The Compensatory Alterations оf the Relaxability and Distensibility of the Myocardium at Weakening of Its Contractility

Abstract

Abstract—The contractile function of the heart is carried out due to the coordinated interaction of the basic properties of the myocardium – distensibility, contractility and relaxability. Violation of myocardial contractility due to any reason creates a situation of chronic heart failure (CHF). The severity of CHF is determined by the ability of the circulatory system to a certain extent to compensate for the weakening of the contractility of the heart, the criterion of which is the value of the ejection fraction. The form of CHF with preserved ejection fraction is defined as diastolic dysfunction. It is the first stage of CHF, its distinctive features are delayed relaxation and increased diastolic pressure in the left ventricle. The review is devoted to the consideration of the structure of diastole in 4 types of CHF – ischemic heart disease in myocardial infarction or microinfarctions caused by isoproterenol, myocardial damage induced by doxorubicin and type 1 diabetes. A common sign of all types of CHF is an increase in myocardial extensibility and a slowdown in relaxation. It has been shown that they are based on a change in the properties of connectin (titin) – a sacromeric protein that connects the ends of myosin filaments with the boundaries of the sarcomere. Its properties determine the distensibility and relaxation of the myocardium, and these changes underlie the primary compensatory reaction of the heart at weakening its contractility. Also mechanisms are mobilized that increase the inflow to the heart and reduce peripheral resistance. The degree of their mobilization depends on the degree of reduction in myocardial contractility. Along with this, each form of CHF has its own specifics, which must be taken into account when choosing the means of therapy.