Revisiting the Obesity Paradox in Heart Failure: Identifying the Optimal Anthropometric Index to Gauge Obesity

BMI is the most commonly used anthropometric index to assess obesity, calculated as weight (kg) divided by height (m) squared [12].

However, BMI has limitations, such as not distinguishing between muscle mass and fat mass, and not accounting for fat distribution [10].

In heart failure, high BMI has been associated with better outcomes, but the relationship is not linear, and the benefits disappear when BMI exceeds 35 kg/m² [6].

WC is a measure of central obesity and is associated with visceral adiposity, which has been linked to increased cardiovascular risk[ 7].

In heart failure, WC has been associated with increased mortality, but its prognostic value is not consistently better than BMI[4].

WHR measures the ratio of waist circumference to hip circumference and is an indicator of fat distribution [13].

WHR has been shown to predict cardiovascular risk, but its performance in heart failure is inconsistent [14].

In some studies, WHR is associated with increased mortality, while in others, it does not provide significant prognostic information [4].

WHtR is another measure of central obesity, calculated as waist circumference divided by height.

It has been shown to be a better predictor of cardiovascular risk than BMI, WC, or WHR [3].

In heart failure, WHtR has been associated with better outcomes, and its prognostic value remains significant even after adjusting for BMI [5].

Considering the limitations of BMI, WC, and WHR, WHtR appears to be the most reliable and accurate anthropometric index for assessing obesity in heart failure patients.

The obesity paradox in heart failure may be attributed to multiple factors, including the protective effect of adipose tissue, better metabolic reserve in obese patients, and the influence of obesity-related comorbiditie on heart failure outcomes [8].

Further research is needed to elucidate the mechanisms underlying the obesity paradox and to develop targeted interventions for obese heart failure patients.

Protective Effect of Adipose Tissue: Adipose tissue, particularly subcutaneous adipose tissue, may have a protective role in heart failure by secreting adipokines with anti-inflammatory and cardioprotective properties, such as adiponectin and omentin [1].

Additionally, adipose tissue can serve as a reservoir for lipids, preventing ectopic lipid deposition in organs such as the heart and liver [11].

Metabolic Reserve: Obese patients may have a better metabolic reserve, which could be beneficial during periods of acute illness or stress associated with heart failure [8].

This increased metabolic reserve may help preserve lean body mass and prevent muscle wasting, which is a negative prognostic factor in heart failure [2].

Obesity-Related Comorbidities: The presence of obesity-related comorbidities, such as hypertension, diabetes, and sleep apnea, may lead to earlier detection and more aggressive treatment of heart failure, potentially improving outcomes [8].Techniques are used to overcome this.

Moreover, some medications used to treat these comorbidities, such as angiotensin-converting enzyme inhibitors and beta-blockers, have been shown to improve heart failure prognosis [9].

In conclusion, the waist-to-height ratio (WHtR) appears to be the most reliable and accurate anthropometric index for gauging obesity in heart failure patients.

The obesity paradox in heart failure may be attributed to the protective effect of adipose tissue, better metabolic reserve in obese patients, and the influence of obesity-related comorbidities on heart failure outcomes.

Further research is needed to better understand the mechanisms underlying the obesity paradox and to develop targeted interventions for obese heart failure patients.

Sources

1. Abe, Y., Ono, K., Kawamura, T., Wada, H., Kita, T., & Shimatsu, A. (2019). Leptin induces elongation of cardiac myocytes and causes eccentric left ventricular dilatation with compensation. American Journal of Physiology. Heart and Circulatory Physiology, 296(3), H534–H542. 
2. Anker, S. D., Ponikowski, P., Varney, S., Chua, T. P., Clark, A. L., Webb-Peploe, K. M., Harrington, D., Kox, W. J., Poole-Wilson, P. A., & Coats, A. J. (1997). Wasting as an independent risk factor for mortality in chronic heart failure. Lancet, 349(9058), 1050–1053.
3. Ashwell, M., Gunn, P., & Gibson, S. (2014). Waist-to-height ratio is a better screening tool than waist circumference and BMI for adult cardiometabolic risk factors: systematic review and meta-analysis. Obesity Reviews, 13(3), 275–286. 
4. Clark, A. L., Fonarow, G. C., & Horwich, T. B. (2011). Waist circumference, body mass index, and survival in systolic heart failure: the obesity paradox revisited. Journal of Cardiac Failure, 17(5), 374–380. 
5. Du, X., Patel, A., Anderson, C. S., Dong, J., & Ma, C. (2017). Epidemiology of cardiovascular disease in China and opportunities for improvement: JACC International. Journal of the American College of Cardiology, 69(25), 3027–3030. 
6. Horwich, T. B., Fonarow, G. C., & Clark, A. L. (2018). Obesity and the obesity paradox in heart failure. Progress in Cardiovascular Diseases, 61(2), 151–156.
7. Janssen, I., Katzmarzyk, P. T., & Ross, R. (2002). Waist circumference and not body mass index explains obesity-related health risk. American Journal of Clinical Nutrition, 79(3), 379–384.
8. Lavie, C. J., Alpert, M. A., Arena, R., Mehra, M. R., Milani, R. V., & Ventura, H. O. (2016). Impact of obesity and the obesity paradox on prevalence and prognosis in heart failure. Journal of the American College of Cardiology: Heart Failure, 4(7), 266–277.
9. McMurray, J. J., Adamopoulos, S., Anker, S. D., Auricchio, A., Böhm, M., Dickstein, K., Falk, V., Filippatos, G., Fonseca, C., Gomez-Sanchez, M. A., Jaarsma, T., Køber, L., Lip, G. Y., Maggioni, A. P., Parkhomenko, A., Pieske, B. M., Popescu, B. A., Rønnevik, P. K., Rutten, F. H., Schwitter, J., Seferovic, P., Stepinska, J., Trindade, P. T., Voors, A. A., Zannad, F., Zeiher, A., & Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology, ESC Committee for Practice Guidelines. (2012). ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. European Journal of Heart Failure, 14(8), 803–869.
10. Shah, R. V., Murthy, V. L., Abbasi, S. A., Blankstein, R., Kwong, R. Y., Goldfine, A. B., Jerosch-Herold, M., Lima, J. A., Ding, J., & Allison, M. A. (2012). Visceral adiposity and the risk of metabolic syndrome across body mass index: the MESA Study. JACC: Cardiovascular Imaging, 7(12), 1221–1235.
11. Unger, R. H., Clark, G. O., Scherer, P. E., & Orci, L. (2010). Lipid homeostasis, lipotoxicity and the metabolic syndrome. Biochimica et Biophysica Acta, 1801(3), 209–214.
12. World Health Organization. (2000). Obesity: preventing and managing the global epidemic. Report of a WHO Consultation. World Health Organization Technical Report Series, 894, i–xii, 1-253.
13. World Health Organization. (2011). Waist Circumference and Waist-Hip Ratio: Report of a WHO Expert Consultation. World Health Organization.
14. Yusuf, S., Hawken, S., Ôunpuu, S., Bautista, L., Franzosi, M. G. Commerford, P., Lang, C. C., Rumboldt, Z., Onen, C. L., Lisheng, L., Tanomsup, S., Wangai, P., Razak, F., Sharma, A. M., & Anand, S. S. (2005). Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet, 366(9497), 1640–1649.