Abstract 18709: Myostatin Expression is Markedly Increased after Biventricular Mechanical Support in Congenital Heart Disease
Purpose: Myostatin directly inhibits skeletal muscle proliferation and development; however, its role in cardiac muscle and function in early congenital heart disease (CHD) is unknown. We studied myostatin expression in cardiac tissue at varying degrees of myocardial dysfunction and after biventricular support.
Methods: Myocardial tissue samples were collected in patients with A) no evidence of HF undergoing CHD surgery (Normal, n=2), B) complex CHD with left HF at the time of cardiac transplantation (OHT, n=4), and C) at the time of cardiac transplantation after acute decompensated HF requiring biventricular assist device support (BiVAD, n=3). Myostatin protein levels were quantified by Western blot analysis using a commercially available antibody. Ventricular function and size were assessed via transesophageal echocardiography prior to surgery on a scale of 1–4 (normal to abnormal).
Results: Demographics and clinical data are shown in Table 1. The age and weight of Normal were significantly lower than OHT or BiVAD. No echocardiographic evidence of left or right HF was seen in Normal; in contrast, severe left ventricular (LV) and biventricular dysfunction and dilation were seen in OHT and BiVAD patients, respectively. The duration of HF was longest in OHT patients compared to BIVAD; the duration of BiVAD support was very short. A trend to increased myostatin expression was seen in LV and right ventricle (RV) OHT samples versus Normal. Furthermore, a sharp increase in myostatin levels was seen in both LV and RV BiVAD samples versus both Normal and OHT.
Conclusion: Myostatin expression in CHD is closely correlated with ventricular size and dysfunction. Loss of feedback-inhibition with BiVAD mechanical unloading may alter normal myostatin regulatory pathways. Further investigation into myostatin regulation in CHD and decompensated HF may provide insight into potential myocardial recovery mechanisms.
- © 2010 by American Heart Association, Inc.