Abstract 8956: Association of Serum Irisin Levels with Inflammatory, Biochemical, and Cardiac Imaging Parameters in Patients With Chronic Heart Failure versus Controls

Abstract

Chronic heart failure (CHF) remains one of the most important causes of morbidity and mortality globally. Metabolic and energetic maladaptation has proven to play a critical in the progression of this condition. In this regard, evidence from preclinical studies has shown that irisin, a recently discovered adipomyokine involved in metabolic control, can induce positive cardioprotective effects by improving cardiac remodeling, cardiomyocyte viability, calcium delivery, and reduction of inflammatory mediators. However, data on the clinical associations between irisin levels and inflammatory and functional imaging parameters are scarce in CHF patients. 32 subjects diagnosed with CHF and 32 healthy controls were evaluated in a cross-sectional study. Serum irisin levels were significantly lower in patients with CHF (4.92, IQR [5.4] ng/ml) than controls (6.45, IQR [3.58] ng/ml). We identified a positive correlation between irisin levels and LVEF (R=0.3), fraction shortening (R=0.4), and body fat percentage (R=0.4). In contrast, a negative correlation between irisin levels and BNP (R=-0.4), insulin levels (R=-0.1), and HOMA index (R=-0.2) was reported. Subjects with CHF showed higher levels of TNF-α (22.05 IQR [12.28] pg/ml) and IL-12p70 (5.58 IQR [4.47] pg/ml) in comparison with controls (9.77 IQR [6.24] and 3.05 [1.90] pg/ml ), while controls showed higher levels of IL-10 (16.27 IQR [10.82] pg/ml) in comparison with CHF cases (7.51 IQR [8.47] pg/ml). However, we did not observe significant correlations between irisin levels and inflammatory cytokines. Irisin levels are possibly reduced in patients with CHF due to the intrinsic energetic and metabolic adaptations that occur as a result of the reduction of cardiac output. Reduced irisin levels play a synergic role with the effects of proinflammatory mediators by hazarding the cardiomyocyte viability, adaptation to ventricular remodeling, and response to fibrosis. This additional damage continues compromising cardiac dynamical parameters creating a vicious cycle.