The Molecular Mechanism of Diastolic Heart Failure

Abstract

Diastolic heart failure (DHF) is a group of clinical syndromes related to the performance of the pulmonary circulation and systemic circulation, with normal left ventricular (LV) systolic function. The pathophysiology of diastolic dysfunction includes delayed relaxation, impaired LV filling, and/or increased stiffness. These conditions result in impaired LV diastolic relaxation ability and a decrease in myocardial compliance. In recent years, studies on the mechanisms of DHF have focused on the renin-angiotensin-aldosterone system, inflammatory cytokines, oxidative stress, the process of myocardial calcium cycling, and associated proteins. The pathomechanism has been proven to be due to a deficiency in ATP, and Ca2+ cannot be reduced by sarcoplasmic reticulum calcium pump (SERCA2a), which leads to myocardial diastolic dysfunction. The correlation between the degradation process of ATP and its metabolites and DHF has also been studied in recent years. This paper summarizes the views on the above and analyzes the correlations between the molecular mechanisms.