Abstract 19533: Pro-Inflammatory Biomarkers in Heart Failure With Preserved Ejection Fraction in Stable Versus Acutely Decompensated Patients
Introduction: There is limited information about the pathophysiology of decompensation in heart failure with preserved ejection fraction (HFpEF). One proposed mechanism involves intermittent exacerbation of a chronic pro-inflammatory state. To test this hypothesis we sought to examine whether the levels of several pro-inflammatory biomarkers are elevated in acutely decompensated HFpEF patients (AD-HFpEF) compared with stable HFpEF patients (S-HFpEF).
Methods: Age and sex-matched cohorts of patients from the RELAX trial (S-HFpEF) and the DOSE and ROSE trials (AD-HFpEF) were selected. The cytokines IL-6 and TNF-α and the innate immune factors high sensitivity (hs)-CRP and pentraxin-3 (PTX3) were measured and compared at baseline. We also tested for correlations between biomarker levels and echocardiographic-Doppler diastolic function indices, including left atrial (LA) volume, E/A, E/E’, and left ventricular (LV) structure (mass, relative wall thickness). To determine if biomarker levels have prognostic utility in AD-HFpEF patients we used a Cox model to test for relationships with 60-day outcomes (death, heart failure re-hospitalization) after adjustment for age.
Results: Compared to the S-HFpEF group, the AD-HFpEF group had a 2.4 fold higher level of IL-6 (4.14 vs. 1.71, p < 0.001), a 1.3 fold higher level of TNF-α (11.54 vs. 8.62, p = 0.002), a 3.5 fold higher level of hs CRP (11.90 vs. 3.42, p < 0.001) and a 2.4 fold higher level of PTX3 (3.08 vs. 1.27, p < 0.001). PTX3 levels correlated significantly with LA volume (r = .41, p < 0.002) and LV mass (r = .29, p < 0.05), while TNF-α correlated with E/A ratio (r = .31, p < 0.04). Of the four biomarkers, only age-adjusted IL-6 was found to be a statistically significant predictor of death or heart failure readmission within 60 days (HR 1.097, p < 0.05).
Conclusion: All four pro-inflammatory markers, hs-CRP, IL-6, TNF-α and PTX3, were elevated in AD-HFpEF compared with S-HFpEF, consistent with the hypothesis that worsening of a pro-inflammatory state contributes to AD-HFpEF.
Author Disclosures: A. Abernethy: None. S. Raza: None. R. Tracy: Research Grant; Modest; NHLBI. P. VanBuren: Research Grant; Modest; NHLBI. J. Sun: Research Grant; Modest; NHLBI. S. McNulty: Research Grant; Modest; NHLBI. K. Anstrom: Research Grant; Modest; NHLBI. M. LeWinter: Research Grant; Modest; NHLBI.
- © 2016 by American Heart Association, Inc.