Risks and Benefits of Weight Loss in Heart Failure

Overweight and obesity are well-established risk factors for most cardiovascular diseases (CVD), including coronary heart disease (CHD), heart failure (HF), and atrial fibrillation. Despite the strong link between excess adiposity and risk of CVD, growing evidence has demonstrated an obesity paradox in patients with CVD. This phenomenon is characterized by a better prognosis in overweight and mildly obese CVD patients than their leaner counterparts. Moreover, the worst outcomes are often incurred by underweight CVD patients, followed by those of normal weight or severely obese. The obesity paradox is now a well-established phenomenon across different types of CVD, and it occurs regardless of age and ethnicity of patients, and severity of CVD. Physical inactivity and low cardiorespiratory fitness (CRF) have long been recognized as major risk factors for CVD. In contrast, high levels of physical activity (PA) and CRF largely neutralize the adverse effects of excess adiposity and other traditional CVD risk factors, including hypertension, metabolic syndrome, and type-2 diabetes. Higher CRF also results in better CVD outcomes across different BMI groups and significantly alters the obesity paradox in patients with HF and CHD. Prognostic benefits of overweight/obesity tend to be limited to unfit patients with HF and CHD, and the obesity paradox usually disappears with improved levels of CRF. Nevertheless, increased PA and exercise training, to maintain or improve CRF, are effective, safe, and proven strategies for primary and secondary prevention of CVD in all weight groups. In this review, we discuss the current concepts of individual and combined contributions of fatness and fitness to CVD risk and prognosis. We then examine the influence of fitness on the obesity paradox in individuals with CVD.

Overweight and obesity, usually defined by high body mass index (BMI), have become a public health problem worldwide. Obesity is a major risk factor for cardiac remodeling and development of heart failure (HF). BMI usually correlates with HF risk in a dose-dependent fashion. A complex interaction between several mechanisms underlies the strong relationship between obesity and HF.

It is now well established that an obesity paradox exerts a protective effect once HF is manifest. This obesity paradox, characterized by a better prognosis in overweight or mildly obese HF patients compared to their leaner counterparts, is observed across different ethnicities and regardless of the type, acuity or etiology of HF. The interaction between BMI and prognosis of HF is usually nonlinear with an abrupt increase in the risk of adverse outcomes in underweight and to a lesser extent in severely obese HF patients. Mechanisms of the obesity paradox remain poorly understood. Recent evidence has suggested that the protective effect of obesity is significantly influenced by lean body mass (rather than fat mass), nutritional status, muscle strength, and cardiorespiratory fitness (CRF). Weight loss, achieved via diet, exercise, and/or bariatric surgery can result in significant improvements of obesity-associated hemodynamic alterations, cardiac dysfunction, and morphologic changes. However, scientific evidence on the safety, efficacy, and strategies of purposeful weight loss in obese HF patients remains limited. Intentional weight loss seems to be reasonable in severely obese HF patients because of proven detrimental effects of severe obesity in this patient population. More importantly, interventions in obese HF patients should focus on increasing physical activity, exercise training (ET) and improving CRF, regardless of the effect on BMI.

In this chapter, we discuss the current concepts of the relation of overweight/obesity with cardiac remodeling and dysfunction, and development of HF. We then examine the current evidence on the clinical utility of natriuretic peptides in obese individuals. We also review the prognostic implications of obesity in HF in light of the obesity paradox. Finally, we discuss the current data on the benefits and risks of weight loss and the prognostic impact of ET and cardiorespiratory fitness in patients with HF.

High-output heart failure (HF) is an unusual cause of cardiac failure that has not been well-characterized.

This study sought to characterize the etiologies, pathophysiology, clinical and hemodynamic characteristics, and outcomes of high-output HF in the modern era.

We performed a retrospective analysis of all consecutive patients referred to the Mayo Clinic catheterization laboratory for hemodynamic assessment between 2000 and 2014. Subjects with definite HF, as defined by the Framingham criteria, were compared to controls of similar age and sex.

The most common etiologies of high-output HF (n = 120) were obesity (31%), liver disease (23%), arteriovenous shunts (23%), lung disease (16%), and myeloproliferative disorders (8%). Compared with controls (n = 24), subjects with high-output HF displayed eccentric left ventricular remodeling, greater natriuretic peptide activation, higher filling pressures, pulmonary hypertension, and increased cardiac output, despite similar ejection fraction. Elevated cardiac output in high-output HF patients was related to both lower arterial afterload (decreased systemic vascular resistance) and higher metabolic rate. Mortality was increased in high-output HF as compared with controls (hazard ratio: 3.4; 95% confidence interval: 1.6 to 7.6). Hemodynamics and outcomes were poorest amongst patients with the lowest systemic vascular resistance.

High-output HF is an important cause of clinical HF in the modern era that is related to excessive vasodilation, and most frequently caused by obesity, arteriovenous shunts, and liver disease. Given the high mortality and increasing prevalence of these comorbidities in Western countries, high-output HF must be considered in the differential diagnosis of patients presenting with dyspnea, congestion, and a normal ejection fraction.