尽管门到气球的时间大大减少了,ST段抬高型心肌梗死(MI)患者的死亡率和心力衰竭发生率已趋于稳定.在再灌注时代进一步减小MI尺寸仍然存在未满足的需求。大多数增强心肌抢救的辅助疗法都失败了,但有些人表现出了希望。目前,一项关键试验显示梗死面积减少的唯一辅助治疗是局部给予过饱和氧(SSO2)治疗.这篇综述提供了先前减少梗死面积的工作背景。作者描述了显示SSO2在减少MI大小方面的有效性的临床前数据,改善局部心肌血流量和心功能,和减少不良左心室重塑-可能是通过减少再灌注危险区内残余缺血的斑片状区域。描述了SSO2有益的潜在机制,包括通过血浆向缺血区输送高水平的溶解氧,但可行,血管和心肌细胞,从而允许他们的生存和功能。然后作者描述了SSO2临床试验,证明在前ST段抬高MI患者中,SSO2治疗安全有效地减少梗死面积,改善心脏功能,减少左心室重塑。
Despite the fact that door-to-balloon times have been greatly reduced, the rates of death and the incidence of heart failure in patients with ST-segment elevation myocardial infarction (MI) have plateaued. There is still an unmet need to further reduce MI size in the reperfusion era. Most adjunctive therapies to enhance myocardial salvage have failed, but some have shown promise. Currently, the only adjunctive therapy in a pivotal trial that has demonstrated reductions in infarct size is localized delivery of supersaturated oxygen (SSO2) therapy. This review provides background on prior infarct size reduction efforts. The authors describe the preclinical data that shows the effectiveness of SSO2 in reducing MI size, improving regional myocardial blood flow and cardiac function, and reducing adverse left ventricular remodeling-presumably by reducing patchy areas of residual ischemia within the reperfused risk zone. Potential mechanisms by which SSO2 is beneficial are described, including the delivery of high levels of dissolved oxygen through plasma to ischemic, but viable, vascular and myocardial cells, thus allowing their survival and function. The authors then describe the SSO2 clinical trials, demonstrating that in patients with anterior ST-segment elevation MI, SSO2 therapy safely and effectively reduces infarct size, improves cardiac function, and reduces adverse left ventricular remodeling.