Erlinge David
Department of Cardiology, Lund University, Skane University Hospital , Lund, Sweden .
Ther Hypothermia Temp Manag. 2011;1(3):129-41. doi: 10.1089/ther.2011.0008.
Hypothermia is an established form of treatment employed following cardiac arrest to limit cerebral injury. The question addressed in this review is whether it is possible to use hypothermia to protect the heart during ischemia resulting from ST-elevation myocardial infarction (STEMI). Mild hypothermia (32°C-35°C) may be of benefit as an adjunctive treatment for STEMI by reducing the extent of the infarct and the effects of the four components of ischemia reperfusion injury: myocardial stunning, microvascular obstruction, reperfusion arrhythmia, and lethal reperfusion injury. To reduce cerebral injury after cardiac arrest, hypothermia can be initiated after reperfusion, and should be maintained for 24-48 hours. However, evidence suggests that to protect the heart in cases of STEMI, hypothermia should be initiated as early as possible after the onset of ischemia, at least before reperfusion. Clinical and experimental results indicate that it is of paramount importance to achieve a body temperature below 35°C before reperfusion to reduce the size of the infarct in the treatment of STEMI patients, and that treatment need only be continued for a relatively short period after reperfusion. Hypothermia has wide-ranging effects on most of the mechanisms involved in ischemia and reperfusion injury, which may explain the potent, highly reproducible cardioprotective effects seen in a large number of studies in different species. Subjecting conscious patients with STEMI to hypothermia is safe, feasible, and well tolerated, but antishivering strategies must be employed. Clinical studies are ongoing to evaluate hypothermia as an adjunctive treatment for myocardial infarction. This review discusses the experimental basis for using mild hypothermia to provide cardioprotection, methods of inducing hypothermia, the timing and duration of treatment, and ways in which the knowledge gained can be translated into clinical treatment.
低温是心脏骤停后用于限制脑损伤的一种既定治疗方式。本综述探讨的问题是,在ST段抬高型心肌梗死(STEMI)导致的缺血期间,是否有可能利用低温来保护心脏。轻度低温(32°C - 35°C)作为STEMI的辅助治疗可能有益,可减少梗死范围以及缺血再灌注损伤四个组成部分的影响:心肌顿抑、微血管阻塞、再灌注心律失常和致死性再灌注损伤。为减少心脏骤停后的脑损伤,低温可在再灌注后开始,并应维持24 - 48小时。然而,有证据表明,为在STEMI病例中保护心脏,低温应在缺血发作后尽早开始,至少在再灌注前开始。临床和实验结果表明,在STEMI患者的治疗中,在再灌注前将体温降至35°C以下对于减小梗死面积至关重要,且再灌注后仅需持续相对较短的一段时间进行治疗。低温对缺血和再灌注损伤所涉及的大多数机制都有广泛影响,这可能解释了在大量不同物种的研究中所观察到的强大且高度可重复的心脏保护作用。让清醒的STEMI患者接受低温治疗是安全、可行且耐受性良好的,但必须采用抗寒战策略。目前正在进行临床研究以评估低温作为心肌梗死辅助治疗的效果。本综述讨论了使用轻度低温提供心脏保护的实验依据、诱导低温的方法、治疗的时机和持续时间,以及如何将所获得的知识转化为临床治疗。