A modern view of the pathophysiological aspects of the development of chronic heart failure on the background of ischemic heart disease

Authors

  • O.M. Godlevska Kharkiv Medical Academy of Postgraduate Education, Kharkiv, Ukraine
  • O.V. Bilchenko Kharkiv Medical Academy of Postgraduate Education, Kharkiv, Ukraine
  • Ya.Yu. Samburg Kharkiv Medical Academy of Postgraduate Education, Kharkiv, Ukraine

DOI:

https://doi.org/10.22141/2224-0586.16.7-8.2020.223708

Keywords:

heart failure with mid-range ejection fraction, ische­mic heart disease, fibrosis, diastolic dysfunction, review

Abstract

In the guidelines of the European Society of Cardiology for heart failure in 2016, the term “heart failure with mid-range ejection fraction” was introduced to refer to the patients with heart failure and a slightly reduced ejection fraction of 40–
49 %. Today, it was found that about 20 % of people with heart failure fall into this category. It is proved that ischemic heart disease is one of the leading factors for the formation and progression of diastolic disorders of the left ventricle. More than 90 % of patients with ischemic heart disease have varying degrees of diastolic dysfunction, which may be based on disorders of active relaxation and fibrotic processes in the myocardium, which occur due to progressive atherosclerotic cardiosclerosis or acute myocardial infarction. In this regard, it is important to analyze recent data on the mechanisms involved in the formation of myocardial fibrosis of ischemic origin and its role in the pathogenesis of heart failure. It has been proved that chronic hypoxic ischemic myocardial damage is accompanied by necrosis of cardiomyocytes, in the place of which reparative fibrosis develops, and the collagen fibers that appeared fill the place of cardiomyocytes. Reactive fibrosis (perivascular and interstitial) develops in the border zone between the scar, which is formed due to reparative fibrosis, and the zone of hibernating myocardium, to a lesser extent in the intact myocardium. Its formation is indirectly caused by the pressure overload and overstretching of cardiomyocyte fibers. Myofibroblasts express contractile proteins, similar to smooth muscle actin that provide mechanical tension in the remodeled matrix, thereby reducing the scar area. In any case, the development of fibrosis in the extracellular matrix is an integral part of myocardial remodeling and requires continuing researches aimed at addressing the problem of participation of all mechanisms in the pathogenesis of chronic heart failure on the background of ischemic heart disease depending on its types.

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Published

2021-04-05

Issue

Section

Scientific Review