Impacts of Cardiac Dyssynchrony and Resynchronisation on Cellular Metabolism and Mitochondria: Current Understanding for Future Applications

Ventricular dyssynchrony serves as a cause of heart failure, resulting from impaired electrical conduction within the heart, commonly from bundle branch block or right ventricular pacing. It exceeds structural remodelling to cause significant cellular dysfunction, particularly in aberrant myocardial metabolism, alterations to myocardial oxygen consumption and cardiac efficiency, along with compromised mitochondrial activity. CRT is a therapeutic strategy that is used for the dyssynchronous ventricle by correcting electrical aberrance, while also improving cellular metabolic homeostasis, cardiac efficiency and mitochondrial function. This article provides a comprehensive review of the mechanisms responsible for ventricular dyssynchrony-induced cardiac remodelling and its reversal through cardiac resynchronisation therapy, focusing on the influence that these mechanisms exert on cellular metabolism and mitochondrial function. Additionally, it underscores the potential for risk assessment and individualised treatment targeting in dyssynchronous heart failure, using metabolic profiles, mitochondrial function indicators and metabolomic evaluation to enhance the efficacy of CRT and improve patient outcomes.