LECTURE № 2. Diseases of the cardiovascular system. Cardiomyopathy. Dilated cardiomyopathy

1. Cardiomyopathy

Cardiomyopathy - primary isolated myocardial lesions of a non-inflammatory nature of unknown etiology (idiopathic), they are not associated with valvular defects or intracardiac shunts, arterial or pulmonary hypertension, coronary heart disease or systemic diseases (such as: collagenoses, amyloidosis, hemochromatosis, etc.), and in the final stage of the disease, severe congestive heart failure and complex disturbances of the heart rhythm and patency develop.

The classification of cardiomyopathies is as follows:

1) dilated cardiomyopathy:

a) idiopathic;

b) toxic;

c) infectious;

d) with collagenoses;

2) hypertrophic;

3) restrictive;

4) arrhythmic dysplasia of the right ventricle;

5) a combination of one of the 4 types of cardiomyopathies with arterial hypertension.

2. Dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is a disease of the heart muscle characterized by a diffuse expansion of all chambers of the heart (mainly the left ventricle), in which the pathology of the pumping function of the heart is in the foreground and, as a result, chronic heart failure (hence the second name is congestive, when the heart is not able to fully pump blood and it "stagnates" in the tissues and organs of the body). The muscular wall of the heart remains either unchanged or hypertrophied to varying degrees.

Diseases and factors that preceded the development of DCM are described in the table below (see Table 5).

Table 5

Diseases and factors that preceded the development of DCMP

This is the most common form of damage to the heart muscle. The incidence is 5-8 cases per 100 people per year. There is no clear family history for these patients. Men get sick 000-2 times more often than women.

Pathogenesis. As a result of the inflammatory process in the heart muscle (myocarditis), the death of individual cells occurs in its various parts. In this case, inflammation is viral in nature, and cells affected by the virus become foreign agents for the body. Accordingly, when antigens appear in the body, a complex of immune response reactions develops aimed at their destruction. Gradually, dead muscle cells are replaced by connective tissue, which does not have the ability to extensibility and contractility inherent in the myocardium. As a result of the loss of basic myocardial functions, the heart loses its ability to function as a pump. In response to this (as a compensatory reaction), the chambers of the heart expand (i.e., they dilate), and in the remaining part of the myocardium thickening and compaction occurs (i.e., its hypertrophy develops). To increase the delivery of oxygen to the organs and tissues of the body, a persistent increase in heart rate occurs (sinus tachycardia).

This compensatory response only temporarily improves the pumping function of the heart. However, the possibilities of myocardial dilatation and hypertrophy are limited by the amount of viable myocardium and are individual for each specific case of the disease. With the transition of the process to the stage of decompensation, chronic heart failure develops. However, at this stage, another compensatory mechanism comes into play: the tissues of the body increase the extraction of oxygen from the blood compared to a healthy body.

But this mechanism is insufficient, since a decrease in the pumping function of the heart leads to a decrease in the supply of oxygen to organs and tissues, which is necessary for their normal functioning, while the amount of carbon dioxide in them increases.

In 2/3 of patients in the cavities of the ventricles in the late stages of the disease, parietal thrombi form (due to a decrease in the pumping function of the heart, as well as uneven contraction of the myocardium in the chambers of the heart), followed by the development of embolism in the pulmonary or systemic circulation.

Pathohistological and pathomorphological changes in the heart. The shape of the heart becomes spherical, its mass increases from 500 to 1000 g, mainly due to the left ventricle. The myocardium becomes flabby, dull, with noticeable whitish layers of connective tissue, there is a characteristic alternation of hypertrophied and atrophic cardiomyocytes.

Microscopically, diffuse fibrosis is detected, it can be combined with both atrophy and hypertrophy of cardiomyocytes, in which there is a significant increase in the volume of nuclei, the number of mitochondria, hyperplasia of the Golgi apparatus, an increase in the number of myofibrils, free and associated with the endoplasmic reticulum ribosomes, an abundance of glycogen granules.

clinical picture. There are no specific signs of the disease. The clinical picture is polymorphic and is determined by:

1) symptoms of heart failure;

2) rhythm and conduction disturbances;

3) thromboembolic syndrome.

All these phenomena develop in the terminal stage of the disease, and therefore the recognition of DCM before the appearance of these symptoms presents significant difficulties.

In most cases, the prognosis of the disease is determined by the defeat of the left ventricle of the heart. Before the onset of heart failure, DCM is latent. The most frequent complaints of already onset heart failure are complaints of decreased performance, increased fatigue, shortness of breath during exertion, and then at rest. At night, he has a dry cough (the equivalent of cardiac asthma), later - typical asthma attacks. Patients present with characteristic anginal pain. With the development of congestion in the systemic circulation, heaviness appears in the right hypochondrium (due to an enlarged liver), swelling of the legs.

Diagnostics. When diagnosing the disease, an important sign is a significant enlargement of the heart (there are no signs of valvular heart disease or arterial hypertension). Cardiomegaly is manifested by expansion of the heart in both directions, determined by percussion, as well as a displacement of the apical impulse to the left and down. In severe cases, a gallop rhythm, tachycardia, and sounds of relative insufficiency of the mitral or tricuspid valves are heard. Atrial fibrillation develops in 20% of cases. Blood pressure is usually normal or slightly elevated (due to heart failure).

Biochemical studies of blood and urine can detect various toxic substances, as well as vitamin deficiencies. Instrumental research methods make it possible to detect:

1) signs of cardiomegaly;

2) changes in indicators of central hemodynamics;

3) rhythm and conduction disturbances.

There are no characteristic changes on the ECG or the shifts are nonspecific. These are signs of an increase in the size of the heart, conduction disturbances in the form of a blockade of the anterior branch of the left leg of the atrioventricular bundle (His bundle) or a complete blockade of the left leg (15% of cases); as well as persistent sinus tachycardia (heart rate often exceeds 100 beats per minute).

Phonocardiogram confirms auscultatory data in the form of a gallop rhythm, a fairly frequent detection of systolic murmur (due to relative insufficiency of the mitral or tricuspid valve). With congestion in the pulmonary circulation, an accent of the II tone is revealed.

X-ray reveals a significant increase in the ventricles (often in combination with a moderate increase in the left atrium) and stagnation of blood in the pulmonary (small) circulation. Violations in the pulmonary circulation are manifested by an increase in the pulmonary vascular pattern, as well as the appearance of transudate in the pleural cavities, which is formed due to increased pressure in the vessels of the lungs.

The method of echocardiography is one of the main methods in the diagnosis of the disease. Echocardiography helps to detect dilatation of both ventricles, hypokinesia of the posterior wall of the left ventricle, paradoxical movement of the interventricular septum during systole. In addition, echocardiography allows you to clarify the increase in the amplitude of movement of the unchanged leaflets of the mitral valve.

Additional instrumental studies are not mandatory for making a diagnosis, but their results allow us to detail the degree of hemodynamic disorders and the nature of morphological changes in the myocardium.

A radioisotope study of the heart (myocardial scintigraphy) is performed to clarify the state of the pumping function of the heart, as well as to determine the zones of the dead myocardium. The study of indicators of central hemodynamics reveals a low minute and stroke volume (minute and stroke indices), an increase in pressure in the pulmonary artery.

Angiocardiographically, the same changes are detected as on the echocardiogram. Live myocardial biopsy is not informative for determining the etiology of cardiomyopathy. In some cases, a viral antigen or an increase in the content of LDH, as well as a decrease in energy production by mitochondria, can be detected in the biopsy. However, this surgical method can be used to clarify the etiology of the disease and further therapy. The manipulation is carried out as follows: under local anesthesia, a large artery and vein are pierced (punctured), then a special instrument with small scissors at the end is passed along their course to the heart. When myocardial biopsy is combined with coronary angiography (injection of a contrast agent into the coronary arteries supplying the heart), it becomes possible to exclude coronary artery disease in a patient as one of the diseases that has symptoms similar to DCM.

These two studies are performed under X-ray television control.

Differential diagnostics. It is produced primarily with myocarditis and myocardial dystrophies, i.e. with those conditions that are sometimes unreasonably called secondary cardiomyopathies.

Myocardial biopsy provides significant assistance in the differential diagnosis of dilated cardiomyopathy and heart disease, occurring with a pronounced increase in it:

1) with severe diffuse myocarditis, cellular infiltration of the stroma is found in combination with dystrophic and necrotic changes in cardiomyocytes;

2) with primary amyloidosis occurring with heart damage (the so-called cardiopathic variant of primary amyloidosis), there is a significant deposition of amyloid in the interstitial tissue of the myocardium, combined with atrophy of muscle fibers;

3) with hemochromatosis (a disease caused by a violation of iron metabolism), deposits of iron-containing pigment are found in the myocardium, various degrees of dystrophy and atrophy of muscle fibers, and proliferation of connective tissue are observed. As a variant of DCM, drug-induced and toxic cardiomyopathies can be considered.

Numerous agents can cause toxic damage to the myocardium: ethanol, emetine, lithium, cadmium, cobalt, arsenic, isoproterenol and other poisons. Histopathological changes in the tissues of the heart muscle appear as focal dystrophies. In the future, the development of microinfarctions occurs, accompanied by a peripheral inflammatory reaction. The most striking example of toxic cardiomyopathy is cardiomyopathy, which occurs in people who consume excessive beer. It is due to the presence of cobalt in it, which is added to beer to improve foam. Cobalt blocks the action of vitamin B₁, and also directly affects the change in the enzymatic processes of the cell. In the acute stage of the course of cobalt cardiomyopathy, the presence of hydropic and fatty degeneration, destruction of intracellular organelles, and focal necrosis of cardiomyocytes are noted.

In the future, diffuse or small-focal interstitial fibrosis develops, the final result is the formation of extensive scars. Cobalt cardiomyopathy is more severe than alcoholic cardiomyopathy. If the diagnosis is made on time, then a clinical cure of patients is observed.

Alcoholic cardiomyopathy. Ethanol has a direct toxic effect on cardiomyocytes. In addition, with chronic ethyl intoxication, there is often a lack of nutrition. It has been proven that alcohol leads to commulation of fatty acids in cardiomyocytes, since there is a lack of energy, which is necessary for their activity. Acetaldehyde, formed during the metabolism of alcohol, can be a factor in direct toxic effects on protein synthesis. Alcoholism is also accompanied by the activation of latent viruses.

Macroscopically, the myocardium is flabby, clay-like, sometimes small scars are observed. The coronary arteries are intact. Microscopic examination shows a combination of dystrophy (hydropic and fatty), atrophy and hypertrophy of cardiomyocytes, possibly the presence of foci of cardiomyocyte lysis and sclerosis. The affected areas of the myocardium contrast with unchanged ones. Electron microscopic examination of heart biopsy specimens shows cystic expansion of the sarcoplasmic reticulum and T-system of cardiomyocytes, which is characteristic of alcoholic cardiomyopathy. Complications of alcoholic cardiomyopathy - sudden death as a result of ventricular fibrillation or chronic heart failure, thromboembolic syndrome.

Treatment. Therapy of cardiomyopathies is a difficult task, since the specific causes of their occurrence are not known. The general principles of treatment of DCM do not differ significantly from the treatment of chronic heart failure. In cases of secondary DCM, the previous disease (heart valve disease, etc.) is additionally treated, and all measures are taken to eliminate the causes of DCM.

In essence, we can talk about the treatment of patients with cardiomyopathy only when clinical signs appear. In heart failure, cardiac glycosides are ineffective. Patients quickly develop intolerance to drugs (glycoside intoxication), and therefore it is necessary to use glycosides that are rapidly excreted from the body (strophanthin, isolanide). Peripheral vasodilators are quite effective, especially with concomitant anginal syndrome (nitrong, sustak, nitrosorbide). These drugs should be prescribed for severe heart failure, difficult to treat with glycosides and diuretics. With anginal syndrome, it becomes necessary to use antianginal drugs, preferably prolonged nitrates (sustak, nitrong, nitrosorbide). Adrenoblockers are effective (they are prescribed in the absence of signs of heart failure).

Of the modern methods of surgical treatment of DCMP, the most effective is heart transplantation (transplantation). However, the possibilities of carrying out this operation are significantly limited. For this reason, as an alternative to heart transplantation in modern treatment, to increase the life expectancy of patients with DCMP, reconstructive surgeries have been developed and are being performed, which are aimed at eliminating insufficiency of the mitral and tricuspid heart valves. Operative elimination of insufficiency of these valves allows for some time to "slow down" the onset of the final stage of the disease. Another alternative to heart transplantation in patients with DCM was the partial removal of the left ventricle in order to reduce its size (Baptiste operation).

Not so long ago, for the treatment of patients with DCMP, special models of pacemakers were developed, they allow you to make the work of the ventricles of the heart synchronous. This leads to an improvement in the filling of the ventricles of the heart with blood and an increase in the pumping function of the heart.

A separate issue should be considered DCM in children, which is 5-10 cases per 100 children per year. It is noteworthy that the disease can develop in different age groups, including infants. The data obtained in the study of a group of children are as follows: patients received 000 options for therapy (monotherapy with prednisolone, monotherapy with digoxin or prednisolone + digoxin). The effectiveness of the treatment was evaluated according to the following criteria: the heart rate was determined before and after the treatment, the respiratory rate, the state of the ejection fraction and the contractility fraction. The analysis of the obtained results shows that the greatest effect in the treatment of dilated cardiomyopathy in young children is achieved with a combination of corticosteroids and glycosides (prednisolone and digoxin). After completion of the main course of treatment (prednisolone administered 3 mg/kg per day for 2 days, digoxin), there was a pronounced decrease in heart rate, a decrease in shortness of breath. Against the background of monotherapy with prednisolone, a decrease in heart rate occurs. Monotherapy with digoxin leads to a decrease in tachycardia and dyspnea. Given the inadvisability of prescribing cytostatic drugs in young children, since a significant number of treatment complications were observed, it is more optimal in pediatrics to use long-acting cardiac glycosides in combination with corticosteroid hormones in dilated cardiomyopathy.

Prevention. Prevention of DCM involves avoiding alcohol, cocaine, and carefully monitoring cardiac parameters during tumor chemotherapy.

It is useful to harden the body from an early age. Complete abstinence from alcohol in alcoholic DCM improves heart contractility and may eliminate the need for a heart transplant.

The fact that in most cases the diagnosis occurs at the stage of heart failure can also lead to negative results in treatment. Early diagnosis of dilated cardiomyopathy can be performed with random (screening) echocardiography, which is performed during the annual medical examination, as well as when examining people with heredity burdened by this disease. It is in this case that it is possible to increase the effectiveness of drug treatment of DCM.

Author: Mostovaya O.S.

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