Abstract
Chronic heart failure (CHF) and obesity are two conditions frequently associated and which, despite all the advances made in their management in the recent years, their prevalence continues to rise. Obese patients present unique challenges in the diagnosis of CHF and also therapeutic particularities. The genetic differences may be a possible explanation for the fact that some people, irrespective of their lifestyle and common classical cardiovascular risk factors, are more susceptible to develop heart failure. Moreover, the adipose tissue, a huge endocrine organ which secretes adipokines, is also a well-established source of all renin-angiotensin-aldosterone system components, being strongly involved in the pathogenesis of CHF. That is why this review will explore the possible links between the RAS genetic polymorphisms and leptin secretion in obese HF patients, trying to bring a more precise understanding of this relationship, which will undoubtedly facilitate a more appropriate treatment of HF in obese patients. We also try to explain the possible incriminated mechanisms, and plausible biological explanations for the relationship between RAS genetic polymorphisms and adipokines secretion in obese heart failure patients.