Long-term benefit of postconditioning
Long-term benefit of postconditioning
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DOI：
10.1161/circulationaha.107.729780
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发表时间：
2008-02-26
期刊：
影响因子：
37.8
通讯作者：
Ovize, Michel
中科院分区：
文献类型：
--
作者：
Thibault, Helene;Piot, Christophe;Ovize, Michel
背景-我们先前证实缺血后处理减少了急性心肌梗死患者肌酸激酶的释放，肌酸激酶是梗死面积的替代标志物。我们的目的是确定缺血后处理是否能够提供（1）持续的梗死面积限制和（2）梗死后几个月心肌收缩功能的改善恢复。方法和结果-胸痛发作6小时内出现的患者，怀疑首次ST段抬高心肌梗死，并且临床决定接受经皮冠状动脉介入治疗的患者有资格入组。直接支架再灌注后，38例患者被随机分配到对照组（无干预; n = 21）或后处理组（血管成形术球囊重复充盈和回缩; n = 17）。通过再灌注早期心肌酶释放和急性心肌梗死后6个月的（201）铊单光子发射计算机断层扫描来评估心肌梗死的大小。在1年时，通过超声心动图评价整体和局部收缩功能。急性心肌梗死后6个月，单光子发射计算机断层扫描静息-再分布指数（梗死面积的替代物）平均为11.8 ± 10.3%，后处理组与对照组的平均值为19.5 ± 13.3%（P = 0.04），与后处理组与对照组相比，肌酸激酶和肌钙蛋白I的释放显著减少（分别为-40%和-47%）。在1年，后处理组表现出7%的增加，左心室射血分数与对照组相比（P = 0.04）。结论-后处理提供持续的梗死面积减少，并改善长期功能恢复急性心肌梗死患者。
Background- We previously demonstrated that ischemic postconditioning decreases creatine kinase release, a surrogate marker for infarct size, in patients with acute myocardial infarction. Our objective was to determine whether ischemic postconditioning could afford (1) a persistent infarct size limitation and (2) an improved recovery of myocardial contractile function several months after infarction.Methods and Results- Patients presenting within 6 hours of the onset of chest pain, with suspicion for a first ST-segment-elevation myocardial infarction, and for whom the clinical decision was made to treat with percutaneous coronary intervention, were eligible for enrollment. After reperfusion by direct stenting, 38 patients were randomly assigned to a control (no intervention; n = 21) or postconditioned group (repeated inflation and deflation of the angioplasty balloon; n = 17). Infarct size was assessed both by cardiac enzyme release during early reperfusion and by (201)thallium single photon emission computed tomography at 6 months after acute myocardial infarction. At 1 year, global and regional contractile function was evaluated by echocardiography. At 6 months after acute myocardial infarction, single photon emission computed tomography rest-redistribution index (a surrogate for infarct size) averaged 11.8 +/- 10.3% versus 19.5 +/- 13.3% in the postconditioned versus control group (P = 0.04), in agreement with the significant reduction in creatine kinase and troponin I release observed in the postconditioned versus control group (-40% and -47%, respectively). At 1 year, the postconditioned group exhibited a 7% increase in left ventricular ejection fraction compared with control (P = 0.04).Conclusions- Postconditioning affords persistent infarct size reduction and improves long-term functional recovery in patients with acute myocardial infarction.