Cardiac Remodeling in Obesity

Abstract

Obesity has generated much interest within the cardiovascular community within the past 2 decades.1 It is now recognized that obesity is an important contributor to cardiac and all-cause mortality,1,2 independent of its association with other cardiovascular risk factors and increases the risk for cardiovascular morbidity, including heart failure (Figure 1).2–4 The malefic consequences of obesity are due both to the associated structural and functional cardiac alterations as well as the high prevalence of coexisting conditions, such as coronary artery disease, hypertension, sleep–disordered breathing (SDB), and diabetes mellitus.1–7 To better understand the relationship between obesity and heart failure, we will review what is known about cardiac structural remodeling in obesity as well as the evidence for preclinical abnormalities in left-ventricular (LV) systolic and diastolic functions. We will place particular emphasis on newer concepts and findings suggested by contemporary imaging methods. Figure 1. The population attributable risk of heart failure because of overweight is 14% in women and 8.8% in men. In obesity, the corresponding population attributable risks in women and men are 13.9 and 10.9%, respectively. From Kenchaiah et al,4 used with permission. By National Institutes of Health criteria, obesity is defined as a body mass index (BMI) ≥30 kg/m2 and severe obesity as a BMI≥40 kg/m2.8 Obesity involves the growth of both lean body mass and adipose tissue and is characterized by a disproportionate growth of adipose tissue in relationship to lean body mass.9 It is now recognized that adipose tissue is not a homogeneous organ, but is differentiated in relation to its metabolic activity. Whereas fat accumulating in the subcutaneous region does not require substantial blood supply,10 fat surrounding organs (abdominal, epicardial) is metabolically active, requires energy, and produces a number of compounds …