Hospital therapy. Pathogenesis of dilated cardiomyopathy (DCM) (most important)

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Hospital therapy. Pathogenesis of dilated cardiomyopathy (DCM) (most important)

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7. Pathogenesis of dilated cardiomyopathy (DCM)

Pathogenesis. As a result of the inflammatory process in the heart muscle (myocarditis), individual cells die in its various parts. Inflammation in this case is viral in nature, and the 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, the 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 the main functions of the myocardium, 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 thickening and thickening occurs in the remaining part of the myocardium (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 (sinus tachycardia) occurs.

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.

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