Abstract
Chronic heart failure (CHF) in most cases is due to a decrease in myocardial contractility. In particular, this results in a reduction in the maximum rate of the pressure development in the left ventricle. At the same time the maximal rate of pressure fall at relaxation is also reduced. This is not surprising, since both depend on Ca ++ myoplasmic concentration. But most of cardiac pathologies have been associated with the impairement of myocardial relaxation to a greater extent than the contraction. In the review a new view has been proposed according to which this phenomenon is attributable to restructuring of titin, the sarcomeric protein that connects the ends of myosin filaments with the sarcomeric board, lines Z. A spring-like molecule of titin shrinks at sarcomeric contraction and straightens in parallel with removing of Ca ++ from myofibrils. A reduction of its stiffness, facilitating the filling of the left ventricle, can reduce restoring force of titin and thereby slow relaxation. The survey provides information about the functions of the calcium transport system and titin in the normal heart and in CHF observed both in experimental models and in patients.
Highlights
in most cases caused by decreased myocardial contractility
This is due to the fact that both parameters depend on the Ca2
myocardial relaxation is impaired to a greater extent than contraction
Summary
Внимательное изучение степени изменений сократимости и расслабимости миокарда позволило установить, что при патологии сердца расслабление снижается даже в большей степени, чем сокращение. Эти данные позволили сделать вывод, что процесс расслабления более чувствительный, чем процесс сокращения, к действию факторов внешней среды, и его изменения могут повлечь изменения сократимости миокарда [11]. Но оно также возрастает и при нарушении этого транспорта – в условиях гипоксии.
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