Being overweight or obese is a worldwide epidemic. Adiposity can cause fat mass-related cardiovascular disease (CVD). Adiposity may also cause adipocyte and adipose tissue anatomic and functional abnormalities, termed adiposopathy (adipose-opathy) or "sick fat," that result in endocrine and immune derangements. Adiposopathy may directly contribute to CVD through pericardiac and perivascular effects on the myocardium and blood vessels. Adiposopathy may also indirectly contribute to CVD through promoting or worsening major CVD risk factors such as type 2 diabetes mellitus, high blood pressure, and dyslipidemia. Despite CVD being the most common cause of mortality among overweight individuals, the pathophysiologic relationship between adiposity and CVD is often thought mysterious, as evidenced by "obesity paradoxes." Underlying this uncertainty are suggestions that excessive body fat does not always increase the risk of CVD and, in some cases, may actually decrease such risks. These paradoxical findings are made less paradoxical when the pathogenic potential of excessive body fat is assessed based on adipose tissue dysfunction rather than simply on increased fat mass alone. This introductory review 1) provides a brief historical perspective of the pathogenic potential of adipose tissue; 2) describes the relationships between adipose tissue (histology, embryology, and adipogenesis) and cardiovascular medicine; 3) outlines the anatomic, functional, endocrine, and immune manifestations of adiposopathy; and 4) describes the importance of cross talk and/or interactions of adipose tissue with other body tissues. Finally, this review describes how "sick fat" helps account for various clinical obesity/cardiovascular paradoxes, supporting adiposopathy as a cardiovascular disease.
Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.