Narins C R, Miller D P, Califf R M, Topol E J
Department of Cardiology and the Joseph J. Jacobs Center for Vascular Biology, The Cleveland Clinic Foundation, Ohio 44195, USA.
J Am Coll Cardiol. 1999 Mar;33(3):647-53. doi: 10.1016/s0735-1097(98)00620-2.
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.
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.
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.
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).
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.
我们试图确定经皮冠状动脉血运重建术中并发的围手术期心肌梗死是否与随后的临床再狭窄相关,这通过靶血管血运重建的需求来判断。
尽管血管成形术后心肌酶升高与晚期死亡率增加相关,但其对随后临床再狭窄的影响(通过晚期靶血管血运重建(TVR)的需求来评估)尚不清楚。
在“IIb/IIIa血小板受体拮抗剂7E3预防缺血并发症(EPIC)试验”中,对2099例行血管成形术或旋切术的患者进行了系列心肌酶测定。对30天存活者进行了为期三年的前瞻性随访,观察不良临床事件,包括死亡和TVR需求。
在研究人群中,围手术期肌酸激酶(CK)升高是晚期死亡率的预测指标。然而,在CK升高的患者中,晚期TVR需求却出现了矛盾的下降。随着CK释放量的增加,这种关系变得越来越明显。CK未升高的患者中晚期TVR发生率为29.8%,CK升高至正常上限3倍以上的患者为24.8%,CK升高至正常上限10倍以上的患者为16.9%(风险比0.51,95%可信区间0.29,0.91)。
在EPIC研究中,通过TVR需求衡量,围手术期心肌梗死患者发生临床再狭窄的可能性较小。从机制上讲,尽管CK升高本身不太可能预防血管再狭窄,但心肌坏死会损害再狭窄的临床表现,从而减少缺血驱动的TVR需求。这一新发现1)突出了再狭窄血管造影和临床测量之间潜在的不一致性,2)对临床试验有影响,因为减少围手术期心肌梗死的治疗方法在通过TVR需求衡量时可能与感知到的再狭窄过多相关。