Abstract

Background: Ghrelin is a novel growth hormone (GH)-releasing peptide, originally isolated from the stomach, which has been identified as an endogenous ligand for the GH secretagogues receptor (GHS-R). Previous studies revealed that chronic administration of ghrelin suppresses cardiac sympathetic activity and prevents left ventricular (LV) remodeling after acute myocardial infarction (AMI). However clinical role of ghrelin after AMI is still not clear. We examined the role of ghrelin in LV remodeling after AMI. Objectives: To elucidate the role of ghrelin in LV remodeling after AMI. Subjects and methods: We employed patients with the first AMI (n=41, mean age 61.9±8.9 years old). We obtained peripheral blood on 1, 7, 14 days and 6 months after the onset. Plasma total ghrelin levels were measured by enzyme-linked immunosorbent assay. Patients were treated by percutaneous coronary intervention within 12 hours after onset. Successful myocardial reperfusion (TIMI flow grade 2 or 3) was accomplished in all patients. To analyze LV remodeling, all patients submitted to two serial left ventriculographies carried out on the day of admission and 6 months after the onset (mean 199±13 days). LV volume index (LVEDVI) was calculated by QCA-CMS software. Results: Plasma total ghrelin levels increased after the onset of AMI (day 0: 28.4±6.4, day 7: 75.1±12.2, day 14: 89.9±14.8 pg/ml, 6months: 46.5±6.6 fmol/ml, p<0.001). There was a significant positive correlation between plasma ghrelin levels on day 14 after the onset and changes in LVEDVI (r=+0.53, p<0.001). The stepwise multivariate regression analysis showed that the plasma ghrelin level on day 14 is a significant explanatory variable for the changes in LVEDVI (F=8.77, p<0.01, β=+0.40). Conclusions: The elevation of Ghrelin levels might be a compensatory mechanism to prevent LV remodeling. These results first indicate that ghrelin has a critical role in the progression of left ventricular remodeling after AMI.

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