Background: The recently discovered myokin Irisin, a peptide originated by a proteolytic cleavage of the transmembrane protein fibronectin type III domain containing 5 (FNDC5) whose expression is induced by exercise and/or by increasing peroxisome proliferator-activated receptor (PPAR)-γ co-activator 1α (PGC-1α), has been considered a prognostic factor in Chronic Ischemic Cardiomyopathy and Acute Heart Failure. Nevertheless, no data are available on Irisin levels in Chronic Heart Failure, both with preserved (HFpEF) or reduced (HFrEF) ejection fraction, matched for age and NYHA classes.
Materials and methods: Therefore, we have evaluated basal plasma irisin levels, by immunoenzymatic method, in these two subtypes of Heart Failure (n=22 HFpEF, age range 5988 years, mean±S.E.M. BMI 28.9±1.3 kg/m2; n=18 HFrEF, 5488 years, BMI 26.5±0.9) and correlated them with metabolic parameters (HOMA-index) and Total Antioxidant Capacity (TAC), as a parameter of Oxidative Stress, measured with a spectrophotometric method, using the system H202-metmyoglobin and the chromogen ABTS.
Results: The two groups did not show significant differences in NT-proBNP levels (2548.8±551.1 ng/ml in HFpEF vs 6007.1±2297.2 in HFrEF). Fasting Irisin levels were significantly lower in HFrEF (mean±S.E.M. 2.77±0.77 ng/ml) in respect to HFpEF (mean±S.E.M. 7.72±0.76 ng/ml). Moreover, a significant inverse correlation between Irisin and LAG values in HFpEF was found (r2=0.145, P<0.05). On the contrary, in HFrEF patients, Irisin and LAG presented a trend toward direct correlation although not significant. No others correlations was found between Irisin and BMI or HOMA-IR for both HFrEF and HFpEF groups.
Conclusions: These data may suggest a different pathophysiological mechanism in these two subtypes of CHF, and a possible role of Oxidative Stress in modulation of Irisin levels. They also strengthen the involvement of metabolic factors in HFpEF.
19 May 2018 - 22 May 2018