Relevance. Adaptation of the heart chambers to their volume overload, which increases with diastolic filling of the left ventricle (LV) or systolic regurgitation in the left atrium (LA) in case of mitral valve insufficiency leads to remodeling of the myocardium of these chambers. Longitudinal hypertrophy of cardiomyocytes (CMCs), realized by building up new sarcomeres at the end of existing myofibrils, is an adaptation mechanism in the early stages, but eventually turns into maladjustment, which leads to heart failure. Hypertrophied CMCs, damaged during decompensation, are replaced by connective tissue due to excessive activation of fibroblasts with deposition of the extracellular matrix, which is also an element of the myocardial remodeling. The progression of heart failure is also associated with a mismatch between blood supply and myocardial oxygen demand, since an increase in the size of the CMCs is accompanied by a rarefaction of the intramural network of microvessels. It is believed that the violation of the ratio of the size of the heart, angiogenesis and cardiac function are the basis for the transition of adaptive compensation of the heart to decompensation with the progression of heart failure.
Objective: to study morphological changes in the myocardium of the LV and LA in patients with mitral valve insufficiency.
Materials and methods. Macroscopically, the condition of the myocardium was studied on the material of 14 autopsies of patients who died of NdMK insufficiency. History of NdMK – from 3 months. up to 2.4±1.1 years. As a control, the hearts of 3 deaths without cardiopathology were studied. The material for light microscopy was pieces of myocardium from different segments of the left ventricle, as well as from the walls of the left ventricle, obtained during autopsy.Morphological (macroscopic, histological and electron microscopic), morphometric and statistical research methods were used.
Results. With LV dilatation associated with chronic mitral valve insufficiency, lengthening of each CMCs provides an increase in the area of the myocardial walls, and, accordingly, the size of the cavity of the corresponding chamber of the heart, which compensates to some extent for the increase in diastolic blood volume in the LV and systolic blood volume in the LA. However, the factor limiting this compensation mechanism is the deficiency of the myocardial microvasculature associated with limited capillary growth. The contradiction between the need for the myocardium to lengthen the CMCs and the inability of capillaries to provide them with oxygen leads to a breakdown in compensation with an increase in fibrotic changes. This is a factor limiting the further increase in the volume of the cavity.
Conclusions. Overloading of the myocardium with volume leads to an increase in the length of the CMCs, on average, from 57.3±9.1 µm to 93.7±12.4 µm. The increase in the length of the CMCs is due to the increase in the number of sarcomeres from 43.7±8.4 to 62.5±14.5. The diameter of the CMCs in this case does not increase reliably. Overloading of the heart cavities with volume is often accompanied by desynchronization of the CMCs contraction, which leads to disruption of the integrity of the myocytic "working syncytium" and pronounced interstitial fibrosis.
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