Abstract

BackgroundAlthough obesity is a risk factor for cardiovascular disease, higher body mass index is related to longer event-free survival in patients with heart failure (HF). While previous research demonstrated that higher levels of inflammatory mediators were associated with shorter event-free survival, the effect of inflammation on the association between obesity and outcomes of HF have not been considered. HypothesisBased on the obesity paradox, we hypothesized that patients with higher baseline body mass index (BMI) would experience better event-free survival than those with lower BMI regardless of inflammatory status. MethodA sample of 415 patients with HF (age 61 ± 11.5 years; 31% female) provided blood to measure soluble tumor necrosis factor receptor1 (sTNFR1), a biomarker of inflammation. Patients were divided into 4 groups based on BMI and a median split of sTNFR1 levels: (1) high BMI ≥ 30 and sTNFR1 > 1804 pg/ml, (2) high BMI ≥ 30 and low sTNFR1 ≤ 1804 pg/ml, and (3) low BMI < 30 and high sTNFR1 > 1804 pg/ml vs. (4) low BMI < 30 and sTNFR1 ≤ 1804 pg/ml. Patients were followed for an average of 365 days to determine the time to first event of either all-cause hospitalization or death. ResultsThere were 177 patients (43%) who experienced either an all-cause hospitalization or death. In a Cox regression, high BMI and high sTNFR1 category predicted time to event (hazard ratio = 1.7, 95% confidence interval = 1.01–2.9) with age, gender, race, left ventricular ejection fraction, New York Heart Association functional class (I/II versus III/IV), log-transformed N-terminal Pro-B-type natriuretic peptide levels, prescribed statin (yes/no), and comorbidity as covariates. ConclusionBeing in a higher inflammation group was associated with shorter event-free survival regardless of BMI. This study provides evidence that inflammation is an important consideration in the association between obesity and better outcomes in patients with HF.

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