Abstract 2824: Drug Eluting Stents Implantation In Acute Myocardial Infarction Significantly Delays Healing And Increases Stent Thrombosis

Abstract

Background Although early clinical results of DES implantation for acute myocardial infarction (AMI) show no significant differences in late thrombosis however, long-term safety is still unclear. We evaluated the pathologic responses following DES implantation in AMI patients and compared to stents implanted in non-AMI lesions. Methods From CVPath DES autopsy registry of 116 cases, we identified 22 who presented with AMI at the time of DES implantation and had underlying plaque rupture (PR) or thin-cap fibroatheroma (TCFA). Morphometric analysis was performed using calibrated software (IPLab, Scanalytics) in patients who died ≥30 days after DES implantation. The percentage of struts with fibrin deposition, inflammation (>10 cells/strut), and uncovered struts were also recorded. We assessed arterial healing, by comparing culprit to non-culprit sites within each stented section. Furthermore, age and stent duration matched non-AMI patients who had underlying fibroatheroma (FA) lesion were selected as controls. Results Of the 22 patients with AMI, 14 died ≥30 days (mean duration: 285±277 days) and stent thrombosis was documented in 7 (50%, mean duration: 333±396 days), whereas in non-AMI patients with underlying FA, thrombosis was significantly less frequent (8%). Morphometric analysis revealed neointimal thickness was significantly less in culprit sites as compared to non-culprit sites in AMI patients. The percentages of uncovered struts, and struts with inflammation were significantly greater in culprit sites as compared to non-culprit sites in AMI lesions. Lesions in non-AMI patients were significantly different from AMI patients with greater neointimal thickness, less fibrin around struts, inflammation and uncovered struts (Table ). Conclusions A higher prevalence of stent thrombosis was observed in patients with AMI than those without AMI and is associated with substantial delayed in arterial healing especially at culprit sites. Pathologic and Morphmetric Analysis, Culprit vs. Non-Culprit and AMI vs. Non-AMI