C R Narins1, D P Miller, R M Califf, E J Topol. 1. Department of Cardiology and the Joseph J. Jacobs Center for Vascular Biology, The Cleveland Clinic Foundation, Ohio 44195, USA.
Abstract
OBJECTIVES: We sought to determine whether periprocedural myocardial infarction complicating percutaneous coronary revascularization is associated with subsequent clinical restenosis, as judged by the need for target vessel revascularization. BACKGROUND: Although myocardial enzyme elevation following angioplasty is associated with increased late mortality, its effect on subsequent clinical restenosis, as assessed by the need for late target vessel revascularization (TVR), is unknown. METHODS: Serial myocardial enzyme determinations were performed on 2,099 patients who underwent angioplasty or atherectomy in the Evaluation of IIb/IIIa platelet receptor antagonist 7E3 in Preventing Ischemic Complications (EPIC) trial. Thirty-day survivors were prospectively followed for three years for adverse clinical events including death and need for TVR. RESULTS: Within the study population, periprocedural creatine kinase (CK) elevation was a predictor of late mortality. Among patients with elevated CK, however, a paradoxical decrease in the need for late TVR was present. This relationship became progressively more profound as the magnitude of CK release increased. Late TVR occurred in 29.8% of patients with no CK elevation, 24.8% with CK elevation to >3 times normal, and 16.9% with >10 times elevation (hazard ratio 0.51, 95% CI 0.29, 0.91). CONCLUSIONS: In the EPIC study, patients with periprocedural MI were less likely to develop clinical restenosis as measured by the need for TVR. Mechanistically, although it is unlikely that CK elevation prevents vascular renarrowing per se, myocardial necrosis impairs the clinical manifestation of restenosis, thereby reducing the need for ischemia-driven TVR. This novel finding 1) highlights the potential discordance between angiographic and clinical measures of restenosis, and 2) has implications for clinical trials, as therapies that reduce periprocedural MI may be associated with a perceived excess of restenosis when measured by the need for TVR.
RCT Entities:
OBJECTIVES: We sought to determine whether periprocedural myocardial infarction complicating percutaneous coronary revascularization is associated with subsequent clinical restenosis, as judged by the need for target vessel revascularization. BACKGROUND: Although myocardial enzyme elevation following angioplasty is associated with increased late mortality, its effect on subsequent clinical restenosis, as assessed by the need for late target vessel revascularization (TVR), is unknown. METHODS: Serial myocardial enzyme determinations were performed on 2,099 patients who underwent angioplasty or atherectomy in the Evaluation of IIb/IIIa platelet receptor antagonist 7E3 in Preventing Ischemic Complications (EPIC) trial. Thirty-day survivors were prospectively followed for three years for adverse clinical events including death and need for TVR. RESULTS: Within the study population, periprocedural creatine kinase (CK) elevation was a predictor of late mortality. Among patients with elevated CK, however, a paradoxical decrease in the need for late TVR was present. This relationship became progressively more profound as the magnitude of CK release increased. Late TVR occurred in 29.8% of patients with no CK elevation, 24.8% with CK elevation to >3 times normal, and 16.9% with >10 times elevation (hazard ratio 0.51, 95% CI 0.29, 0.91). CONCLUSIONS: In the EPIC study, patients with periprocedural MI were less likely to develop clinical restenosis as measured by the need for TVR. Mechanistically, although it is unlikely that CK elevation prevents vascular renarrowing per se, myocardial necrosis impairs the clinical manifestation of restenosis, thereby reducing the need for ischemia-driven TVR. This novel finding 1) highlights the potential discordance between angiographic and clinical measures of restenosis, and 2) has implications for clinical trials, as therapies that reduce periprocedural MI may be associated with a perceived excess of restenosis when measured by the need for TVR.
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