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Obesity and the heart: an ever-growing problem. (Editorial).

Recent evidence indicates that the prevalence of overweight and obesity in the United States has been increasing at epidemic proportions over the past two decades, and that the impact of obesity and cardiovascular diseases is being appropriately and increasingly recognized. (1,2) There is now no question that obesity exerts a "heavy" toll on the entire cardiovascular system, especially the heart.

Hypertension

Obesity and essential hypertension are closely related disorders. Although both disorders are extremely prevalent, each occurs more frequently with the other disorder than in the normal population. (3-5) Obese patients are more likely to be hypertensive than lean patients, and weight gain is typically associated with increases in arterial pressure. The wealth of data now indicate that both obesity and hypertension result from a common pathophysiologic mechanism largely involving insulin resistance, and that obesity certainly begets hypertension, and hypertension possibly even begets obesity via reduced insulin sensitivity.

Cardiac Structure

Hypertension and obesity typically produce different cardiac adaptations. (4) The fundamental response to an isolated increase in arterial pressure, or afterload, in hypertension is left ventricular hypertrophy (LVH) of the concentric type (thickening of the ventricular wall without chamber dilation), whereas obesity causes a marked increase in preload, which leads to left ventricular (LV) dilation, with only minimal increase in wall thickness (or eccentric LVH). When obesity and hypertension coexist, as is so prevalent in our society, these conditions exert a dual burden on the heart, leading to both dilation and hypertrophy and markedly increasing the premature risk of many cardiovascular disorders.

Cardiac Function

Although LVH may initially serve as an adaptive and compensatory mechanism (according to Laplace's law, a compensatory increase in wall thickness reduces wall stress), clearly, as LVH progresses, it is associated with numerous adverse cardiovascular abnormalities and morbid cardiac events. (3-5) In studies from the Ochsner Clinic, we have demonstrated that all types of LVH, including concentric, isolated septal and, particularly, the eccentric LVH in obese hypertensive patients is associated with increased prevalence and complexity of ventricular dysrhythmias. (6-10) As with increased ventricular ectopic activity, our studies also demonstrated that LV diastolic abnormalities accompany all types of LVH, including concentric, isolated septal, and eccentric LVH, with the most marked abnormalities occurring in those with both obesity and hypertension, particularly those with left atrial abnormalities by electrocardiography. (8,11,12)

Early in obesity and hypertension, systolic function, especially when assessed by preload-independent indices (eg, ejection fraction), is generally preserved. (11) However, well over a decade ago, we demonstrated an early reduction in contractility in obese and, especially, hypertensive obese patients as measured by a preload-independent index (end-systolic stress/end-systolic volume index). (13) Alpert et al (14-17) have confirmed the adverse effects of significant obesity on diastolic and systolic ventricular function. In a study of 74 morbidly obese patients, Alpert et al (14) demonstrated that nearly one third had clinical evidence of congestive heart failure (CHF), and the probability of CHF increased with the increased duration of morbid obesity (at 20 and 25 years of obesity duration, the probability of CHF was 66% and 93%, respectively). A recent epidemiologic study from the Framingham Heart Study indicates that overweight and obesity are potent predictors of subsequent CHF. (18)

Coronary Disease

Obesity is known to have significant adverse effects on many of the coronary artery disease (CAD) risk factors, including arterial pressure, insulin resistance, plasma lipids (especially increasing triglycerides and decreasing high-density lipoprotein cholesterol), physical activity, inflammation, exercise capacity, and LVH. (19,20) Despite adversely affecting all of these individual risk factors, data from both the Framingham Heart Stud (21) and a large cohort of female U.S. nurses (22) have indicated that obesity is an independent risk factor for major CAD events in men and, particularly, women. Several studies indicate a progressive increase in all-cause mortality associated with overweight and, especially, with frank obesity. (1,2)

Weight Reduction

Weight loss clearly lowers arterial pressure, preload, afterload, and sympathetic stimulation to the cardiovascular system. (3-5) MacMahon et al (23) demonstrated that even a small weight loss (approximately 15 lb) in mildly obese hypertensive subjects was associated with benefits on pressure and LVH that were superior to reductions achieved with [beta]-blocking agents. Alpert et al (14) demonstrated that New York Heart Association functional class improved in 12 of 14 morbidly obese patients who achieved marked weight loss (>30% of total weight) after gastroplasty by an average of greater that one functional class. Weight loss was also associated with marked improvements in LV chamber size, LV end-systolic wall stress, and diastolic and systolic ventricular function in these patients. In our cardiac rehabilitation program of patients with CAD, where nearly 40% met criteria for obesity, even small reductions in body weight (eg, >5% or average 10%) were associated with marked improvements in obesity indices, lipids, and exercise capacity compared with obese patients who did not lose weight. (19) The improvements in cardiac structure and function in a patient with hypertrophic cardiomyopathy after significant weight loss discussed in this issue of the Southern Medical Journal extends the potential cardiovascular benefits of marked weight reduction.

Despite all of this evidence, busy clinicians often recognize that efforts at purposeful weight reduction often involve some "wishful thinking." Despite the "obesity paradox" that we and others have recently described in select patients after CAD procedures (24,25) and with significant systolic heart failure, (26-28) we believe that purposeful weight reduction remains a viable therapy for the prevention and treatment of most cardiovascular disorders. Better efforts at caloric restriction to promote weight loss and exercise training to prevent weight gain (and help with weight loss), along with better and safer pharmacologic approaches, are desperately needed in the primary and secondary prevention of cardiovascular diseases.

Accepted September 11, 2002.

References

(1.) Krauss RM, Winston M, Fletcher BJ, Grundy SM. Obesity: Impact on cardiovascular disease. Circulation 1998;98: 1472-1476.

(2.) Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med 1998;158:1855-1867.

(3.) Lavie CJ, Messerli FH. Cardiovascular adaptation to obesity and hypertension. Chest 1986;90:275-279.

(4.) Messerli FH. Cardiovascular effects of obesity and hypertension. Lancet 1982;2:1165-1168.

(5.) Lavie CJ, Ventura HO, Messerli FH. Len ventricular hypertrophy. Post-grad Med 1992;91:134-143.

(6.) Lavie CJ, Nunez BD, Garavaglia GE, Messerli FH. Hypertensive concentric left ventricular hypertrophy: when is ventricular ectopic activity increased? South Med J 1988;81:696-700.

(7.) Messerli FH, Ventura HO, Elizardi DJ, Dunn FG, Frohlich ED. Hypertension and sudden death: Increased ventricular ectopic activity in left ventricular hypertrophy. Am J Med 1984;77:18-22.

(8.) Nunez BD, Lavie CJ, Messerli FH, Schmieder RE, Garavaglia GE, Nunez M. Comparison of diastolic left ventricular filling and cardiac dysrhythmias in hypertensive patients with and without isolated septal hypertrophy. Am J Cordial 1994;74:585-589.

(9.) Messerli FH, Nunez BD, Ventura HO, Snyder DW. Overweight and sudden death: Increased ventricular ectopy in cardiopathy of obesity. Arch Intern Med 1987;147:1725-1728.

(10.) Lavie CJ, Ventura HO, Messerli FH. Hypertension, obesity, left ventricular hypertrophy, complex ventricular ectopic activity, and increased risk for sudden death: Review of Ochsner Studies and the literature. J Cardiopulm Rehabil 1993;13:264-270.

(11.) Lavie CJ, Amodeo C, Ventura HO, Messerli FH. Left atrial abnormalities indicating diastolic ventricular dysfunction in cardiopathy of obesity. Chest 1987;92:1042-1046.

(12.) Grossman E, Oren S, Messerli FH. Left ventricular filling and stress response pattern in essential hypertension. Am J Med 1991;91:502-506.

(13.) Garavaglia GE, Messerli FH, Nunez BD, Schmieder RE, Grossman E. Myocardial contractility and left ventricular function in obese patients with essential hypertension. Am J Cordial 1988;62:594-597.

(14.) Alpert MA, Terry BE, Mulekar M, Cohen MV, Massey CV, Fan TM, et al. Cardiac morphology and left ventricular function in normotensive morbidly obese patients with and without congestive heart failure, and effect of weight loss. Am J Cardiol 1997;80:736-740.

(15.) Alpert MA, Lambert CR, Terry BE, Cohen MV, Mukerji V, Massey CV, et al. Interrelationship of left ventricular mass, systolic function and diastolic filling in normotensive morbidly obese patients. Int J Obes Relat Metab Disord 1995;19:550-557.

(16.) Alpert MA, Terry BE, Lambert CR, Kelly DL, Panayiotou H, Mukerji V, et al. Factors influencing left ventricular systolic function in nonhypertensive morbidly obese patients, and effect of weight loss induced by gastroplasty. Am J Cardiol 1993;71:773-737.

(17.) Alpert MA, Lambert CR, Terry BE, Kelly DL, Panayiotou H, Mukerji V, Effect of weight loss on left ventricular mass in nonhypertensive morbidly obese patients. Am J Cardiol 1994;73:918-921.

(18.) Kenchaiah S, Evans JC, Levy D, wilson PW, Benjamin EJ, Larson MG, et al. Obesity and the risk of heart failure. N Engl J Med 2002;347:305-313.

(19.) Lavie CJ, Milani RV. Effects of cardiac rehabilitation, exercise training, and weight reduction on exercise capacity, coronary risk factors, behavioral characteristics, and quality of life in obese coronary patients. Am J Cardiol 1997;79:397-401.

(20.) Lavie CJ, Milani RV. Effects of cardiac rehabilitation and exercise training on peak aerobic capacity and work efficiency in obese patients with coronary artery disease. Am J Cardiol 1999;83:1477-1480.

(21.) Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an independent risk factor for cardiovascular disease: A 26-year follow-up of participants in the Framingham Heart Study. Circulation 1983;67:968-977.

(22.) Manson JE, Colditz GA, Stampfer MJ, Willett WC, Rosner B, Monson RR, et al. A prospective study of obesity and risk of coronary heart disease in women. N Engl J Med 1990;322:882-889.

(23.) MacMahon SW, Wilcken DE, Macdonald GJ. The effect of weight reduction on left ventricular mass: A randomized controlled trial in young, overweight hypertensive patients. N Engl J Med 1986;314:334-339.

(24.) Gruberg L, Weissman NJ, Waksman R, Fuchs S, Deible R, Pinnow EE, et al. The impact of obesity on the short-term and tong-term outcomes after percutaneous coronary intervention: The obesity paradox? J Am Coll Cardiol 2002;39:578-584.

(25.) Gurm HS, Whitlow PL, Kip KE. The impact of body mass index on short- and long-term outcomes in patients undergoing coronary revascularization: Insights from the Bypass Angioplasty Revascularization Investigation (BARI). J Am Coll Cardiol 2002;39:834-840.

(26.) Horwich TB, Fonarow GC, Hamilton MA, McLellan WR, Woo MA, Tillisch JH. The relationship between obesity and mortality in patients with heart failure. J Am Coll Cardiol 2001;38:789-795.

(27.) Lavie CJ, Osman AF, Milani RV, Mehra MR. Body composition and prognosis in chronic systolic heart failure: The obesity paradox. Am J Cordial 2003;91:891-894.

(28.) Lavie CJ, Milani R, Mehra MR, Ventura HO, Messerli FH. Obesity, weight reduction and survival in heart failure. J Am Call Cardiol 2002; 39:1563-1564 (letter).

From the Ochsner Heart and Vascular Institute, New Orleans, LA.

Reprint requests to Carl J. Lavie, MD, Department of Cardiology, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121. Email: clavie@ochsner.org

Copyright [c] 2003 by The Southern Medical Association 0038-4348/03/9606-0535
COPYRIGHT 2003 Southern Medical Association
No portion of this article can be reproduced without the express written permission from the copyright holder.
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Author:Messerli, Franz H.
Publication:Southern Medical Journal
Article Type:Editorial
Geographic Code:1USA
Date:Jun 1, 2003
Words:1824
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