Abstract 10270: Increased Circulating Myostatin is Predictive of Mortality in Congestive Heart Failure.
Background: Myostatin (Mstn), a member of transforming growth factor beta (TGF-ß) family, regulating skeletal muscle mass, is emerging as a regulator of cardiomyocytes trophicity. Recent observations show that plasma concentrations of Mstn are significantly increased in heart failure patients and related to the severity of the disease. In the present study we examine whether Mstn could also predict long term mortality.
Methods: Mstn circulating concentrations were measured in 73 fully treated heart failure (HF) patients, and the risk-adjusted survival was analyzed over a 6-year follow-up period. Patients' characteristics: age 68±13 years; 56 males, 17 females; ejection fraction: 22±6%; NYHA II-IV; etiology: ischemic n=54, dilated cardiomyopathy n=19. The Mstn concentrations were determined with a two-site enzyme immunoassay (Immundiagnostik, Bensheim, Germany). Mstn was used as categorical variable allocated on the basis of the median, and its prognostic value was assessed using univariate or multivariate COX proportional hazard model. Survival curves of patients with Mstn below and above the median were compared by the Kaplan-Meier method (Log-Rank test).
Results: Of the 73 patients enrolled, 43 died (worsening HF n=29; sudden death n=11; other cardiovascular death n= 3) and 6 patients underwent a heart transplant. Twenty-four patients were alive at the end of the follow-up. Geometric mean [95% CI] of Mstn was higher in CHF 63.9 ng/mL [28.5-144.5] than in controls 43.0 ng/mL [13.5-69.0] (p < 0.01). Mstn was predictive of mortality (p=0.0253) in univariate COX analysis. Kaplan-Meier curves differ significantly (Log-Rank=0.0255). At the end of follow-up, only 10% of the patients with Mstn above median were still alive; in contrast 50% with Mstn below median survived.
Conclusions: Mstn identifies a subgroup of patients with a very high long term mortality risk which could improve the selection process for more aggressive therapies.
- © 2011 by American Heart Association, Inc.