At the Heart of Severe Obesity: Chronic Heart Failure and the Role of Bariatric Surgery

| September 1, 2019

by Michael W. Foster, MD; Colleen M. Tewksbury, PhD, RD; Gerard Hoeltzel; Noel N. Williams, MD; J. Eduardo Rame, MD, MPhil; and Kristoffel R. Dumon, MD

Drs. Foster, Tewksbury, Williams, and Dumon and Mr. Hoeltzel are with the Department of Surgery, Division of Gastrointestinal Surgery at Penn Metabolic and Bariatric Surgery Center, and Drs. Foster and Rame are with the Department of Medicine, Division of Cardiovascular Medicine at the Hospital of the University of Pennsylvania in Philadelphia, Pennsylvania.

Funding: No funding was provided.

Disclosures: The authors report no conflicts of interest relevant to the content of this article.

Abstract: Patients with obesity are likely to be diagnosed with chronic heart failure earlier than those with normal weight. Despite the maladaptive effects that obesity has on cardiac structure and function, patients with obesity live longer than their normal-weight counterparts after diagnosis of heart failure is made. Known as the “obesity paradox,” this phenomenon and the likely mechanisms underlying this observation are discussed by the authors of this review article, along with the potential benefits of bariatric surgery for patients with heart failure who also suffer from severe obesity.

Keywords: obesity, chronic heart failure, cardiomyopathy, neurohumoral, obesity paradox, bariatric surgery

Bariatric Times. 2019;16(9):14–16.

Among the myriad comorbidities associated with obesity, cardiac structure and function are adversely affected with increasing body mass index (BMI).1,2 Both systolic and diastolic dysfunction, which can lead to chronic heart failure (CHF), occur at higher rates among patients with obesity.3,4 According to a study of over 5,000 Framingham Heart Study participants, the risk of heart failure is increased by five percent in men and seven percent in women for every 1kg/m2 increase in BMI.3 The metabolic syndrome is more prevalent among patients with obesity than those with normal BMI.5 Hyperlipidemia, hypertension, and insulin resistance associated with metabolic syndrome lead to atherosclerotic changes to the coronary vasculature, which predisposes patients to coronary artery disease and eventually myocardial infarction (MI). Cardiac ischemia during an MI can result in ischemic cardiomyopathy, a type of heart failure with reduced ejection fraction (HFrEF), as the heart might not adequately contract during systole after the insult.6

Diastolic dysfunction, or the inability to relax the heart sufficiently during diastole, is also prevalent among patients with obesity and is often referred to as obesity cardiomyopathy.7 Hypertension can cause left ventricular hypertrophy and subsequent heart failure with preserved ejection fraction (HFpEF) if blood pressure is not controlled.7,8 This is because the left ventricle must squeeze harder to eject blood into the aorta when afterload is increased. The adiposity among patients with severe obesity increases the total blood volume, which increases the pressure of blood filling the left ventricle during diastole. This leads to left ventricular (LV) enlargement, increased cardiac wall stress, and eventual HFpEF.5 This process can also result in pulmonary hypertension and right ventricular (RV) failure if blood is backed up into the pulmonary vasculature for a prolonged period.6

Additionally, obesity hypoventilation syndrome (OHS) can result in RV failure.6 OHS is a restrictive lung disease that is caused by an overabundance of abdominal adipose, which restricts contraction of the diaphragm and prevents ventilation by decreasing lung compliance, causing hypoxemia. Hypoxic vasoconstriction occurs as a result of insufficient alveolar oxygenation within the lung itself. Normally, when the pulmonary capillaries are not receiving enough oxygen, arterioles constrict in an effort to shunt blood to parts of the lung that are oxygenating. But in the setting of OHS, the entire lung is not oxygenating properly, and the result is pulmonary arterial hypertension, which puts a strain on the RV as it pumps against higher pressures.6 This leads to RV hypertrophy and eventual RV failure.6 Avoiding obesity would help to prevent the adverse cardiovascular consequences it causes, including heart failure, but there exists a counterintuitive phenomenon known as the “obesity paradox” present in the literature that suggests that obesity might be protective in CHF.9 So even if intentional weight loss is possible, would it be beneficial for this population?

Unraveling the Mysteries of the Obesity Paradox

Often referred to as the “obesity paradox,” it is the observation that patients with overweight or obesity and cardiovascular disease (CVD), including CHF, live longer from the time of diagnosis than their matched counterparts with normal BMI.9 According to several meta-analyses, patients with CHF and a BMI greater than 30kg/m2 were shown to have a reduction in mortality risk of up to 33 percent compared to patients with a BMI between 18.5 and 29.9kg/m2.10–13 Since the obesity paradox was first described in heart failure using BMI cutoffs, several studies improved the predictability of survival using other anthropometric measures of adiposity, including waist circumference, percent body fat mass, and bioelectrical impedance.14,15 Central obesity and percent body adiposity are more specific measures of overall metabolic status, risk of insulin resistance, and earlier-onset of both CVD and CHF than BMI alone.16 Between the differences in onset of disease, metabolic profile, and lack of cardiac cachexia among the population with obesity, there are several explanations for the improved survivability of those with higher levels of adiposity compared to individuals with normal fat distribution and BMI.17,18

Explanations for the obesity paradox in CHF can be separated into three categories: observational, hormonal/metabolic, and hemodynamic tolerance.

Observational. Patients with obesity tend to present and are given a CHF diagnosis earlier than their normal-weight counterparts.5 This could be due to lower cardiopulmonary fitness or restrictive lung disease, leading to acute shortness of breath and further evaluation by medical staff upon arrival to the emergency department or primary care office. Tests performed to evaluate acute shortness of breath might reveal underlying heart failure earlier than usual given the patient’s risk stratification. Despite the observation that patients with obesity are less likely to seek care and obtain follow-up treatment, CHF diagnosis is still made earlier for this population, likely due to the disturbing and debilitating nature of acute decompensated heart failure. Another reason for their earlier presentation could be due to a lower level of the circulating atrial natriuretic peptides (ANP) and brain natriuretic peptides, (BNP), which are released into the blood as a result of left atrial stretch from volume overload and/or left ventricular failure.19 ANP and BNP are responsible for renal clearance of excess sodium and fluids, in addition to vasodilation and reduction of cardiac afterload.19 Patients with obesity have lower levels of these peptides, which might result in earlier-onset shortness of breath secondary to CHF. If patients are diagnosed with CHF earlier, improvement in survival, if measured from the time of diagnosis as previous studies have done, could be due to a lead-time bias. That is, if diagnosis is made earlier, survival appears longer. Lastly, since patients with obesity have differing etiologies for heart failure (they are more likely to have HFpEF predominance),6,10,11 survivability discrepancies can be expected.

Hormonal/metabolic. Perhaps the most investigated explanation for the obesity paradox, hormonal and metabolic changes that occur with obesity should be viewed through two different lenses. First, is the patient metabolically healthy and therefore able to store fat and acquire obesity, whereas patients that are unable to gain weight are at a metabolic disadvantage? And second, does adiposity itself have protective effects on the long-term outcome for patients with CHF? Patients with chronic illness, including cancer and CHF, undergo cachexia, whereby the inflammatory cytokines tumor necrosis factor-alpha, interleukin-6, and interferon gamma induce deterioration of muscle through the ubiquitin-proteasome pathway and adipose tissue via lipolysis.20 This highly inflammatory, catabolic state is associated with both normal or underweight BMI and increased mortality.21 Patients with obesity are likely not undergoing this process, which suggests that they are at a metabolic advantage compared to patients with lower levels of adiposity.

The adipose tissue itself could have a protective effect on survival, but this is not well understood, and more research is needed to shed light on this possibility. Although diet-induced obesity and impaired insulin signaling from metabolic syndrome result in lipotoxicity, or excess lipid accumulation in tissues, adaptive mechanisms provide some protection from overwhelming cardiac damage (Figure 1). Leptin, an adipokine, is produced in adipocytes and promotes satiety through a hypothalamic signal mechanism and mobilizes fat stores to regulate body weight.22,23 The mobilization of fats allows tissues, including the heart, to utilize them as a metabolic substrate for energy. According to a study by Bedi et al,24 the failing heart uses ketones, derived from fat, for metabolic energy, instead of glucose for glycolysis and free fatty acids for beta oxidation in a normally functioning heart. While it is controversial, it is possible that the insulin resistance associated with the metabolic syndrome could be beneficial, as it would promote ketogenesis over glucose utilization, which, for the failing heart, might provide additional access to its preferred metabolic fuel. According to this paradigm, the mobilization of fats by leptin, insulin resistance, and the increase in pericardial fat available for lipolysis and subsequent ketogenesis among patients with obesity, progression to late-stage heart failure might be delayed by readily available substrates for metabolism.24,25

Hemodynamic tolerance. Hypertension associated with obesity allows for higher levels of cardioprotective medications, such as beta-adrenergic blockers, angiotensin-converting-enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs), and aldosterone antagonists, to be administered to patients with CHF. The increase in activity of the renin-angiotensin-aldosterone and beta adrenergic mechanisms contribute to pathologic myocardial remodeling that contribute to heart failure, so inhibition of these pathways is beneficial and has been shown to promote “reverse remodeling” where the pre-CHF structure and function of the heart is at least partly re-established.26,27 Additionally, the effect of Entresto (sacubitril/valsartan), a neprilysin inhibitor/ARB combination drug that has been proven to reduce mortality and heart failure hospitalizations, could be enhanced in patients with obesity.28 Sacubitril inhibits the breakdown of ANP and BNP, which is deficient in patients with obesity, so up-regulation of these hormones could be especially beneficial to this population and further confer a survival benefit.28 Whether it is the tolerability to neurohumoral blockade among patients with obesity/hypertension or the increased dosages of the medications themselves, it is reasonable to conclude that the ability to take more cardioprotective medications is beneficial to delay the progression of heart failure.27,28

The debate concerning whether obesity might play a protective role in the progression to end-stage heart failure might be ongoing, but for patients with severe obesity, the message is clear: the obesity paradox regarding heart failure shows a benefit for patients with overweight and low-level obesity, but not those with severe obesity who would be potential candidates for bariatric surgery.29 The potential metabolic, hormonal, and hemodynamic benefits of having a higher-than-normal BMI have a diminishing effect once obesity becomes severe.2,5 It seems there is a “sweet spot” for the cardiometabolic benefit to adiposity, but for the bariatric population whose obesity is severe, intentional weight loss is preferred.5,30–32

The Role of Bariatric Surgery in Patients with Severe Obesity and Chronic Heart Failure

Despite the documented obesity paradox, patients with CHF and obesity are encouraged to lose weight to improve cardiovascular function.30,31 The reduction in hypertension, hyperlipidemia, and diastolic dysfunction that results from successful weight reduction has been demonstrated to improve outcomes for patients with CVD and Class 2 or 3 (“severe”) obesity, defined as having a BMI of 35 to 40kg/m2 or greater than 40kg/m2, respectively.30–32 In addition to potentially improving cardiac symptoms, these patients might also benefit from improvements in insulin sensitivity and metabolic health.32 Although there is some speculation that insulin resistance has a protective effect for the failing heart, this research is ongoing and can be considered speculative. In 2015, the American Heart Association and the American Diabetes Association released a joint scientific statement underscoring the importance of diabetes management via intentional weight loss for the prevention of CVD.32 The cardiac benefits of weight loss are not limited to those with severe obesity; remission from lower levels of obesity has been shown to improve cardiac morphology and function.33 A study by Hou et al33 demonstrated favorable reduction in LV and RV chamber size, LV wall thickness, left ventricular end diastolic diameter (LVEDD), and an increased left ventricular ejection fraction (LVEF) following weight reduction from moderate obesity.

Although lifestyle modification, including eating pattern changes and exercise, are helpful for any patient with diabetes, patients with severe obesity are also encouraged to consider bariatric surgery for effective risk management and possible diabetes reversal.34 For patients with severe obesity, intensive behavioral therapy, including dietary changes, increases in exercise, and lifestyle modification, produces clinically meaningful improvements in blood pressure, serum lipids, and insulin sensitivity but is not an effective method for sustained, significant weight loss.36–38 Although some patients might lose weight with intensive behavioral therapy, weight regain is common with time and less intensive intervention. Bariatric surgery remains the primary evidenced method for long-term and durable weight loss in patients with severe obesity.39

A meta-analysis of 4,070 patients who underwent bariatric surgery reported an overall Type 2 diabetes mellitus (T2DM) resolution rate of 78 percent following the procedure.34 Weight loss following bariatric surgery is accompanied by dramatic improvements in coronary artery disease and its risk factors and potential reversal of diabetes and dyslipidemia.34,35,40,41 This leads to the potential for prevention of ischemic cardiomyopathy along with the possibility for myocardial reverse remodeling.33 Recently, a study by Fisher et al42 showed that patients with severe obesity and T2DM had reductions in macrovascular events and improved outcomes following bariatric surgery. Furthermore, reduction in total blood volume following significant, maintained weight loss can prevent diastolic dysfunction, while decreased abdominal adiposity can relieve RV stress in the setting of OHS. For patients with advanced heart failure, bariatric surgery might still play a role in disease management.

Late- and end-stage heart failure might require additional support or heart transplant (HT) in order to prolong life.43 For these patients with advanced heart failure (New York Heart Association Functional Class IV), cardiac output is devastatingly low. Some patients with HFrEF might require inotropes such as milrinone, which helps the heart to squeeze harder during systole.44 But when cardiac function worsens or the patient does not tolerate higher doses of inotropes, next steps include the implantation of a left ventricular assist device (LVAD), which is a form of mechanical circulatory support (MCS), or HT. Many patients with severe obesity are limited by BMI cutoffs for HT (not typically performed in patients with BMI ≥35kg/m2), so bariatric surgery following LVAD implantation is their only viable option.46 MCS can therefore be given to patients with advanced heart failure as a bridge to transplant if they are able to have enough intentional weight loss to qualify for HT. For these critically ill patients, bariatric surgery is the difference between MCS as a palliative/destination therapy option and MCS as a bridge to cardiac transplantation.


The impressive improvements in metabolic and cardiovascular health, including prevention and improvement in CHF, have led to a sharp increase in the number of bariatric surgery cases per year (158,000 cases in 2011 compared to 228,000 cases in 2017).46 Despite the clear cardiovascular benefits of bariatric surgery for patients with heart failure and severe obesity, clinicians might be hesitant to prescribe a proven method of rapid, long-lasting weight loss because of the possible protective effect of overweight and low-level obesity.47 It is important to differentiate patients with severe obesity who are candidates for bariatric surgery from those with BMI less than 35kg/m2 who might benefit from adiposity in the setting of catabolic disease. Intentional weight loss is beneficial for patients with CHF and severe obesity, including the recommendations to do so, and bariatric surgery is the only proven method of long-lasting, durable weight loss in this population.36–39


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