarditis caused by enterovirus infection in mice, accompanied by persistent immune dysfunction, and finally form DCM, After long-term follow-up of patients with acute viral myocarditis, 6 to 48% can be converted to DCM. It has been reported that chronic viral myocarditis develops into DCM after 1 to 8 years of follow-up, accounting for about 30% of the total DCM of this group. O'Connell and Kenllund List 20 common viruses that can cause myocarditis, Coxsackie A, B virus, Echo virus, influenza A, B, poliovirus, herpes simplex virus, herpes zoster virus, Epstein-Barr virus, African lymphoma Virus, rotavirus, rabies virus, hepatitis B virus, arbovirus, Junim virus, human HIV, the most common development of DCM after infection with Coxsackie virus.

Autoimmune response (30%):

In the past 10 years, the immuno-molecular mechanism of DCM has proposed viral/immunological theory, immunological abnormalities of DCM, including abnormal autoreactivity of humoral and cellular immunity to cardiomyocytes, decreased activity of self-clearing cells, and abnormal cell-inhibiting activity. Currently, immune-mediated injury is considered to be the etiology and pathogenesis of DCM. In conclusion, the autoimmune process, causing myocardial cell structure and dysfunction at the molecular level, may be one of the important mechanisms that may cause the onset of DCM.

Genetic factors (10%):

About 20% of DCM has a familial pathogenesis, but it is less common than hypertrophic cardiomyopathy (HCM). The familial DCM is mainly an autosomal dominant genetic disease, and the myosin heavy chain (, -MHL) gene is abnormal. Not only seen in HCM, but also in DCM patients, it has been found that myocardial tissue of DCM patients has a fetal myosin heavy chain. The re-expression of this fetal myosin is related to the pathogenesis of DCM. Mtmtoni pointed out that the pathogenic gene of DCM lies in muscle nutrition. The dystropin gene is defective and protrudes from the heart, causing the membranous cell scaffold of cardiomyocytes to break, and finally forming DCM. In DCM, the number of chromosomes such as HLA-DR4 and A11, B12 is also increased, and Ts cell function is accompanied. Low, is a high-risk carrier of DCM.

Myocardial energy metabolism disorders (20%):

Energy metabolism is the basic guarantee for maintaining the normal structure and function of cardiomyocytes. The energy metabolism in cardiomyocytes and the high-energy phosphate bond provided are directly similar to the phosphorylation and dephosphorylation processes of membrane channel proteins, contractile proteins, receptors and protein kinases. The process involves almost all regulation and life function in cardiomyocytes. The amount of ATP in myocardium of hamsters (HCM and DCM) is 28% lower than that of the control rats. The CK activity in the myocardium of DCM patients is directly reduced by 30% to 50%. Phosphate creatine, a substrate for the synthesis of ATP, decreased by 60%; magnetic resonance imaging (31p NMR) and PET detected a decrease in CK activity and a decrease in ATP and CK in heart failure animals.

Other factors (10%):

In recent years, data show that the activity of the adrenal nervous system in patients with chronic heart failure is locally changed, the activity of adrenaline in the heart, kidney and peripheral nerve is increased, the density of noradrenergic nerve in the heart tissue is reduced, and the G receptor protein adenylate cyclase of DCM (Receptor-G proteinadenylase-cyclase, RGC) complexes often change significantly, 1 receptor density is reduced by 60% to 70% in severe heart failure, 2 receptor density is unchanged, but due to 2 receptor dissociation, 2 receptor The agonist reactivity decreased by about 30%, and the inhibitory Gi protein activity increased by 30% to 40%. The 2 receptor dissociation may be related to the increase of Gi protein activity. The receptor dissociation is obvious after myocardial infarction, and the 1 receptor is down-regulated. , 2 receptor dissociation and low-grade norepinephrine can be manifested in DCM, heart failure caused by myocardial infarction and myocardial overload, RGC system is an important target for drug regulation of -adrenergic pathway.

Pathogenesis

DCM is mainly characterized by heart pumping disorders. DCM patients have myocardial lesions, imbalance of contraction of heart muscles in various parts of the heart, so that myocardial contractility is weakened, cardiac output is reduced, and early heart rate can be compensated by late heart rate. Volume and cardiac output decreased, ventricular diastolic and end-systolic volume increased, ejection fraction decreased, the heart gradually expanded, resulting in relative closure of the mitral and tricuspid valves, due to increased ventricular end-diastolic pressure, atrial pressure also increased, Pulmonary circulation and systemic venous pressure are also increased and congested, congestive heart failure occurs, and pulmonary embolism and pulmonary arterioles repeatedly cause thromboembolism in the late stage, which can lead to pulmonary hypertension, and the performance of right heart failure is more prominent. In addition, myocardial fibers Chemotherapy can involve the sinus node pacemaker and conduction system, can occur a variety of arrhythmia, reduced cardiac output, renal perfusion, stimulate the renin-angiotensin-aldosterone system, increase peripheral vascular resistance, make the heart row The blood volume is even more reduced.

The pathophysiological changes in elderly patients are more prominent. Because of the increased ventricular blood storage and slow blood flow, it is conducive to the formation of wall thrombus, which can cause embolism of the heart, lungs, kidneys, limbs and other external organs, such as pulmonary embolism. The right heart load is further aggravated.

The color of the myocardium is pale, slack, the heart is enlarged, the ventricle is enlarged more than the atrium, the left ventricle is especially, the heart enlargement is often more than twice that of normal people, and there is a certain degree of cardiac hypertrophy, which is caused by the expansion of the heart and the weight of the heart is increased. In general, the weight of the heart in adult cases is usually 400-750g, a few more than 100%, the mitral and tricuspid annulus increases, and occasionally the edge of the valve leaf is thickened, and multiple small scars are visible on both sides of the ventricular cavity. Scar fiber stoves are common in the papillary muscle and 1/2 of the inner side of the ventricular wall, to local thinning to less than 3mm, 50% to 70% of autopsy can be seen in the heart of each cavity with a wall thrombus, the left ventricular apex is most common, prone to occur Pulmonary circulation and systemic embolism.

Under light microscopy, the diseased myocardium is mainly focal fibrosis, occasionally small pieces of necrosis, myocardial cells have different degrees of hypertrophy, atrophy, vacuolar degeneration and basophilic degeneration, interfiber tissue thickening, interstitial different degrees Thickening, extensive and varying sizes of fibrotic lesions and lymphocytic infiltration around blood vessels and cardiomyocytes.

Electron microscopy showed decreased myofibrillar content, increased mitochondria, increased sputum rupture or disappearance, sarcoplasmic reticulum expansion, increased glycogen, nuclear enlargement, nuclear membrane folding, deformation, interstitial thickening with edema, and increased collagen fibers. Histochemical examination, succinate dehydrogenase, phosphonate and glycogen were reduced to varying degrees, calcium-dependent ATPase, maleate dehydrogenase, glutamate dehydrogenase and 5' nucleotidase were reduced, but Increased levels of LDH and LDH5 reflect changes in cardiac structure and metabolic function.

Elderly patients with dilated cardiomyopathy

There are no effective preventive measures, and early detection and early diagnosis are the key to the prevention and treatment of this disease. Effectively control heart failure and arrhythmia, relieve immune-mediated myocardial damage, and improve the quality of life and survival of patients with dilated cardiomyopathy. Prevention of predisposing factors: Once diagnosed, patients are often highly nervous, anxious, depressed, and seriously concerned, frequently seeking medical treatment, and urgently require medication to control symptoms. Avoid smoking, alcoholism, overwork, nervousness, agitation, overeating, indigestion, colds and fever, excessive intake of salt, low blood potassium, low blood magnesium.

Elderly patients with dilated cardiomyopathy Complications arrhythmia pulmonary embolism

Patients may have arrhythmia, and some patients have systemic embolism and pulmonary embolism.

Symptoms of dilated cardiomyopathy in the elderly Common symptoms Congestive fatigue, weakness, arrhythmia, liver enlargement, high fever, sudden heart rate, increased angina, right heart failure

Symptom

DCM usually has a slow onset. In the early stage of the disease, it can be asymptomatic or has few symptoms. About one-third of patients have cardiac dysfunction III to IV at the time of treatment. Some patients are found during physical examination or other diseases. Cardiac enlargement or electrocardiogram showing arrhythmia, further examination and diagnosis of DCM, heart function decline but in the compensation period, can be expressed as fatigue, weakness, shortness of breath after activity, labor ability decreased significantly, the disease progressed to a certain stage, showing congestive Heart failure, when there is left heart failure, there may be cough, hemoptysis, chest tightness, gradual occurrence of paroxysmal dyspnea at night, sitting breathing, even acute pulmonary edema, general severity of left heart failure and duration of disease and left ventricular dilatation In proportion, the symptoms of right heart failure appear in the later stage of the disease, manifested as digestive tract congestion, hepatomegaly, tenderness and pain in the liver area, lower extremity edema, multiple serous effusions, etc., a small number of patients with serous effusion occurred earlier.

Some patients complain of chest discomfort, chest pain is not easy to distinguish between angina pectoris, may be pleural chest pain, and heart enlargement to pericardial extension, myocardial hypoxia, ischemia, tachycardia, ectopic rhythm, pulmonary embolism, may also be pericardial lesions And caused by fatigue.

About one-third of DCM patients have arrhythmia, 20% have atrial fibrillation, 37% have complex ventricular arrhythmias, and 15% to 60% have non-sustained ventricular tachycardia.

About 18% of DCM patients have embolism, which can be seen at any stage of the disease. Some patients have embolism as the first symptom. For example, lung, brain, kidney, coronary artery, peripheral blood vessel embolism, etc. may have corresponding symptoms and signs.

Sudden death can occur in patients with DCM, the cause of which is related to fatal arrhythmias and embolism.

2. Signs

There are very few heart-positive signs in the early stage. Sometimes the heart auscultation can smell the obvious third heart sound or the fourth heart sound. It is the most important sign of early DCM. Patients can have sinus tachycardia at rest, and arrhythmia or mild heart. Enlargement, when the disease progresses to a serious stage, signs of congestive heart failure may occur, the heart enlarges, the left ventricle enlarges obviously, the apex shifts to the left, diffuse or lifted, the heart rate increases, and the first heart sound of the apex Low blunt, you can hear the third heart sound or the fourth heart sound. Because the heart is enlarged, the apical area or the tricuspid area can smell the full systolic murmur of the hair styling. After the heart function is improved, the murmur can be weakened or disappeared. There is a pulmonary artery. In the high pressure, the second sound of the pulmonary valve area is hyperthyroidism, and there is complete left bundle branch block. The second heart sound is reversed. The blood pressure is mostly normal, but it can be increased in heart failure. The main increase in diastolic blood pressure is pulse pressure. Reduced, in addition, can also be manifested as cyanosis, jugular vein engorgement, weak pulse, wet lungs at the bottom of the lungs, swollen liver and pulsation, lower extremity or systemic edema, may have pleural or abdominal effusion, some suffering You may have pericardial effusion.

DCM still lacks a unified specific diagnostic criteria. In addition to other organic heart disease, combined with clinical and laboratory examinations to confirm the diagnosis, the domestic Jiang has proposed diagnostic criteria for senile dilated cardiomyopathy:

1 age is greater than 60 years old;

2 after the activity, palpitations, shortness of breath, clinical manifestations of congestive heart failure (heart function NYHA-III, IV);

3 physical examination, X-ray and echocardiography have heart enlargement, heart / chest ratio > 0.5;

4 heart auscultation first heart sounds weakened, pathological S3, S4; 5 history of syncope or arterial embolism;

6 arrhythmia showed diversity, variability, myocardial strain, abnormal Q wave;

7 Except for other organic heart disease and secondary cardiomyopathy, clinically, when the elderly have unexplained heart failure, other causes can not be found, such as hypertension, ischemic cardiomyopathy, valvular disease, etc., should be considered To the possibility of senile cardiomyopathy, the most common clinical manifestations are decreased cardiac reserve function and cardiac insufficiency. Heart failure due to senile cardiomyopathy may not be common, often under stress conditions such as hyperthyroidism and anemia. Surgery, infection, fatigue, excessive heat, induced heart failure symptoms when the infusion rate is too fast.

Examination of elderly patients with dilated cardiomyopathy

ESR increased, liver function SGPT, SGOT and globulin increased in heart failure, and occasionally, serum myocardial enzyme increased slightly.

Electrocardiogram

It is characterized by diversity, complexity, and lack of specificity. Because of the abnormality of myocardial ultrastructure in the early stage of the disease, such as myocardial cell degeneration, myocardial fibrosis, myocardial fiber arrangement disorder, the myocardial cells are electrically unstable. Therefore, various arrhythmias can occur in the early stage of the disease, including ectopic heart rhythm, early atrial, early room, atrial fibrillation and conduction block. 80% of patients have pacing and conduction disorders, and sick sinus syndrome can occur. Conduction block, left bundle branch block, branch block and non-specific indoor block, right bundle branch block is rare.

2. Echocardiography

Echocardiographic examination of the characteristics of DCM is helpful for identification of other heart diseases and cardiomyopathy. The more the left ventricular ejection fraction is reduced, the higher the wall stress and the worse the prognosis.

3. X-ray inspection

In the early stage of the disease, there is no change. With the development of the disease, the atrium of different degrees is displayed, the ventricular cavity is enlarged, the heart is weak, the heart shadow is large, and it can be approximate spherical. In a few cases, the left ventricle and the left and right atrium are enlarged, and the heart is present. Appearance of the mitral valve, enhanced lung texture or pulmonary interstitial edema, often accompanied by pleural effusion, may have pericardial effusion, heart to chest ratio greater than 0.6.

4. Radionuclide inspection

DCM radionuclide examination mainly includes dynamic visualization of cardiac blood pool and myocardial perfusion imaging, dynamic visualization of blood pool, observation of wall motion, calculation of cardiac systolic and diastolic function and phase analysis by ventricular wall volume curve, DCM The characteristics of the blood pool imaging are: the heart cavity is obviously enlarged, the left ventricle cavity is enlarged, the heart chamber volume is increased, the heart is expanded and dilated, forming a spherical or elliptical shape, the wall motion is generally weakened, and the left ventricular ejection fraction is obvious. Lower, can be reduced to below 20%, the initial 1/3 ejection fraction (1/3EF), peak ejection rate (PER), peak filling rate (PFR), 1/3 filling score (1/3FF) are reduced, Peak ejection time (TPER) and peak filling time (TPFR) were significantly prolonged, indicating that the patient's left ventricular systolic and diastolic function were impaired, but the systolic function was more impaired. The phase analysis showed that the left ventricular phase histogram was half. The height and width and phase angle increased significantly, reflecting the significant decrease in the coordination of ventricular motion.

5. MRI examination

MRI can provide reliable and reproducible quantitative information on the cardiac structure of patients with cardiomyopathy, contribute to the classification of cardiomyopathy and evaluate the therapeutic effect, and also apply to biochemical analysis in vivo. In 1990, Schaefer reported phosphodiester, phosphoric acid in DCM patients. The increase of citrate and phosphodiester ATP provides a non-invasive method for further study of myocardial metabolism. MRI examination shows left and right ventricle enlargement, uniform left ventricular wall thickness, and increased left ventricular mass, which can provide myocardial thickness. Changes in ventricular contraction, changes in ventricular volume and cardiac cycle capacity, can also provide information about the nature of myocardial abnormalities.

6. Cardiac catheterization and cardiovascular angiography

At DCM, there was no characteristic change in hemodynamics in cardiac catheterization. In patients with heart failure, cardiac output and stroke output decreased, left ventricular end-diastolic pressure, left atrial pressure, pulmonary capillary and pulmonary arterial pressure increased. The venous blood oxygen difference is increased. In the absence of heart failure, cardiac output and stroke volume are normal at rest, but in some patients, the left and right atrial average pressures may be slightly increased, and the left and right ventricular end-diastolic pressures are also Can be slightly increased.

Left ventricular angiography showed diffuse enlargement of the left ventricle, weakened contractile force, and generally low wall motion. In some cases, localized abnormal wall motion was observed, and there may be mild to moderate mitral regurgitation and left atrial enlargement. Occasionally, intracardiac thrombosis, coronary angiography showed no stenotic lesions.

7. CT examination

In DCM, the left ventricle is visible, the interventricular septum and free wall are thin, and the left ventricular cavity is significantly dilated, causing the septal bulge to the right ventricular outflow tract and exhibiting right ventricular obstruction, ie, Bernheim syndrome, with a few cases of left atrium or right. The ventricle is mainly enlarged, and sometimes there is a wall thrombus with filling defects in the heart. It can also measure the increase of myocardial weight, increase the left ventricular volume, and also see pleural effusion, pericardial effusion and pulmonary thromboembolism. which performed.

8. Endomyocardial biopsy

In 1963, Konno and Sakakiara pioneered intravenous endocardial myocardial biopsy (EMB). In 1981, clinical application began. EMB is not specific to DCM, but it is helpful for differential diagnosis of secondary cardiomyopathy and acute myocarditis, but biopsy. Normal tissue can not rule out the disease, which may be related to the number and location of the obtained specimens. In DCM, the myocardial cells under different light microscopes show different degrees of hypertrophy and degeneration, mainly nuclear hypertrophy, deformity and deep staining, myogenic The fibers are reduced, and the perinuclear vacuoles appear. The heavier ones have myofibrolysis, the myocardial cells are cavitation, the myocardial interstitial has different degrees of hyperplasia, the myocardial cells are disordered, and the endocardium can be normal or varying degrees of fibrosis. A small amount of wall thrombosis can be seen.

Diagnosis and identification of dilated cardiomyopathy in the elderly

Diagnostic criteria

In October 1995, the diagnostic reference criteria for idiopathic DCM developed by the National Myocarditis and Cardiomyopathy Symposium were as follows:

Clinical manifestation

Cardiac enlargement, reduced ventricular systolic function with or without congestive heart failure, often arrhythmia, complications of embolism and sudden death.

2. Auxiliary inspection

(1) X-ray examination, heart-thorax ratio >0.5.

(2) The echocardiogram shows the whole heart enlargement, especially the enlargement of the left ventricle. The left ventricular end-diastolic volume is 80ml/m2, the heart can be spherical, the wall motion is diffusely weakened, and the ejection fraction is reduced.

3. Other specific cardiomyopathy must be excluded

4. Detection of serum anti-cardiomyocyte peptide antibodies in patients

Such as anti-myocardial mitochondrial ADP/ATP carrier antibody, anti-myosin antibody, anti-1 receptor antibody, anti-M2 cholinergic receptor antibody, can be used as adjunctive diagnosis of this disease, detecting HLA phenotype and genotype of patients and their members It is helpful to predict susceptible populations. Endocardial myocardial biopsy is not specific for the diagnosis of this disease, but it is helpful for differential diagnosis of secondary cardiomyopathy and acute myocarditis.

Differential diagnosis

Coronary heart disease

A small number of patients with severe coronary heart disease have severe myocardial ischemia, often with multiple small infarction areas or extensive myocardial fibrosis. The heart chamber is enlarged with chronic heart failure and can be similar to DEM, but patients with coronary heart disease There are generally risk factors for coronary heart disease, such as obesity, hyperlipidemia, hyperglycemia, high blood pressure, etc., typical symptoms of angina pectoris, history of acute myocardial infarction, auscultation of the second aorta of the aorta, S3, S4 rare, systolic The murmur is constant, while the second auscultation of the DCM auscultation aorta is low, often with S3, S4, apical systolic murmur can be alleviated or disappeared with heart failure, abnormal Q wave and ST-T changes in coronary heart disease according to coronary blood supply The site appears in the corresponding lead. Echocardiography is mainly caused by left ventricular involvement in coronary heart disease. If there is myocardial necrosis, there is segmental reverse motion. Selective coronary angiography and radionuclide examination are helpful for differential diagnosis.

2. Rheumatic heart valve disease

DCM can have murmur of the mitral or tricuspid valve and enlargement of the left atrium, so it should be differentiated from rheumatic heart disease. If there is no such noise before the heart is significantly enlarged in the past history, the noise is louder in heart failure, after heart failure control The noise is weakened or disappeared, accompanied by the third heart sound or the fourth heart sound running the horse, etc., which suggests the possibility of the disease. The rheumatic heart disease is mainly mitral stenosis, which may have characteristic mitral diastolic murmur, sometimes Accompanied by two, tricuspid regurgitation systolic murmur and left atrial enlargement, but the murmur is weak in heart failure, the murmur is enhanced after heart failure control, echocardiography has characteristic valvular lesions, and the electrocardiogram shows right axis deviation. The mitral valve type P wave , X-ray shows that the valve has calcification shadow, characteristic compartment enlargement.

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