Heart failure is a complex progressive clinical syndrome which is initiated by risk factors (e.g., hypertension, obesity, and diabetes), then proceeds to asymptomatic maladaptive left ventricular remodeling and dysfunction, and finally evolves into clinically overt, symptomatic heart failure, disability, and death. The progression of left ventricular dysfunction is associated with changes in cardiac energy metabolism. Mitochondria play a central role in a variety of cardiomyocytes functions, including oxidative energy production, storage of calcium ions, and programmed cell death. The mitochondrial DNA (mtDNA) content correlates with the size and number of mitochondria, which change under different energy demands and oxidative stress. Experimental studies demonstrated that any genetic manipulation resulting in significantly decreased mtDNA could accelerate the ageing process and cause adverse myocardial remodeling and dysfunction. On the other hand, preservation of the mtDNA copy number in mouse hearts delays the development of heart failure after myocardial infarction. Recent general population study also demonstrated that echocardiographic indexes of left ventricular structure and function are significantly and independently associated with mtDNA content measured at peripheral blood cells in cross-sectional and longitudinal analyses. In this chapter, we will discuss the recent experimental, clinical and epidemiological data of the possible impact of mtDNA content on cardiac structure and function.
Keywords: Echocardiography; Left ventricle; Mitochondrial DNA content.