(Circulation. 1997;96:3248-3250.)
© 1997 American Heart Association, Inc.
Articles |
Obesity and Heart Disease
A Statement for Healthcare Professionals From the Nutrition Committee, American Heart Association
Key Words: AHA Medical/Scientific Statements • obesity • cardiovascular diseases • coronary disease • heart failure
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Introduction |
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 Top Introduction Definition of ObesityObesity and Coronary Heart...Congestive Heart FailureTreatment of Obesity and...References |
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Obesity is an increasingly prevalent metabolic disorder affecting not only the US population but also that of the developing world. It is estimated from the third National Health and Nutrition Examination Survey (NHANES III) (1988-1991) that 33% of the US population is obese, compared with 25% in NHANES II (1976-1980).1 Fatness is associated with a number of comorbidities, including several forms of heart disease. Although heredity explains 30% to 70% of cases of obesity, environmental contributions to the increasing prevalence of obesity must be sought since the gene pool has remained stable over the same interval. Diets high in fat (and calories)2 and a reduced expenditure of energy in the form of physical activity3 are the most likely explanations. However, in the United States, despite the reduction in consumption of fat from approximately 40% of calories in 1965 to 34% of calories in 1991,4 a decrease in incidence of obesity has not occurred. This is likely attributable to both maintenance of fat intake with an increase in total caloric intake and reduced physical activity. Interestingly, in developing countries some comorbidities are seen at a lesser degree of excess weight, suggesting that relative weight may be as important as absolute adiposity.
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Definition of Obesity |
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TopIntroductionDefinition of ObesityObesity and Coronary Heart...Congestive Heart FailureTreatment of Obesity and...References |
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The definition of obesity, or being overweight,5 remains controversial. In the United States, mortality data provided by the Metropolitan Life Insurance Company historically have been used to define obesity.6 Yet these data relate to mortality only, and the definition depends on a person's frame (size), which is arbitrary and not independently related to obesity-related mortality or comorbidities. Body mass index (BMI) has recently gained favor as a better measure of adiposity.7 8 BMI is defined as weight in kilograms divided by height in meters squared (kg/m2). A threshold level of BMI to define obesity is not entirely appropriate because in women, a BMI <21 may be associated with the greatest protection from coronary heart disease mortality.9 Yet for many women a BMI near 30 may still not be of concern when the increase in adipose tissue is distributed in the pelvis and not the abdomen. Substantial evidence now indicates that an increased waist circumference, or waist-to-hip ratio, predicts comorbidities and mortality from obesity.10 11 Unfortunately, a BMI-based definition fails to take body fat distribution into account.
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Obesity and Coronary Heart Disease |
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TopIntroductionDefinition of ObesityObesity and Coronary Heart...Congestive Heart FailureTreatment of Obesity and...References |
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Until recently the relation between obesity and coronary heart disease was viewed as indirect, ie, through covariates related to both obesity and coronary heart disease risk,12 including hypertension; dyslipidemia, particularly reductions in HDL cholesterol; and impaired glucose tolerance or non–insulin-dependent diabetes mellitus. Insulin resistance and accompanying hyperinsulinemia are typically associated with these comorbidities.13 Although most of the comorbidities relating obesity to coronary artery disease increase as BMI increases, they also relate to body fat distribution. Long-term longitudinal studies, however, indicate that obesity as such not only relates to but independently predicts coronary atherosclerosis.9 14 15 This relation appears to exist for both men and women with minimal increases in BMI. In a 14-year prospective study, middle-aged women with a BMI >23 but <25 had a 50% increase in risk of nonfatal or fatal coronary heart disease,9 and men aged 40 to 65 years with a BMI >25 but <29 had a 72% increased risk.16 The overall relation between obesity and coronary artery disease morbidity and mortality is less clear for Hispanics,17 Pima Indians,18 and African-American women.19
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Congestive Heart Failure |
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TopIntroductionDefinition of ObesityObesity and Coronary Heart...Congestive Heart FailureTreatment of Obesity and...References |
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Left ventricular hypertrophy is common in patients with obesity and to some extent is related to systemic hypertension.20 However, abnormalities in left ventricular mass and function also occur in the absence of hypertension21 and may be related to the severity of obesity.22 Hypertension is approximately three times more common in obese than normal-weight persons.23 This relationship may be cause-and-effect in that when weight increases, so does blood pressure,24 whereas when weight decreases, blood pressure falls.25
Increased left ventricular volume and wall stress in addition to increased stroke volume and cardiac output are commonly seen in systemic hypertension.21 26 The hypertrophy of the left ventricle is both concentric and eccentric, and diastolic dysfunction is common. When obesity is present but systemic hypertension is absent, left ventricular volume is often increased, but wall stress usually remains normal. However, in obese patients without hypertension, increases in stroke volume and cardiac output as well as diastolic dysfunction are seen. These changes in the left ventricle are related to sudden death in obese patients. When 22 patients with severe obesity were examined postmortem, dilated cardiomyopathy was most frequently associated with sudden death (n=10), with severe coronary atherosclerosis (n=6), concentric left ventricular hypertrophy without dilatation (n=4), pulmonary embolism (n=1), and hypoplastic coronary arteries (n=1) also found.22 Thus, dilated cardiomyopathies, presumably with concomitant cardiac arrhythmias, may be the most common cause of sudden death in patients with severe obesity. The prolonged QT interval also seen in obesity27 may predispose to such arrhythmias.
Changes in the right heart also occur in obesity. The pathophysiology is related to obstructive sleep apnea and/or the obesity hypoventilation syndrome, which produce pulmonary hypertension and right ventricular hypertrophy, dilatation, progressive dysfunction, and finally failure.28 29 However, right ventricular dysfunction can also occur as a consequence of left ventricular dysfunction, and the heart failure that develops is often biventricular.21
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Treatment of Obesity and Heart Disease |
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TopIntroductionDefinition of ObesityObesity and Coronary Heart...Congestive Heart FailureTreatment of Obesity and...References |
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In patients with congestive heart failure, sodium restriction and small reductions in weight may dramatically improve ventricular function and oxygenation.30 31 In addition, several studies suggest that the more extensive weight reduction that follows gastrointestinal surgery for obesity reduces cardiovascular mortality32 and in persons with non–insulin-dependent diabetes, both cardiovascular and total mortality.33 Moreover, although many studies have demonstrated the beneficial effects of weight reduction on cardiovascular risk factors such as hypertension25 34 35 and dyslipidemia,36 37 recent studies from Sweden indicate that the major reduction of body weight that follows gastrointestinal surgery for obesity also reduces incidence of non–insulin-dependent diabetes mellitus.38 Shortening of the QT interval also follows weight reduction.39 Thus, weight reduction appears efficacious in reducing risks of coronary heart disease and congestive heart failure and potentially preventing heart disease in obese patients.
Treatment of obesity should be based on its severity and the presence
of comorbidities, eg, congestive heart failure,
dyslipidemia, hypertension, non–insulin dependent
diabetes, and obstructive sleep apnea. Maintaining a BMI <25
throughout adult life has been recently recommended.40 For
most patients with a BMI between 25 and 30, lifestyle modifications
including diet and exercise are appropriate. Diets should be modestly
restricted in calories; evidence suggests that obese patients who have
slower rates of weight reduction have the same long-term outcomes as
patients undergoing more rapid weight reduction.41
Restricting consumption of fat to <30% of total calories should also
be prescribed because low-fat diets may also promote weight
reduction.42 When rapid weight loss is needed, eg, for
severe biventricular heart failure, more severe caloric
restriction, eg, 
800 calories daily, with at least 0.75 g/kg
bioavailable protein, can be used.43 For less-urgent
weight reduction, a loss of 0.45 kg (1 lb) per week is
reasonable.44 This rate of weight loss would require a
caloric deficit of about 400 calories per day.
Training programs that increase physical activity have had a variable effect on body mass and composition.45 46 However, simply changing daily routines, eg, parking farther away and using the stairs rather than the elevator, may also be effective.47 Once weight loss has been achieved, a more vigorous exercise program may also enhance maintenance of reduction in weight.48
Pharmaceuticals should be considered with a BMI >30 or with less-severe obesity and comorbidities.49 50 The rationale for use and discussion with the patient about adverse effects of the medications should be documented in the patient's record. If the risk from obesity is sufficiently serious to indicate use of antiobesity drugs, long-term use should be anticipated. However, a case-control study in Europe demonstrated that patients treated with dexfenfluramine for more than 3 months had an odds ratio of 23.1 (95% confidence interval, 6.9 to 77.7) of developing primary pulmonary hypertension.51 A potential link between fenfluramine therapy of obese patients with valvular heart disease has also been raised.52 As a result, both fenfluramine and dexfenfluramine have been withdrawn from the market. Few drug choices remain. Like other nonsurgical therapies for obesity, once antiobesity drugs are discontinued, weight gain typically follows.53
When the BMI is >35 and comorbidities exist, gastrointestinal surgery becomes a consideration. When the BMI is >40, surgery is the treatment of choice. The experience of the surgeon and type of operation chosen predict outcome. In general, a Roux-en-Y gastric bypass is superior to gastric plication.54
Although weight reduction is not recommended for patients with a BMI <25, some patients in this category clearly have risks related to body fat distribution. Although measurement of waist circumference may help identify such patients, this assessment is crude, and other approaches are more expensive, ie, magnetic resonance imaging and computed tomography. Moreover, the radiation risk with some techniques (eg, computed tomography) precludes their use in children.
No matter what the therapeutic approach, it is important to realize that obesity is a disorder and recidivism is common, with <5% of patients maintaining their reduced weight at 4 years.55 Thus, therapeutic regimens must be maintained indefinitely; even then, only surgery has been proved to produce substantial sustained long-term weight loss. Prevention of obesity by diet and regular physical activity remains the highest priority for maintaining cardiovascular health. This is particularly important for small children and adolescents.
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Footnotes |
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"Obesity and Heart Disease" was approved by the American Heart Association Science Advisory and Coordinating Committee in August 1997.
A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0130.
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H. Eyre, R. Kahn, and R. M. Robertson Preventing Cancer, Cardiovascular Disease, and Diabetes: A common agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association Diabetes Care, July 1, 2004; 27(7): 1812 - 1824. [Abstract] [Full Text] [PDF]
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H. Eyre, R. Kahn, R. M. Robertson, the ACS/ADA/AHA Collaborative Writing Committee, ACS/ADA/AHA Collaborative Writing Committee Member, N. G. Clark, C. Doyle, Y. Hong, T. Gansler, T. Glynn, et al. Preventing Cancer, Cardiovascular Disease, and Diabetes: A Common Agenda for the American Cancer Society, the American Diabetes Association, and the American Heart Association Circulation, June 29, 2004; 109(25): 3244 - 3255. [Abstract] [Full Text] [PDF]
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