Abstract 3662: Sirolimus-eluting Stent Implantation Adversely Affects Microvascular Endothelial Function in the Infarct-related Coronary Artery in Patients with Acute Anterior Myocardial Infarction
Myocardial ischemia-reperfusion causes endothelial injury in the vasculature of the infarct-related coronary artery, which contributes to infarct extension and poor prognosis after acute myocardial infarction (AMI). Sirolimus-eluting stents (SES) inhibit re-endothelialization at the site of stenting. Thus, this study assessed the hypothesis that SES implantation may impair recovery of endothelial vasomotor function from ischemia-reperfusion injury at a site distal to the site of stenting of the infarct-related coronary artery in AMI.
Methods: This study included 24 consecutive patients with a first AMI due to occlusion of the left anterior descending coronary artery (LAD) and successful reperfusion therapy using SES (n = 12) or bare metal stents (BMS, n = 12). No residual stenosis was present in LAD in all patients. Coronary blood flow responses of the LAD to intracoronary infusion of acetylcholine (ACh, 5, 10, and 50 μg/min) were measured by an intracoronary flow wire at 2 weeks after AMI. Levels of vascular endothelial growth factor (VEGF) were measured by ELISA in plasma obtained from the aortic root (AO) and the anterior interventricular vein (AIV) at the same time in all patients.
Results: Time to reperfusion, peak CK levels, and myocardial blush grade just after reperfusion were similar between the SES and BMS groups. At 2 weeks after AMI, the increase in coronary blood flow in response to ACh was lower in the SES than the BMS group (p < 0.01 by two-way AVOVA) (% increase from baseline flow, 35 ± 4% vs. 110 ± 12% at 10 μg/min of ACh, respectively, p < 0.01). The epicardial coronary artery was more severely constricted to response to ACh in the SES than in the BMS group (p < 0.05 by two-way ANOVA). The 2 groups had comparable coronary blood flow and epicardial coronary diameters at baseline and similar changes in epicardial diameter in response to nitrates. VEGF levels were significantly lower in the AIV than in the AO in the SES group (114 ± 9 vs. 135 ±11 pg/ml, respectively, p < 0.01) but not in the BMS group (128 ± 13 vs. 130 ± 14 pg/ml, respectively, p = ns).
Conclusion: During the course of AMI, SES implantation adversely affects endothelium-dependent vasomotor function in resistance and large coronary arteries in association with a reduction in myocardial VEGF secretion.