Background: Although 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.
Hypothesis: Based 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.
Method: A 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.
Results: There 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.
Conclusion: Being 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.
Keywords: Health outcome; Heart failure; Inflammation; Obesity.
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