Thibault Hélène, Piot Christophe, Ovize Michel
Hôpital Cardiologique and Pneumologique Louis Pradel, Hospices Civils de Lyon, 59 Boulevard Pinel, 69394 Lyon cedex 03, France.
Heart Fail Rev. 2007 Dec;12(3-4):245-8. doi: 10.1007/s10741-007-9033-2.
Acute myocardial infarction is the leading cause of morbidity and mortality in industrialized countries. Ischemic postconditioning, that consists of repeated brief episodes of ischemia-reperfusion performed just after reflow following a prolonged ischemic insult, dramatically reduces infarct size in animal models. Recent data indicate that it might involve the activation of the PI3-kinase-Akt-eNOS as well as PKC signalling pathways and inhibition of the opening of the permeability transition pore. A recent clinical study demonstrated that postconditioning protects the human heart. Repeated brief episodes of inflation-deflation of the angioplasty balloon performed immediately after re-opening of the culprit coronary artery reduced infarct size by 36%. Additional studies are required to determine whether infarct size limitation by postconditioning would improve functional recovery as well as patient's outcome. Further research is needed to find new pharmacological agents that would mimick postconditioning in order to treat all patients with ongoing acute myocardial infarction.
急性心肌梗死是工业化国家发病和死亡的主要原因。缺血后处理是指在长时间缺血损伤后的再灌注后立即进行的反复短暂缺血-再灌注发作，在动物模型中可显著减小梗死面积。最近的数据表明，其可能涉及PI3激酶-Akt-eNOS以及PKC信号通路的激活，以及抑制通透性转换孔的开放。最近一项临床研究表明，后处理可保护人类心脏。在罪犯冠状动脉重新开通后立即对血管成形术球囊进行反复短暂的充气-放气，可使梗死面积减小36%。需要进一步的研究来确定后处理对梗死面积的限制是否会改善功能恢复以及患者的预后。还需要进一步研究以找到能够模拟后处理的新药，以便治疗所有正在发生急性心肌梗死的患者。
