CRT's Obesity Paradox in Heart Failure: Long-term Survival Rises With BMI

October 01, 2015

NATIONAL HARBOR, MD — How well a patient with heart failure responds to cardiac resynchronization therapy (CRT) over the long term could partly depend on their body-mass index (BMI) when the device is implanted, suggests a small cohort study[1]. It found significantly greater 10-year survival on CRT for patients who were obese by standard criteria, compared with those of normal weight, an effect that was partly mediated by the etiology of their heart failure and whether they had diabetes. The effect was also graded in that 10-year survival for overweight patients was between that for the normal-weight and obese.

This single-center exploratory analysis of only 113 patients with CRT isn't strong enough to prove a direct interaction between obesity and long-term CRT outcomes, according to Dr Alison L Wand (University of Pennsylvania, Philadelphia). But it does suggest a wrinkle in the well-recognized but poorly understood inverse relationship between obesity and heart-failure mortality.

"What we can say is that the 'obesity paradox' that we see in patients with heart failure is preserved in patients who undergo cardiac resynchronization therapy. We see the same kind of effect both when they're treated medically and when they're treated with CRT," she told heartwire from Medscape.

Dr Alison Wand

Having diabetes shortened survival regardless of BMI, but obese diabetics still fared better than normal-weight nondiabetic patients.

The findings, she and her colleagues propose, could potentially help in predicting which patients with heart failure are likely to respond best to CRT. Wand presented the analysis here at the Heart Failure Society of America 2015 Scientific Meeting.

The 33 patients that were normal weight (BMI <25 kg/m2), 47 that were overweight (BMI 25–29 kg/m2), and 33 obese (BMI >30 kg/m2) showed similar prevalence of diabetes and atrial fibrillation and similar cardiovascular medications and left atrial dimensions. Over 10 years, the 113 patients met 88 primary end points, including death in 73 cases.

In multivariate analysis, the hazard ratio (HR) for the primary end point was 0.90 (95% CI 0.85–0.97, P=0.003) for every 1-point increase in BMI.

A similar graded survival benefit for 10-year mortality from CRT was seen for the three BMI categories. Compared with those initially normal weight, the HR for those overweight was 0.54 (95% CI 0.28–1.02, P=0.06) and obese was 0.32 (95% CI 0.14–0.70, P=0.005) after adjustment for age, sex, glomerular filtration rate (GFR), insulin use, QRS width, cardiomyopathy etiology, LVEF, NYHA functional class, left ventricular size, left atrial size, and right ventricular function.

Diabetes interacted with obesity such that it attenuated the survival benefit for both the obese and nonobese. Obese nondiabetic patients fared the best and nonobese diabetics the worst.

10-Year Survival (%) for CRT Patients by Obesity Status and Diabetes Status (trend, P=0.002)

Diabetes status Nonobese Obese
Diabetic 7.7 29.4
Nondiabetic 20.4 43.8

There was a similar gradient of survival by etiology of heart failure, with the highest survival seen in the obese with nonischemic HF and the lowest for the nonobese with nonischemic disease (P=0.03). The obese and nonobese with ischemic cardiomyopathy showed intermediate, similar survival curves.

Wand had no relevant financial relationships.

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