Department of Coronary Heart Disease, Skane University Hospital, Lund University, Lund, Sweden.
Circ Cardiovasc Interv. 2010 Oct;3(5):400-7. doi: 10.1161/CIRCINTERVENTIONS.110.957902. Epub 2010 Aug 24.
Experimental studies have shown that induction of hypothermia before reperfusion of acute coronary occlusion reduces infarct size. Previous clinical studies, however, have not been able to show this effect, which is believed to be mainly because therapeutic temperature was not reached before reperfusion in the majority of the patients. We aimed to evaluate the safety and feasibility of rapidly induced hypothermia by infusion of cold saline and endovascular cooling catheter before reperfusion in patients with acute myocardial infarction.
Twenty patients with acute myocardial infarction scheduled to undergo primary percutaneous coronary intervention were enrolled in this prospective, randomized study. After 4 ± 2 days, myocardium at risk and infarct size were assessed by cardiac magnetic resonance using T2-weighted imaging and late gadolinium enhancement imaging, respectively. A core body temperature of <35°C (34.7 ± 0.3°C) was achieved before reperfusion without significant delay in door-to-balloon time (43 ± 7 minutes versus 40 ± 6 minutes, hypothermia versus control, P=0.12). Despite similar duration of ischemia (174 ± 51 minutes versus 174 ± 62 minutes, hypothermia versus control, P=1.00), infarct size normalized to myocardium at risk was reduced by 38% in the hypothermia group compared with the control group (29.8 ± 12.6% versus 48.0 ± 21.6%, P=0.041). This was supported by a significant decrease in both peak and cumulative release of Troponin T in the hypothermia group (P=0.01 and P=0.03, respectively).
The protocol demonstrates the ability to reach a core body temperature of <35°C before reperfusion in all patients without delaying primary percutaneous coronary intervention and that combination hypothermia as an adjunct therapy in acute myocardial infarction may reduce infarct size at 3 days as measured by MRI.
URL: http://www.clinicaltrials.gov. Unique identifier: NCT00417638.
实验研究表明，在急性冠状动脉闭塞再灌注前诱导低温可减少梗死面积。然而，先前的临床研究未能显示出这种效果，这主要被认为是因为在大多数患者中，再灌注前未能达到治疗温度。我们旨在评估在急性心肌梗死患者中，通过输注冷盐水和血管内冷却导管在再灌注前快速诱导低温的安全性和可行性。
这项前瞻性、随机研究纳入了 20 名计划接受直接经皮冠状动脉介入治疗的急性心肌梗死患者。在 4 ± 2 天后，通过心脏磁共振 T2 加权成像和晚期钆增强成像分别评估心肌危险区和梗死面积。在再灌注前，核心体温<35°C（34.7 ± 0.3°C），且门球时间无明显延迟（低温组 43 ± 7 分钟，对照组 40 ± 6 分钟，P=0.12）。尽管缺血持续时间相似（低温组 174 ± 51 分钟，对照组 174 ± 62 分钟，P=1.00），但低温组梗死面积与危险区的比值比对照组降低了 38%（低温组 29.8 ± 12.6%，对照组 48.0 ± 21.6%，P=0.041）。低温组肌钙蛋白 T 的峰值和累积释放均显著降低（P=0.01 和 P=0.03），支持了这一结果。
该方案表明，在不延迟直接经皮冠状动脉介入治疗的情况下，所有患者均能达到再灌注前<35°C的核心体温，急性心肌梗死中联合低温作为辅助治疗可能会降低磁共振测量的 3 天梗死面积。
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