Join the 200th Anniversary Celebration

Correspondence

Obesity and the Risk of Heart Failure

N Engl J Med 2002; 347:1887-1889December 5, 2002

Article

To the Editor:

The report by Kenchaiah et al. (Aug. 1 issue)1 and the accompanying editorial by Massie2 show the important association between any increased body-mass index and the risk of heart failure. However, several reports have now indicated that abdominal fat may be at least as important as body-mass index in determining cardiac risk. Lakka et al.3 found that the waist-to-hip ratio provided additional information beyond body-mass index that helped in predicting coronary heart disease, whereas the reverse did not apply. That study, involving 1346 Finnish men 42 to 60 years of age, showed an increase by nearly a factor of three in the risk of coronary events in men with a waist-to-hip ratio of 0.91 or greater.

During eight years of follow-up in the Nurses' Health Study, Rexrode et al.4 found that the waist-to-hip ratio and waist circumference were strongly and independently associated with an increased risk of coronary heart disease among women with a body-mass index of 25 or less. They noted that after adjustment for body-mass index and other cardiac risk factors, women with a waist-to-hip ratio of 0.88 or higher had a relative risk of coronary heart disease of 3.25, as compared with those with a ratio below 0.72. The more recent focus on visceral fat as an even more sensitive risk factor for vascular disease and diabetes5 may be a further refinement.

Gerard O'Brien, M.D.
Monroeville Medical Associates, Monroeville, PA 15146

5 References
  1. 1

    Kenchaiah S, Evans JC, Levy D, et al. Obesity and the risk of heart failure. N Engl J Med 2002;347:305-313
    Full Text | Web of Science | Medline

  2. 2

    Massie BM. Obesity and heart failure -- risk factor or mechanism? N Engl J Med 2002;347:358-359
    Full Text | Web of Science | Medline

  3. 3

    Lakka HM, Lakka TA, Tuomilehto J, Salonen JT. Abdominal obesity is associated with increased risk of acute coronary events in men. Eur Heart J 2002;23:706-713
    CrossRef | Web of Science | Medline

  4. 4

    Rexrode KM, Carey VJ, Hennekens CH, et al. Abdominal adiposity and coronary heart disease in women. JAMA 1998;280:1843-1848
    CrossRef | Web of Science | Medline

  5. 5

    Boyko EJ, Fujimoto WY, Leonetti DL, Newell-Morris L. Visceral adiposity and the risk of type 2 diabetes: a prospective study among Japanese Americans. Diabetes Care 2000;23:465-471
    CrossRef | Web of Science | Medline

To the Editor:

Kenchaiah and colleagues report an increase in the risk of heart failure with increasing body-mass index in women but not in men. In the light of the epidemiologic data suggesting that heart failure in patients with normal or preserved ejection fraction (so-called diastolic heart failure) predominantly affects elderly women,1,2 it would be interesting to know whether their findings are applicable to the subgroup with preserved systolic function.

Mathew S. Maurer, M.D.
Columbia University, New York, NY 10032

2 References
  1. 1

    Rich MW. Epidemiology, pathophysiology, and etiology of congestive heart failure in older adults. J Am Geriatr Soc 1997;45:968-974
    Web of Science | Medline

  2. 2

    Klapholz M, Mitchell J, Meisner JS, et al. Clinical characteristics and co-morbid conditions of patients hospitalized for heart failure with normal systolic function: results of the New York Heart Failure Consortium Registry on Diastolic Dysfunction. Circulation 2001;104:Suppl II:II-689 abstract.

To the Editor:

The report on obesity as a risk factor for heart failure and the accompanying editorial bring to mind the fact that the heart normally oxidizes fat for contraction.1 Why, then, does the heart fail in the midst of plenty? Experiments in obese rats suggest that impaired oxidation of fatty acids by the heart results in the accumulation of triglycerides in cardiomyocytes.2 It seems that Rudolph Virchow already had it right in 1858 when he wrote that “the hearts described by the old anatomists as fatty were in a great measure only hearts infiltrated with fat; on the other hand, what is meant at the present day when genuine fatty degeneration (metamorphosis) of the heart is spoken of is not this obesity of the heart, this interlarding of its fibers with fat cells, but rather a real transformation of its substance, going on in the interior of the fibers. In the latter case the fat lies in, in the former between, the primitive fasciculi.”3 Despite our best efforts, the state of our knowledge in this matter remains where it was a century and a half ago.

Heinrich Taegtmeyer, M.D., D.Phil.
Christopher R. Wilson, B.S.
University of Texas Houston Medical School, Houston, TX 77030

3 References
  1. 1

    Taegtmeyer H, Hems R, Krebs HA. Utilization of energy-providing substrates in the isolated working-rat heart. Biochem J 1980;186:701-711
    Web of Science | Medline

  2. 2

    Young ME, Guthrie PH, Razeghi P, et al. Impaired long-chain fatty acid oxidation and contractile dysfunction in the obese Zucker rat heart. Diabetes 2002;51:2587-2595
    CrossRef | Web of Science | Medline

  3. 3

    Virchow RLK. Die Cellularpathologie und ihrer Begründung auf physiologische und pathologische Gewebelehre. Berlin, Germany: A. Hirschwald, 1858.

To the Editor:

In the recent study by Kenchaiah et al. and the accompanying editorial by Massie, the relation between obesity and heart failure is discussed in great detail. However, only passing reference is made to obstructive sleep apnea in these patients as a possible contributing factor. As Massie notes, “obesity-related hypoventilation and sleep apnea may also contribute.” In the literature, obstructive sleep apnea is a well-documented coexisting condition in obese persons and has been considered an important contributory factor to cardiovascular complications, including hypertension, congestive heart failure, arrhythmias, stroke, and even sudden death syndrome.1-3 Furthermore, increasing obesity and more severe obstructive sleep apnea are often noted to occur in parallel. Is it possible that obstructive sleep apnea may have had a bigger role in the risk of heart failure that occurred with worsening obesity in this population?

Richard A. Dart, M.D.
Marshfield Clinic, Marshfield, WI 54449

3 References
  1. 1

    Gislason T, Benediktsdottir B, Bjornsson J, Kjartansson G, Kjeld M, Kristbjarnarson H. Snoring, hypertension, and the sleep apnea syndrome: an epidemiologic survey of middle-aged women. Chest 1993;103:1147-1151
    CrossRef | Web of Science | Medline

  2. 2

    Bonsignore MR, Marrone O, Insalaco G, Bonsignore G. The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms. Eur Respir J 1994;7:786-805
    CrossRef | Web of Science | Medline

  3. 3

    Chan HS, Chiu HF, Tse LK, Woo KS. Obstructive sleep apnea presenting with nocturnal angina, heart failure, and near-miss sudden death. Chest 1991;99:1023-1025
    CrossRef | Web of Science | Medline

To the Editor:

The identification of obesity as a prevalent and modifiable risk factor for congestive heart failure suggests the pressing need for a public health response. A serious public-information campaign coupled with clearly marked calorie counts on food items — especially fast food — might motivate consumers, even subliminally, to develop more healthful habits. The complicity of the food industry in fostering norms of unhealthful eating and in seducing generations of young people ought to be viewed in much the same way as that of the tobacco industry with respect to its promotion of tobacco. The cure for our society's dietary excess and consequent cardiac disease should not be a pharmacopoeia of magic bullets, but rather some sobering doses of education and moderation.

Elizabeth R. Jenny-Avital, M.D.
Jacobi Medical Center, Bronx, NY 10461

Author/Editor Response

The authors reply:

To the Editor: We agree with Dr. O'Brien's observation that assessment of regional indexes of adiposity, such as the waist circumference or waist-to-hip ratio, may provide incremental information regarding the risk of heart failure. We did not evaluate these indexes in our investigation.

With reference to Dr. Maurer's comments, we would like to emphasize the consistency in the relation between body-mass index and the risk of heart failure in women and men in multiple analyses detailed in our report. We presented data on preserved as compared with impaired left ventricular ejection fraction in patients with heart failure in a small subgroup of participants for whom such information was available, and we noted the occurrence of both systolic and diastolic heart failure in obese persons. However, additional studies are required to examine the potential contribution of increased body-mass index to diastolic heart failure.

Dr. Dart notes the possible role of obstructive sleep apnea as a mechanism for heart failure in obese persons. We did not evaluate sleep-disordered breathing in our report. We appreciate the historical perspective provided by Dr. Taegtmeyer and Mr. Wilson, and we agree with Dr. Jenny-Avital's call for urgent and resolute measures to tackle obesity at an individual level and on a societal scale in order to curb the current epidemic1 and to prevent the numerous health hazards associated with excess weight.

Satish Kenchaiah, M.D.
Daniel Levy, M.D.
Ramachandran S. Vasan, M.D.
Framingham Heart Study, Framingham, MA 01702

1 References
  1. 1

    Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999-2000. JAMA 2002;288:1723-1727
    CrossRef | Web of Science | Medline

Author/Editor Response

The editorialist replies:

To the Editor: I agree with Dr. O'Brien that the pattern of fat distribution is probably an important factor in the association between overweight–obesity and heart failure. The paper by Kenchaiah et al. did not report the waist-to-hip ratio, but I speculated that the increased risk of heart failure was in substantial part explained by the metabolic syndrome, an accompaniment of the excessive accumulation of visceral fat, and its consequences, including left ventricular hypertrophy and neurohormonal activation. These are important potential targets for interventions — such as exercise, blockage of the renin–angiotensin system, and other approaches that diminish insulin resistance — that may prevent the cardiovascular complications of obesity.

Taegtmeyer and Wilson raise an important philosophical point by asking why the heart fails “in the midst of plenty,” since fatty acids are the primary metabolic substrate for the working heart. The role of altered substrate utilization and energy availability in the failing heart is a complex and controversial subject — one about which the authors of this letter have a great deal more expertise than I. However, the fatty infiltration of the myocardium described by Virchow is not the typical finding in the failing hearts of today, although fat deposits in the coronary arteries, also well recognized by Virchow, do have an important role. I suspect that overweight and obesity take their greatest toll on the heart through their effects on blood vessels and the resultant damage mediated by hypertension, atherosclerosis, and vascular dysfunction.

Dr. Dart has emphasized a point that space considerations allowed me to mention only cursorily — that obstructive sleep apnea, a condition more prevalent in obese persons, may cause heart failure and thereby explain part of the association between obesity and heart failure reported by Kenchaiah et al. Indeed, the complex interaction between sleep disorders and heart failure is a topic of growing interest.1 The frequency with which obstructive sleep apnea causes heart failure and the mechanisms by which this occurs are uncertain, except in the case of severe pulmonary hypertension and resulting right ventricular failure. It is possible that hypertension or excessive autonomic activity may play an intermediary part. Conversely, it is now clear that heart failure itself is frequently associated with sleep-disordered breathing, which is often central rather than obstructive in origin and is associated with more severe symptoms and a poorer prognosis.2 Trials are under way to determine whether positive airway pressure can be beneficial in affected patients with heart failure.3

Barry M. Massie, M.D.
University of California, San Francisco, San Francisco, CA 94941

3 References
  1. 1

    Leung RS, Bradley TD. Sleep apnea and cardiovascular disease. Am J Respir Crit Care Med 2001;164:2147-2165
    Web of Science | Medline

  2. 2

    Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med 1999;341:949-954
    Full Text | Web of Science | Medline

  3. 3

    Yan AT, Bradley TD, Liu PP. The role of continuous positive airway pressure in the treatment of congestive heart failure. Chest 2001;120:1675-1685
    CrossRef | Web of Science | Medline

Citing Articles (3)

Citing Articles

  1. 1

    Ni-Huiping Son, Shuiqing Yu, Joseph Tuinei, Kotaro Arai, Hiroko Hamai, Shunichi Homma, Gerald I. Shulman, E. Dale Abel, Ira J. Goldberg. (2010) PPARγ-induced cardiolipotoxicity in mice is ameliorated by PPARα deficiency despite increases in fatty acid oxidation. Journal of Clinical Investigation 120:10, 3443-3454
    CrossRef

  2. 2

    Rachel Ash-Bernal, Linda R. Peterson. (2006) The Cardiometabolic Syndrome and Cardiovascular Disease. Journal of the CardioMetabolic Syndrome 1:1, 25-28
    CrossRef

  3. 3

    Constance Th.R.M. Schrander-Stumpel, Leopold M.G. Curfs, Prapto Sastrowijoto, Suzanne B. Cassidy, Jaap J.P. Schrander, Jean-Pierre Fryns. (2004) Prader-Willi syndrome: Causes of death in an international series of 27 cases. American Journal of Medical Genetics 124A:4, 333-338
    CrossRef

Trends: Most Viewed (Last Week)

More Trends