Heart Failure, Obesity and Bariatric Surgery


Address for correspondence:
Juanita Reigle, RN, MSN, APRN, BC, University of Virginia Health System, PO Box 800158, Charlottesville, VA 22908
E-mail: jrl6g@virginia.edu


Mr J, a 43-year-old male with a nonischemic dilated cardiomyopathy and morbid obesity (weight 371 pounds, body mass index [BMI] 50 kg/m2) was referred for bariatric surgery. His cardiac condition made him a suitable candidate for cardiac transplantation but, unfortunately, he was too obese. His past medical history included obstructive sleep apnea, hypertension, hyperlipidemia, degenerative joint disease, gastroesophageal reflux disease, and placement of a biventricular pacemaker and implantable cardioverter defibrillator. For years, he attempted to lose weight but was unsuccessful, despite referral to a nutritionist and exercise physiologist. Mr J had been stable on a typical heart failure regimen, although he continued to exhibit New York Heart Association Class III symptoms. An echocardiogram showed an ejection fraction of 25%, a left ventricular diameter of 5.7 cm, and a left ventricular posterior wall of 1.5 cm. His fasting triglycerides were 368 mg/dL. A right heart catheterization showed a pulmonary artery (PA) wedge pressure of 20 mm Hg and a PA systolic pressure of 45 mm Hg.

Mr J underwent a Roux-en-Y gastric bypass procedure, in which the gastric size is reduced and surgically connected to the jejunum, without complications. He had a relatively uneventful postoperative course and at 6 months his weight was 285 pounds (BMI 38.6 kg/m2) and his triglycerides were 128 mg/dL. Two years after gastric bypass surgery his weight was 198 pounds (BMI 27 kg/m2) and he remained active, walking approximately 3 miles a day. An echocardiogram showed an ejection fraction of 35% to 40%, left ventricular posterior wall of 1.0 cm, and a left ventricular diameter of 5.6 cm. Mr J has resumed work as a bus driver and is followed by the heart failure team.

Obesity is one of the greatest health care risks facing the world's population. The World Health Organization estimated that in 2002 more than 300,000 deaths in the United States were weight-related.1 The burden of this burgeoning epidemic is even more profound when considering the significant sequelae of obesity such as diabetes, arthritis, sleep apnea, hypertension, stroke, cardiovascular disease, heart failure, and premature death.

BMI is one measure used to assess nutritional status and is commonly used as a measure of obesity (see Table I).2 Obesity, defined as a BMI >30 kg/m2, is an important risk factor for development of heart failure.3 After adjustment for known risk factors, data from the Framingham Heart Study revealed a 5% and 7% increased risk of developing heart failure for men and women, respectively, with each 1 Unit incremental increase in BMI.4 Regardless if obesity is the cause of a cardiomyopathy or a coexisting condition, health care professionals must consider the cardiac consequences of obesity and surgical options for weight loss in this population.

Table I. Body Mass Index (BMI) and Weight Classification
  1. BMI=weight in kilograms divided by the square of the height in meters (kg/m2). Available from: http://www.who.int/bmi/index.jsp?introPage=intro_3.html

Obesity (Class 1)30–34.9
Obesity (Class 2)35–39.9
Morbid obesityAbove 40


Obesity is associated with numerous structural and functional cardiovascular abnormalities. In obese individuals, fat deposition moves beyond adipose tissue to organs such as the liver, kidneys, and heart. This phenomenon, known as ectopic fat storage, can impair tissue and organ function. Fat deposition occurs in the heart and vascular system as weight increases. In animal models, cardiac fat pads increase around the base of both ventricles leading to elevated end diastolic pressures, decreased diastolic compliance, and elevated atrial pressures.5 Postmortem evaluation of obese humans found increased heart mass, ventricular hypertrophy, and microscopic myocyte hypertrophy.6,7 Changes in the vascular system occur as blood vessels lose elasticity when fat wraps around and infiltrates the cells. The increased vascular stiffness and high metabolic demands from increased fat and organ mass add to cardiac workload.5,6,8

Changes in the cardiac function and structure may play a significant role in the increased incidence of atrial and ventricular dysrhythmias in the obese. The risk of persistent atrial fibrillation increases as BMI increases.9 In one study, signal-averaged electrocardiograms in individuals with a BMI >30 kg/m2 had significantly more abnormalities compared with healthy, normal weight individuals.10 Obese patients postmyocardial infarction who enrolled in the Multicenter Automatic Defibrillator Implantation Trial-II trial had a significantly more ventricular tachyarrhythmias than nonobese patients.11

Although ectopic fat storage impairs cardiac function, other factors contribute to the development of heart failure. Obesity is associated with dyslipidemia, particularly elevated triglycerides and decreased high-density lipoprotein levels. Elevated free fatty acid levels lead to endothelial dysfunction, decreased nitric oxide production, release of inflammatory cytokines such as interleukin-6 and tumor necrosis factor-α, and vasoconstriction.5,12 The excess adipose tissue is richly supplied with blood vessels resulting in an increased intravascular volume.8 The elevated preload, coupled with the elevated metabolic activity of adipose tissue, leads to chamber dilatation, increased wall stress, increased myocardial oxygen consumption, and eventually contributes to left ventricular dysfunction.8,13


Despite overwhelming evidence that obesity increases the risk of heart failure, once heart failure is present, all-cause mortality and death from worsening heart failure is lower in obese persons. In fact, obesity may predict survival, with mildly obese individuals having the best prognosis.6,14,15 There are several theories for this perplexing fact. First, obese individuals with heart failure may be diagnosed earlier with less severe myocardial dysfunction.15,16 Second, overweight and obese individuals typically have elevated blood pressures at baseline and are better able to tolerate higher doses of angiotensin-converting enzyme inhibitors and β-blockers.14 Third, some speculate that high serum lipoproteins have a protective effect by neutralizing inflammatory cytokines.14,15 Fourth, cardiac cachexia, a wasting syndrome seen in advanced heart failure, is associated with a poor prognosis. However, obese individuals have more calorie and protein stores and may be better able to meet the metabolic demands of chronic heart failure.15,16 Finally, the sympathetic response to exercise in lean individuals is more exaggerated with higher epinephrine and renin levels compared with obese persons, which may confer a better prognosis.14


Despite data suggesting that obesity may offer a mortality benefit for individuals with heart failure, weight loss, especially for morbidly obese individuals, is recommended.17 Nonsurgical weight loss from dietary changes, exercise, or pharmacological therapies can improve functional capacity, reduce the incidence of diabetes, improve the lipid profile, improve left ventricular diastolic function, reduce hypertension, and improve quality of life.18,19 Modest weight loss of 4.5% or more in mildly obese individuals is associated with reduced left ventricular mass and improved diastolic function.16,20

Other treatment options for effective weight loss include surgical interventions, such as gastric banding and gastric bypass. Since 1993, the number of bariatric surgeries performed on obese adults in the United States has increased more than 9-fold.21 Bariatric surgery candidates are generally morbidly obese (BMI ≥40 kg/m2) and have been unsuccessful in losing significant weight by nonoperative means. In the presence of high-risk comorbid conditions, such as obese-related cardiomyopathy, a BMI of 35 kg/m2 is considered criteria for bariatric surgery.22 Bariatric surgery is performed using either open or laparoscopic techniques and depending on the operative procedure used, the risks of preoperative and postoperative complications vary. In general, operative mortality (30-day) is <2% for all surgical approaches.22,23

In the past, obese patients with cardiac disease were considered high risk for preoperative complications such as myocardial infarction, and thus excluded from gastric bypass procedures. Recent case reports and studies have refuted this assumption and indicate that bariatric surgery is an acceptable option in this population.19,23–25 When compared with patients without cardiac disease, patients with coronary artery disease or heart failure had more comorbid conditions before surgery and a slightly longer hospital stay, but no deaths during the hospitalization and no cardiac mortalities for up to 5 years after bariatric surgery.23 Moreover, in long-term follow-up, bariatric surgery patients have significant reductions in cardiovascular risk factors compared with nonsurgical control groups.26,27 In patients with preexisting cardiac disease, including heart failure, gastric bypass results in a reduction of all comorbid conditions, including sleep apnea, degenerative joint disease, hypertension, and diabetes.23 In morbidly obese patients with heart failure, case reports indicate that bariatric surgery has resulted in significantly reduced chamber size and wall thickness and improved systolic function and diastolic filling.19,21,23


Obesity is a risk factor for developing heart failure and is associated with multiple comorbid conditions. Although specific treatment for each comorbid condition is important, weight loss can significantly reduce the long-term harmful consequences and improve quality of life. Bariatric surgery in obese individuals with heart failure appears to provide an overall mortality benefit, particularly with reductions of cardiovascular deaths.24,25,28