Author + information
- Published online February 26, 2018.
- Carl J. Lavie, MD∗ ( and )
- Hector O. Ventura, MD
- Department of Cardiovascular Diseases, John Ochsner Heart and Vascular Institute, Ochsner Clinical School–The University of Queensland School of Medicine, New Orleans, Louisiana
- ↵∗Address for correspondence:
Dr. Carl J. Lavie, Cardiac Rehabilitation, Exercise Laboratories, John Ochsner Heart and Vascular Institute, Ochsner Clinical School–The University of Queensland School of Medicine, 1514 Jefferson Highway, New Orleans, Louisiana 70121-2483.
We have published numerous reports on the obesity paradox in many patients with cardiovascular disease (CVD) (1–3), including patients with heart failure (HF) (2,3). Certainly, it is well recognized that obesity worsens almost all of the established CVD risk factors, including worsening plasma lipid levels, rising blood pressure, increasing glucose levels, and leading to increased levels of inflammation. Considering these adverse effects, it is no surprise that obesity is associated with increased prevalence of almost all CVDs, including coronary heart disease (CHD) and hypertension, which are strong risk factors for the development of HF in adults, as well as an increased prevalence of HF and atrial fibrillation (1–3). Obesity also has adverse effects on left ventricular structure and hypertrophy and adversely affects systolic and, especially, diastolic ventricular function. Thus, it is not surprising that HF with reduced ejection fraction (HFrEF) and, especially, with preserved ejection fraction (HFpEF) are increased in the setting of obesity. Efforts to prevent obesity and its progression, therefore, would be beneficial for the primary prevention of most CVDs, including HF.
However, despite the adverse effects of obesity to increase CVD risk factors and to increase CVD, an obesity paradox has been recognized in CVD and HF, meaning that in cohorts of patients with these established CVDs (including HF), generally overweight and obese patients have a better prognosis and survival compared with similar patients with the same CVD who are not overweight or obese (1–4). This outcome has been shown with HFpEF and especially with HFrEF (4). However, little has been published on the impact of body composition and obesity on prognosis of HF in the pediatric population.
In this issue of JACC: Heart Failure, Castleberry et al. (5) assess data from the largest registry of pediatric cardiomyopathy with information from 98 pediatric cardiac centers in the United States and Canada that included data on dilated cardiomyopathy (DCM). The authors assessed the impact of malnourishment, obesity, or normal body weight (NB) in 904 patients with DCM on risk of death or transplantation. They determined that malnourishment (23.7%; n = 214) was associated with a >2-fold increased mortality but not with significant differences in transplantation rate compared with NB. Although obesity was associated with increased mortality in univariate analysis, it was only associated with a nonsignificant trend of increased mortality (hazard ratio: 1.49; 95% confidence interval: 0.72 to 3.08) in multivariate analysis, and there were no significant differences in the transplantation rate.
The finding of higher mortality in the malnourished group (5) should be no surprise, as almost all groups of patients with low body weight have a higher mortality. This finding has been confirmed in cohorts with CVD, including CHD and HF, and many other groups of patients with non-CVD, and now in a relatively large cohort of pediatric patients (mean age 2.7 ± 4.5 years) with DCM. Although the authors describe this group as malnourished, they mean low body weight (body mass index <5% for ≥2 years or weight-for-length <5% for <2 years), as there was no assessment of true nutritional status. Clearly, pediatric patients with low body weight had considerably higher mortality risk. Conversely, obese patients with DCM (13.3%; n = 120; age 9.0 ± 6.3 years) had a statistically similar survival and transplantation rate as did those with NB; there was no obesity paradox but, on the other hand, obesity was also not associated with a worse prognosis compared with NB pediatric patients with DCM.
In adults with HFpEF and HFrEF, obesity has been associated with better survival (1–4). This outcome has been demonstrated with body mass index in HFrEF and HFpEF, for percent body fat in HFrEF, and abdominal obesity in HFrEF, with surprising findings in HFpEF (better survival in univariate analysis but worse survival in multivariate analysis with abdominal obesity) (4). In the current study of pediatric patients with DCM, details of body composition other than just height and weight were not available, and nor was the “obese” cohort divided into overweight or varying severities of obesity, which is a limitation in this large study.
Finally, our research has also concentrated on the potential benefits of fitness, including cardiorespiratory fitness (CRF) and muscular fitness, to improve prognosis for patients with CVD, including for HF. Clearly, further study is needed to develop both CRF and muscular fitness to improve prognosis in adults and, at least, older children and adolescents with HF. As we recently reviewed (6), improving CRF is needed throughout the life span, from childhood to adolescence, adulthood, and older ages, to improve the health of our population and for the primary prevention of CVD and HF.
↵∗ Editorials published in JACC: Heart Failure reflect the views of the authors and do not necessarily represent the views of JACC: Heart Failure or the American College of Cardiology.
Dr. Lavie is the author of The Obesity Paradox. Dr. Ventura has reported that he has no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
- Lavie C.J.,
- Pandey A.,
- Lau D.H.,
- Alpert M.A.,
- Sanders P.
- Lavie C.J.,
- Milani R.V.,
- Ventura H.O.
- Castleberry C.D.,
- Jefferies J.L.,
- Shi L.,
- et al.
- Lavie C.J.,
- Kokkinos P.,
- Ortega F.B.