Obesity has reached global epidemic proportions in both adults and children and is associated with numerous comorbidities, including hypertension (HTN), type II diabetes mellitus, dyslipidemia, obstructive sleep apnea and sleep-disordered breathing, certain cancers, and major cardiovascular (CV) diseases. Because of its maladaptive effects on various CV risk factors and its adverse effects on CV structure and function, obesity has a major impact on CV diseases, such as heart failure (HF), coronary heart disease (CHD), sudden cardiac death, and atrial fibrillation, and is associated with reduced overall survival. Despite this adverse association, numerous studies have documented an obesity paradox in which overweight and obese people with established CV disease, including HTN, HF, CHD, and peripheral arterial disease, have a better prognosis compared with nonoverweight/nonobese patients. This review summarizes the adverse effects of obesity on CV disease risk factors and its role in the pathogenesis of various CV diseases, reviews the obesity paradox and potential explanations for these puzzling data, and concludes with a discussion regarding the current state of weight reduction in the prevention and treatment of CV diseases.

Obesity has reached epidemic proportions in the United States and worldwide. Considering the adverse effects of obesity on left ventricular (LV) structure, diastolic and systolic function, and other risk factors for heart failure (HF), including hypertension and coronary heart disease, HF incidence and prevalence, not surprisingly, is markedly increased in obese patients. Nevertheless, as with most other cardiovascular diseases, numerous studies have documented an obesity paradox, in which overweight and obese patients, defined by body mass index, percent body fat, or central obesity, demonstrate a better prognosis compared with lean or underweight HF patients. This review will describe the data on obesity in the context of cardiopulmonary exercise testing in HF. Additionally, the implications of obesity on LV assist devices and heart transplantation are reviewed. Finally, despite the obesity paradox, we address the current state of weight reduction in HF.

Omega-3 polyunsaturated fatty acid (omega-3 PUFA) therapy continues to show great promise in primary and, particularly in secondary prevention of cardiovascular (CV) diseases. The most compelling evidence for CV benefits of omega-3 PUFA comes from 4 controlled trials of nearly 40,000 participants randomized to receive eicosapentaenoic acid (EPA) with or without docosahexaenoic acid (DHA) in studies of patients in primary prevention, after myocardial infarction, and most recently, with heart failure (HF). We discuss the evidence from retrospective epidemiologic studies and from large randomized controlled trials showing the benefits of omega-3 PUFA, specifically EPA and DHA, in primary and secondary CV prevention and provide insight into potential mechanisms of these observed benefits. The target EPA + DHA consumption should be at least 500 mg/day for individuals without underlying overt CV disease and at least 800 to 1,000 mg/day for individuals with known coronary heart disease and HF. Further studies are needed to determine optimal dosing and the relative ratio of DHA and EPA omega-3 PUFA that provides maximal cardioprotection in those at risk of CV disease as well in the treatment of atherosclerotic, arrhythmic, and primary myocardial disorders.

Our investigation indicates that a state of reduced natriuretic peptide level exists in the obese individual with heart failure.

Digoxin did not reduce overall mortality, but it reduced the rate of hospitalization both overall and for worsening heart failure. These findings define more precisely the role of digoxin in the management of chronic heart failure.