Internal illnesses. Dilated (congestive) cardiomyopathy (lecture notes)

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Internal illnesses. Dilated (congestive) cardiomyopathy (lecture notes)

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LECTURE No. 16. Dilated (congestive) cardiomyopathy

Cardiomyopathy - diseases of the myocardium of unknown etiology, manifested by cardiomegaly and heart failure, with the exclusion of damage to the heart valves, coronary and pulmonary vessels, arterial hypertension.

Dilated (congestive) cardiomyopathy - damage to cardiomyocytes with the development of their contractile weakness, expansion of the heart cavities and progressive chronic heart failure, resistant to therapy. It is more common in men aged 35-45, but in women the disease is more severe.

Pathogenesis. A hypocirculatory hemodynamic state develops with a decrease in the stroke volume of the heart with increased filling of the heart with blood. Circulatory insufficiency develops as a result of a primary contractile defect in the heart muscle, and myocardial hypertrophy has a secondary compensatory character.

Pathological anatomy. There is a sharp expansion of all cavities of the heart without a significant increase in the thickness of the walls of the ventricles (cor bovinum). The mass of the heart is 2-3 times more than normal. The left ventricle is enlarged compared to the right. The myocardium becomes flabby, dull, areas of hypertrophy and atrophy of cardiomyocytes alternate. The valvular apparatus and coronary vessels do not change. There may be parietal thrombi in the cavities.

Clinic. Extrasystole, ventricular tachycardia appear; atrial fibrillation (an early sign), initially of a paroxysmal type, which quickly becomes permanent. There are signs of circulatory decompensation. Systolic blood pressure decreases while maintaining diastolic blood pressure.

Apical impulse of weak force, spilled; deaf I tone. Due to the increase in end-diastolic pressure, a fourth tone appears in the left ventricle, an accent of the second tone over the pulmonary artery is noted. At the apex of the heart, in the 4th intercostal space on the left side of the sternum, a prolonged systolic murmur appears as a result of mitral regurgitation of blood with the expansion of the mitral orifice or dysfunction of the papillary muscles. Auscultatory signs increase with the progression of heart failure and dilatation of the heart and weaken with improvement in the condition.

The main periods of the disease

В I period there are no asymptomatic complaints. The ejection fraction was reduced to 35%, the end diastolic size of the left ventricle was 6,5 cm.

In II period progressive myocardial damage, symptoms of chronic heart failure appear - NC stage I-II. Ejection fraction 35-25%, end-diastolic size of the left ventricle 7-7,5 cm, volume/weight index of the left ventricle not more than 1,35 mg.

В III period of developed clinical manifestations, a clinic of total heart failure appears - NC IIB-III, severe cardomegaly. Mortality is high from congestive heart failure, thromboembolic complications.

В IV period stabilization occurs complete or significant regression of edema, venous congestion with simultaneous progression of the actual signs of circulatory failure. The inotropic function of the heart and arterial perfusion of organs and tissues decrease, and a small ejection syndrome develops. Index volume / mass of the left ventricle - 1,5 ml / g, ejection fraction up to 20% or less.

В V terminal period there comes a pronounced dystrophy of all internal organs, ischemic damage to the liver, kidneys, dyscirculatory encephalopathy, weight loss due to atrophy of the skeletal muscles, recurrent thromboembolism is possible.

The main criteria for diagnosis are the presence of cardiomegaly, rhythm and conduction disturbances, progressive circulatory failure resistant to cardiotonic therapy, thromboembolic complications.

Additional diagnostic study. It is recommended to conduct a biochemical blood test to establish the presence of dysproteinemia, hypoalbuminemia in congestive heart failure.

An ECG study reveals violations of atrioventricular and intraventricular conduction, repolarization processes (ST segment depression, T wave inversion), high-grade ventricular arrhythmias, atrial fibrillation, pathological Q wave due to severe myocardial fibrosis, complete blockade of the left bundle branch block (in 10% patients); a decrease in the voltage of the R and S waves in standard leads, an increase in the chest leads.

20-hour monitoring of the ECG by Holter, echocardiography is carried out, dilatation of all cavities of the heart, mainly the left ventricle, a decrease in ejection fraction, signs of heart failure: hydropericardium, hydrothorax, increased pressure in the pulmonary artery, ascites, absence of echocardiographic signs of the disease that led to cardiac insufficiency), Doppler echocardiography (mitral and tricuspid regurgitation, intraatrial thrombi (in 25-50%), intraventricular thrombi (in XNUMX%), a significant decrease in systolic function, diastolic dysfunction), x-ray examination (increase in heart size, signs of pulmonary congestion (venous plethora, interstitial pulmonary edema), cavity effusion (hydrothorax, hydropericardium)).

Complications. Complications include a permanent form of atrial fibrillation, thromboembolism.

Differential diagnostics. It is carried out with effusion pericarditis, coronary heart disease, viral myocarditis, alcoholic myocardial dystrophy, rheumatic heart disease, hypertension.

Treatment. In the presence of atrial fibrillation of the tachysystolic form, symptoms of left ventricular failure, cardiac glycosides (digoxin) are used in the treatment.

β-blockers are prescribed after stabilization of the condition with cardiac glycosides and diuretics.

Potassium-sparing diuretics are used (triamterene, veroshpiron, indapamide. If they are used excessively, hypokalemia, a decrease in BCC (circulating blood volume), and a decrease in blood flow to the heart are possible.

ACE inhibitors have a beneficial effect on pre- and afterload with subsequent improvement in hemodynamics.

Additional treatments include peripheral vasodilators. Nitrosorbide reduces preload, lowers the end diastolic pressure in the cavity of the left ventricle, reduces its size.

Antiarrhythmic therapy is also used - cordarone, anticoagulant therapy, blood ultrafiltration to reduce stagnation.

Of the surgical methods of treatment with the ineffectiveness of conservative therapy, implantation of a cardioverter-defibrillator and heart transplantation (with low ejection syndrome and in the period of stabilization) are used.

Flow. The course can be with rapid progression (1-1,5 years), with slow progression or recurrent.

Forecast. Unfavorable, mortality within 5 years is 50%.

Author: Myshkina A.A.

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