Dear Colleagues,

Obesity is a growing worldwide disease and a risk factor for the development of heart failure and sudden cardiac death. Isolated obesity can directly cause cardiomyopathy in humans though its effect on cardiac function and structure may not be easily isolated from those of comorbidities, such as hypertension, diabetes, dyslipidemia, and coronary artery disease. Additionally, obesity per se leads to increased blood volumes along with decreased systemic arterial resistance, resulting in high cardiac output and subsequent cardiac adaptations in structure and function. In any case, obesity and its related comorbidities affect cardiac physiology in an additive and/or synergetic fashion. They can directly attack the myocardium and also coronary arteries by provoking muscle injury and endothelial dysfunction, respectively, leading to cardiomyopathy and vasculopathy. In this scenario, inflammation, hypertrophy and apoptosis are the main tissue responses. Additionally, an increase in fat and fiber depositions as events of steatosis and fibrosis, can worsen the cardiovascular function. Unfortunately, the underlying molecular mechanisms have not yet been discovered, leading to a lack of effective therapeutic strategies and prognostic biomarkers. Likely, alterations in cardiac metabolism might be initial precursors of the cardiac dysfunction under an obesogenic milieu.

Dr. Óscar Lorenzo González
Guest Editor

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• obesity
• cardiomyopathy
• cardiac function
• risk factor
• cardiac morphology
• dyslipidemia