Journal of Cardiac Failure Vol. 20 No. 3 2014
Editorial Comment
Clinical Implications of Weight Loss in Heart Failure CARL J. LAVIE, MD,1,2 AND HECTOR O. VENTURA, MD1 New Orleans and Baton Rouge, Louisiana
Clearly, overweight and obesity are increasing in epidemic proportions in the United States (US) and most of the Westernized world.1,2 Obesity has many adverse effects on cardiovascular (CV) risk factors, including causing dyslipidemia, hypertension (HTN), and left ventricular (LV) hypertrophy (LVH), hyperglycemia/metabolic syndrome/type 2 diabetes mellitus, increasing inflammation, and reducing exercise capacity and fitness.2,3 Because the CV risk factors are all directly responsible for increasing the risk of coronary heart disease (CHD), which is now probably the leading cause of heart failure (HF), this risk, along with HTN and LVH, which also adversely affect systolic and diastolic LV function, not surprisingly leads to obesity markedly increasing the risk of HF, with both preserved and reduced systolic function.3 Probably the best study to demonstrate this increased HF risk with overweight and obesity is from Kenchaiah et al,4 who studied 5,881 Framingham Heart Study participants; they demonstrated a 5% increase in HF prevalence in men and a 7% increase in women for every 1 kg/m2 increase in body mass index (BMI), with the risk of HF increasing along the entire spectrum of BMI. Alpert et al5 demonstrated a strong relationship between morbid obesity and HF prevalence, which is concerning because morbid obesity has been increasing in our society more than obesity per se and has now reached w3% in the US.1e3 Despite the adverse effects that obesity has on CV risk factors and increasing systolic and diastolic abnormalities,
leading to an increased prevalence of CV diseases, including HF, numerous studies and meta-analyses have demonstrated an obesity paradox, in which obese patients with established CV diseases have a better clinical prognosis than do lean patients with these same CV diseases.2,3,6 This obesity paradox has been demonstrated with systolic HF and HF with preserved systolic function, and has been demonstrated in both acute and chronic HF.3,6,7 In fact, we have demonstrated an obesity paradox in both CHD and HF using both BMI as well as percentage of body fat (BF).8e12 Additionally, the obesity paradox in HF has even been demonstrated with central obesity or elevated waist circumference (WC), with the best prognosis being seen in HF patients with increased levels of both BMI and WC.13 In the present study by Aktas et al14 in this issue of Journal of Cardiac Failure, in almost 1,000 patients with class I and II HF from the Cardiac Resynchronization Therapy with Defibrillation (CRT-D) arm of the Multi-center Automated Defibrillator Implantation TrialeCardiac Resynchronization Therapy (MADIT-CRT) study, there was no obesity paradox noted, but those with O2 kg of weight loss had considerably worse clinical prognosis and mortality at 1 year follow-up compared with those who did not lose significant weight, which was particularly noted in those with a left bundle branch block pattern on the electrocardiogram. The study adds to the literature suggesting harmful effects of weight loss (presumably nonpurposeful) in patients with HF. On the other hand, Alpert et al15 have recently reviewed the impact of purposeful weight loss with diet or bariatric surgery on the hemodynamic and structural abnormalities of obesity. Certainly, many patients with LV systolic dysfunction show improvements in LV structure and function with weight reduction; additionally, right ventricular systolic and diastolic function also may improve following weight loss. These improvements in cardiac structure and function, as well as functional classification, following weight loss are generally more noted in patients with more severe obesity. Considering the current level of evidence, how should clinicians currently approach weight loss recommendations for patients with HF? Based on the lack of evidence supporting weight loss in patients with CV diseases,
From the 1John Ochsner Heart and Vascular Institute, Ochsner Clinical SchooleUniversity of Queensland School of Medicine, New Orleans, Louisiana and 2Department of Preventive Medicine, Pennington Biomedical Research Center, Louisiana State University Systems, Baton Rouge, Louisiana. Manuscript received January 2, 2014; revised manuscript accepted January 2, 2014. Reprint requests: Carl J. Lavie, MD, Medical Director, Cardiac Rehabilitation and Prevention, Director, Exercise Laboratories, John Ochsner Heart and Vascular Institute, Ochsner Clinical SchooleUniversity of Queensland School of Medicine, 1514 Jefferson Highway, New Orleans, LA 70121-2483. Tel: (504) 842-1281; fax: (504) 842-5875. E-mail: [email protected] See page 191 for disclosure information. 1071-9164/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.cardfail.2014.01.002
190
Implications of Weight Loss in HF
the recent American College of Cardiology Foundation/ American Heart Association guidelines16 do not make any definitive recommendations for weight loss, although they do make suggestions regarding the high risk associated with severe (or morbid class III obesity, BMI $40 kg/m2).16 Currently, with the lack of data to support weight loss, as well as the considerable data regarding the obesity paradox in HF, we think that in overweight and mildly obese (class I, BMI 30e35 kg/ m2) with HF, emphasis should be placed on increasing physical activity, exercise training, and improving levels of fitness, both cardiorespiratory fitness (CRF) as well as muscular fitness.17e20 ln fact, as with CHD,21 we have demonstrated that there is no obesity paradox in HF patients with systolic dysfunction if they have relatively preserved CRF (peak oxygen consumption O14 mL O2 kg 1 min 1).22 Many of the studies, including the current paper, have assessed weight loss and have not been able to separate purposeful versus nonpurposeful, the latter of which would be expected to be associated with a poor prognosis in HF and many other chronic conditions. On the other hand, considering the very poor prognosis associated with more morbid obesity, and the potential benefits of weight loss in these patients, we currently think that purposeful weight loss should still be encouraged for HF patients with severe obesity.16,23,24 In these patients, weight loss has been associated with reductions in LV mass, improvements in systolic and diastolic dysfunction, and improvements in functional capacity.15 In conclusion, better large-scale purposeful weight loss intervention trials are needed in many groups with CV diseases, including HF. However, currently, the constellation of data still support purposeful weight loss in patients with HF, especially in more severe obesity (certainly with BMI $40 kg/m2 and probably with BMI O35 kg/m2).3,20,24 Considering the importance of CRF to improve prognosis in almost every patient group studied, as well as the clear evidence that high CRF is associated with lower mortality in HF, incorporating physical activity and exercise training and efforts to improve CRF into weight loss efforts appear to be especially promising.18,22,25 Disclosures C.J.L. has served as a consultant and speaker for CocaCola and is publishing a book about the obesity paradox with potential royalties.
References 1. Sturm R. Increases in morbid obesity in the USA: 2000e05. Public Health 2007;121:492e6. 2. Lavie CJ, Milani RV, Ventura HO. Obesity and cardiovascular disease: risk factor, paradox, and impact of weight loss. J Am Coll Cardiol 2009;53:1925e32.
Lavie and Ventura
191
3. Lavie CJ, Alpert MA, Arena R, Mehra MR, Milani RV, Ventura HO. Impact of obesity and the obesity paradox on prevalence and prognosis in heart failure. J Am Coll Cardiol HF 2013;1:93e102. 4. 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;347:305e13. 5. Alpert MA, Terry BE, Mulekar M, Cohen MV, Massey CV, Fan TM, et al. Cardiac morphology and left ventricular function in morbidly obese patients with and without congestive heart failure and effect of weight loss. Am J Cardiol 1997;80:736e40. 6. Oreopoulos A, Padwal R, Kalantar-Zadeh K, Fonarow GC, Norris CM, McAlister FA. Body mass index and mortality in heart failure: a meta-analysis. Am Heart J 2008;156:13e22. 7. Fonarow GC, Srikanthan P, Costanzo MR, Cintron GB, Lopatin M, ADHERE Scientific Advisory Committee and Investigators. An obesity paradox in acute heart failure: analysis of body mass index and in hospital mortality for 108,927 patients in the Acute Decompensated Heart Failure National Registry. Am Heart J 2007;153: 74e81. 8. Lavie CJ, Milani RV, Artham SM, Patel DA, Ventura HO. The obesity paradox, weight loss, and coronary disease. Am J Med 2009;122: 1106e14. 9. Lavie CJ, de Schutter A, Patel D, Artham SM, Milani RV. Body composition and coronary heart disease mortality: an obesity or a lean paradox? Mayo Clin Proc 2011;86:857e64. 10. Lavie CJ, De Schutter A, Patel DA, Romero-Corral A, Artham SM, Milani RV. Body composition and survival in stable coronary heart disease: impact of lean mass index and body fat in the ‘‘obesity paradox’’. J Am Coll Cardiol 2012;60:1374e80. 11. DeSchutter A, Lavie CJ, Patel DA, Artham SM, Milani RV. Relation of body fat categories by Gallagher classification and by continuous variables to mortality in patients with coronary heart disease. Am J Cardiol 2013;111:657e60. 12. Lavie CJ, Osman AF, Milani RV, Mehra MR. Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Am J Cardiol 2003;91:891e4. 13. Clark AL, Chyu J, Horwich TB. The obesity paradox in men versus women with systolic heart failure. Am J Cardiol 2012;110:77e82. 14. Aktas MK, Zareba W, Huang DT, McNitt S, Polonsky S, Chen L, et al. The effect of weight loss on clinical outcomes in patients implanted with a cardiac resynchronization therapy device: a MADIT-CRT sub-study. J Card Fail 2014;20:183e9. 15. Alpert MA, Omran J, Mehra A, Ardhanari S. Impact of obesity and weight loss on cardiac performance and morphology in adults. Prog Cardiovasc Dis 2014;56:391e400. 16. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH, et al. Writing Committee. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;128: e240e319. 17. Kaminsky LA, Arena R, Beckie TM, Brubaker PH, Church TS, Forman DE, et al. The importance of cardiorespiratory fitness in the United States: the need for a national registry: a policy statement from the American Heart Association. Circulation 2013;127:652e62. 18. Lavie CJ, Berra K, Arena R. Formal cardiac rehabilitation and exercise training programs in heart failure: evidence for substantial clinical benefits. J Cardiopulm Rehabil Prev 2013;33:209e11. 19. Artero EG, Lee DC, Lavie CJ, Espa~na-Romero V, Sui X, Church TS, et al. Effects of muscular strength on cardiovascular risk factors and prognosis. J Cardiopul Rehabil Prev 2012;32:351e8. 20. Clark AL, Fonarow GC, Horwich TB. Obesity and obesity paradox in heart failure. Prog Cardiovasc Dis 2014;56:409e14. 21. McAuley PA, Artero EG, Sui X, Lee DC, Church TS, Lavie CJ, et al. The obesity paradox, cardiorespiratory fitness, and coronary heart disease. Mayo Clin Proc 2012;87:443e51. 22. Lavie CJ, Cahalin LP, Chase P, Myers J, Bensimhon D, Peberdy MA, et al. Impact of cardiorespiratory fitness on the obesity
192 Journal of Cardiac Failure Vol. 20 No. 3 March 2014 paradox in patients with heart failure. Mayo Clin Proc 2013;88: 251e8. 23. Nagarajan V, Cauthen CA, Starling RC, Tang WH. Prognosis of morbid obesity patients with advance heart failure. Congest Heart Fail 2013;19:160e4.
24. Lavie CJ, Ventura HO. Analyzing the weight of evidence on the obesity paradox and heart failuredis there a limit to the madness? Congest Heart Fail 2013;19:158e9. 25. Vuori IM, Lavie CJ, Blair SN. Physical activity promotion in the health care system. Mayo Clin Proc 2013;88:1446e61.
Editorial Comment
Clinical Implications of Weight Loss in Heart Failure CARL J. LAVIE, MD,1,2 AND HECTOR O. VENTURA, MD1 New Orleans and Baton Rouge, Louisiana
Clearly, overweight and obesity are increasing in epidemic proportions in the United States (US) and most of the Westernized world.1,2 Obesity has many adverse effects on cardiovascular (CV) risk factors, including causing dyslipidemia, hypertension (HTN), and left ventricular (LV) hypertrophy (LVH), hyperglycemia/metabolic syndrome/type 2 diabetes mellitus, increasing inflammation, and reducing exercise capacity and fitness.2,3 Because the CV risk factors are all directly responsible for increasing the risk of coronary heart disease (CHD), which is now probably the leading cause of heart failure (HF), this risk, along with HTN and LVH, which also adversely affect systolic and diastolic LV function, not surprisingly leads to obesity markedly increasing the risk of HF, with both preserved and reduced systolic function.3 Probably the best study to demonstrate this increased HF risk with overweight and obesity is from Kenchaiah et al,4 who studied 5,881 Framingham Heart Study participants; they demonstrated a 5% increase in HF prevalence in men and a 7% increase in women for every 1 kg/m2 increase in body mass index (BMI), with the risk of HF increasing along the entire spectrum of BMI. Alpert et al5 demonstrated a strong relationship between morbid obesity and HF prevalence, which is concerning because morbid obesity has been increasing in our society more than obesity per se and has now reached w3% in the US.1e3 Despite the adverse effects that obesity has on CV risk factors and increasing systolic and diastolic abnormalities,
leading to an increased prevalence of CV diseases, including HF, numerous studies and meta-analyses have demonstrated an obesity paradox, in which obese patients with established CV diseases have a better clinical prognosis than do lean patients with these same CV diseases.2,3,6 This obesity paradox has been demonstrated with systolic HF and HF with preserved systolic function, and has been demonstrated in both acute and chronic HF.3,6,7 In fact, we have demonstrated an obesity paradox in both CHD and HF using both BMI as well as percentage of body fat (BF).8e12 Additionally, the obesity paradox in HF has even been demonstrated with central obesity or elevated waist circumference (WC), with the best prognosis being seen in HF patients with increased levels of both BMI and WC.13 In the present study by Aktas et al14 in this issue of Journal of Cardiac Failure, in almost 1,000 patients with class I and II HF from the Cardiac Resynchronization Therapy with Defibrillation (CRT-D) arm of the Multi-center Automated Defibrillator Implantation TrialeCardiac Resynchronization Therapy (MADIT-CRT) study, there was no obesity paradox noted, but those with O2 kg of weight loss had considerably worse clinical prognosis and mortality at 1 year follow-up compared with those who did not lose significant weight, which was particularly noted in those with a left bundle branch block pattern on the electrocardiogram. The study adds to the literature suggesting harmful effects of weight loss (presumably nonpurposeful) in patients with HF. On the other hand, Alpert et al15 have recently reviewed the impact of purposeful weight loss with diet or bariatric surgery on the hemodynamic and structural abnormalities of obesity. Certainly, many patients with LV systolic dysfunction show improvements in LV structure and function with weight reduction; additionally, right ventricular systolic and diastolic function also may improve following weight loss. These improvements in cardiac structure and function, as well as functional classification, following weight loss are generally more noted in patients with more severe obesity. Considering the current level of evidence, how should clinicians currently approach weight loss recommendations for patients with HF? Based on the lack of evidence supporting weight loss in patients with CV diseases,
From the 1John Ochsner Heart and Vascular Institute, Ochsner Clinical SchooleUniversity of Queensland School of Medicine, New Orleans, Louisiana and 2Department of Preventive Medicine, Pennington Biomedical Research Center, Louisiana State University Systems, Baton Rouge, Louisiana. Manuscript received January 2, 2014; revised manuscript accepted January 2, 2014. Reprint requests: Carl J. Lavie, MD, Medical Director, Cardiac Rehabilitation and Prevention, Director, Exercise Laboratories, John Ochsner Heart and Vascular Institute, Ochsner Clinical SchooleUniversity of Queensland School of Medicine, 1514 Jefferson Highway, New Orleans, LA 70121-2483. Tel: (504) 842-1281; fax: (504) 842-5875. E-mail: [email protected] See page 191 for disclosure information. 1071-9164/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.cardfail.2014.01.002
190
Implications of Weight Loss in HF
the recent American College of Cardiology Foundation/ American Heart Association guidelines16 do not make any definitive recommendations for weight loss, although they do make suggestions regarding the high risk associated with severe (or morbid class III obesity, BMI $40 kg/m2).16 Currently, with the lack of data to support weight loss, as well as the considerable data regarding the obesity paradox in HF, we think that in overweight and mildly obese (class I, BMI 30e35 kg/ m2) with HF, emphasis should be placed on increasing physical activity, exercise training, and improving levels of fitness, both cardiorespiratory fitness (CRF) as well as muscular fitness.17e20 ln fact, as with CHD,21 we have demonstrated that there is no obesity paradox in HF patients with systolic dysfunction if they have relatively preserved CRF (peak oxygen consumption O14 mL O2 kg 1 min 1).22 Many of the studies, including the current paper, have assessed weight loss and have not been able to separate purposeful versus nonpurposeful, the latter of which would be expected to be associated with a poor prognosis in HF and many other chronic conditions. On the other hand, considering the very poor prognosis associated with more morbid obesity, and the potential benefits of weight loss in these patients, we currently think that purposeful weight loss should still be encouraged for HF patients with severe obesity.16,23,24 In these patients, weight loss has been associated with reductions in LV mass, improvements in systolic and diastolic dysfunction, and improvements in functional capacity.15 In conclusion, better large-scale purposeful weight loss intervention trials are needed in many groups with CV diseases, including HF. However, currently, the constellation of data still support purposeful weight loss in patients with HF, especially in more severe obesity (certainly with BMI $40 kg/m2 and probably with BMI O35 kg/m2).3,20,24 Considering the importance of CRF to improve prognosis in almost every patient group studied, as well as the clear evidence that high CRF is associated with lower mortality in HF, incorporating physical activity and exercise training and efforts to improve CRF into weight loss efforts appear to be especially promising.18,22,25 Disclosures C.J.L. has served as a consultant and speaker for CocaCola and is publishing a book about the obesity paradox with potential royalties.
References 1. Sturm R. Increases in morbid obesity in the USA: 2000e05. Public Health 2007;121:492e6. 2. Lavie CJ, Milani RV, Ventura HO. Obesity and cardiovascular disease: risk factor, paradox, and impact of weight loss. J Am Coll Cardiol 2009;53:1925e32.
Lavie and Ventura
191
3. Lavie CJ, Alpert MA, Arena R, Mehra MR, Milani RV, Ventura HO. Impact of obesity and the obesity paradox on prevalence and prognosis in heart failure. J Am Coll Cardiol HF 2013;1:93e102. 4. 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;347:305e13. 5. Alpert MA, Terry BE, Mulekar M, Cohen MV, Massey CV, Fan TM, et al. Cardiac morphology and left ventricular function in morbidly obese patients with and without congestive heart failure and effect of weight loss. Am J Cardiol 1997;80:736e40. 6. Oreopoulos A, Padwal R, Kalantar-Zadeh K, Fonarow GC, Norris CM, McAlister FA. Body mass index and mortality in heart failure: a meta-analysis. Am Heart J 2008;156:13e22. 7. Fonarow GC, Srikanthan P, Costanzo MR, Cintron GB, Lopatin M, ADHERE Scientific Advisory Committee and Investigators. An obesity paradox in acute heart failure: analysis of body mass index and in hospital mortality for 108,927 patients in the Acute Decompensated Heart Failure National Registry. Am Heart J 2007;153: 74e81. 8. Lavie CJ, Milani RV, Artham SM, Patel DA, Ventura HO. The obesity paradox, weight loss, and coronary disease. Am J Med 2009;122: 1106e14. 9. Lavie CJ, de Schutter A, Patel D, Artham SM, Milani RV. Body composition and coronary heart disease mortality: an obesity or a lean paradox? Mayo Clin Proc 2011;86:857e64. 10. Lavie CJ, De Schutter A, Patel DA, Romero-Corral A, Artham SM, Milani RV. Body composition and survival in stable coronary heart disease: impact of lean mass index and body fat in the ‘‘obesity paradox’’. J Am Coll Cardiol 2012;60:1374e80. 11. DeSchutter A, Lavie CJ, Patel DA, Artham SM, Milani RV. Relation of body fat categories by Gallagher classification and by continuous variables to mortality in patients with coronary heart disease. Am J Cardiol 2013;111:657e60. 12. Lavie CJ, Osman AF, Milani RV, Mehra MR. Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Am J Cardiol 2003;91:891e4. 13. Clark AL, Chyu J, Horwich TB. The obesity paradox in men versus women with systolic heart failure. Am J Cardiol 2012;110:77e82. 14. Aktas MK, Zareba W, Huang DT, McNitt S, Polonsky S, Chen L, et al. The effect of weight loss on clinical outcomes in patients implanted with a cardiac resynchronization therapy device: a MADIT-CRT sub-study. J Card Fail 2014;20:183e9. 15. Alpert MA, Omran J, Mehra A, Ardhanari S. Impact of obesity and weight loss on cardiac performance and morphology in adults. Prog Cardiovasc Dis 2014;56:391e400. 16. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH, et al. Writing Committee. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;128: e240e319. 17. Kaminsky LA, Arena R, Beckie TM, Brubaker PH, Church TS, Forman DE, et al. The importance of cardiorespiratory fitness in the United States: the need for a national registry: a policy statement from the American Heart Association. Circulation 2013;127:652e62. 18. Lavie CJ, Berra K, Arena R. Formal cardiac rehabilitation and exercise training programs in heart failure: evidence for substantial clinical benefits. J Cardiopulm Rehabil Prev 2013;33:209e11. 19. Artero EG, Lee DC, Lavie CJ, Espa~na-Romero V, Sui X, Church TS, et al. Effects of muscular strength on cardiovascular risk factors and prognosis. J Cardiopul Rehabil Prev 2012;32:351e8. 20. Clark AL, Fonarow GC, Horwich TB. Obesity and obesity paradox in heart failure. Prog Cardiovasc Dis 2014;56:409e14. 21. McAuley PA, Artero EG, Sui X, Lee DC, Church TS, Lavie CJ, et al. The obesity paradox, cardiorespiratory fitness, and coronary heart disease. Mayo Clin Proc 2012;87:443e51. 22. Lavie CJ, Cahalin LP, Chase P, Myers J, Bensimhon D, Peberdy MA, et al. Impact of cardiorespiratory fitness on the obesity
192 Journal of Cardiac Failure Vol. 20 No. 3 March 2014 paradox in patients with heart failure. Mayo Clin Proc 2013;88: 251e8. 23. Nagarajan V, Cauthen CA, Starling RC, Tang WH. Prognosis of morbid obesity patients with advance heart failure. Congest Heart Fail 2013;19:160e4.
24. Lavie CJ, Ventura HO. Analyzing the weight of evidence on the obesity paradox and heart failuredis there a limit to the madness? Congest Heart Fail 2013;19:158e9. 25. Vuori IM, Lavie CJ, Blair SN. Physical activity promotion in the health care system. Mayo Clin Proc 2013;88:1446e61.
