中等（32°C）与轻度（35°C）治疗性低温对猪急性心肌梗死的剂量依赖性心脏保护作用。
Dose-Dependent Cardioprotection of Moderate (32°C) Versus Mild (35°C) Therapeutic Hypothermia in Porcine Acute Myocardial Infarction.
机构信息
Division of Cardiovascular Medicine, Stanford University, Stanford, California; Cardiovascular Institute, Stanford University, Stanford, California.
Division of Cardiovascular Medicine, Stanford University, Stanford, California.
出版信息
JACC Cardiovasc Interv. 2018 Jan 22;11(2):195-205. doi: 10.1016/j.jcin.2017.08.056.
OBJECTIVES
The study investigated whether a dose response exists between myocardial salvage and the depth of therapeutic hypothermia.
BACKGROUND
Cardiac protection from mild hypothermia during acute myocardial infarction (AMI) has yielded equivocal clinical trial results. Rapid, deeper hypothermia may improve myocardial salvage.
METHODS
Swine (n = 24) undergoing AMI were assigned to 3 reperfusion groups: normothermia (38°C) and mild (35°C) and moderate (32°C) hypothermia. One-hour anterior myocardial ischemia was followed by rapid endovascular cooling to target reperfusion temperature. Cooling began 30 min before reperfusion. Target temperature was reached before reperfusion and was maintained for 60 min. Infarct size (IS) was assessed on day 6 using cardiac magnetic resonance, triphenyl tetrazolium chloride, and histopathology.
RESULTS
Triphenyl tetrazolium chloride area at risk (AAR) was equivalent in all groups (p = 0.2), but 32°C exhibited 77% and 91% reductions in IS size per AAR compared with 35°C and 38°C, respectively (AAR: 38°C, 45 ± 12%; 35°C, 17 ± 10%; 32°C, 4 ± 4%; p < 0.001) and comparable reductions per LV mass (LV mass: 38°C, 14 ± 5%; 35°C, 5 ± 3%; 32°C 1 ± 1%; p < 0.001). Importantly, 32°C showed a lower IS AAR (p = 0.013) and increased immunohistochemical granulation tissue versus 35°C, indicating higher tissue salvage. Delayed-enhancement cardiac magnetic resonance IS LV also showed marked reduction at 32°C (38°C: 10 ± 4%, p < 0.001; 35°C: 8 ± 3%; 32°C: 3 ± 2%, p < 0.001). Cardiac output on day 6 was only preserved at 32°C (reduction in cardiac output: 38°C, -29 ± 19%, p = 0.041; 35°C: -17 ± 33%; 32°C: -1 ± 28%, p = 0.041). Using linear regression, the predicted IS reduction was 6.7% (AAR) and 2.1% (LV) per every 1°C reperfusion temperature decrease.
CONCLUSIONS
Moderate (32°C) therapeutic hypothermia demonstrated superior and near-complete cardioprotection compared with 35°C and control, warranting further investigation into clinical applications.
目的
本研究旨在探讨心肌再灌注与治疗性低温深度之间是否存在剂量反应关系。
背景
轻度低温对急性心肌梗死（AMI）的心脏保护作用在临床试验中得出了相互矛盾的结果。快速、更深的低温可能会改善心肌再灌注。
方法
对 24 头进行 AMI 的猪进行分组，分别接受常温（38°C）、轻度（35°C）和中度（32°C）低温再灌注。在 1 小时的前壁心肌缺血后，通过快速血管内冷却达到目标再灌注温度。冷却在再灌注前 30 分钟开始。在再灌注前达到目标温度，并维持 60 分钟。在第 6 天使用心脏磁共振、三苯基氯化四氮唑（triphenyl tetrazolium chloride）和组织病理学评估梗死面积（IS）。
结果
三组三苯基氯化四氮唑危险区（AAR）面积相当（p=0.2），但与 35°C 和 38°C 相比，32°C 的 IS 面积分别减少了 77%和 91%（AAR：38°C，45±12%；35°C，17±10%；32°C，4±4%；p<0.001），每单位左心室质量（LV）的减少量也相当（LV 质量：38°C，14±5%；35°C，5±3%；32°C，1±1%；p<0.001）。重要的是，32°C 的 IS AAR 较低（p=0.013），并且与 35°C 相比，免疫组化肉芽组织增加，表明组织再灌注更高。延迟增强心脏磁共振 IS LV 也显示 32°C 时明显减少（38°C：10±4%，p<0.001；35°C：8±3%；32°C：3±2%，p<0.001）。第 6 天的心输出量仅在 32°C 时得到保存（心输出量减少：38°C，-29±19%，p=0.041；35°C：-17±33%；32°C：-1±28%，p=0.041）。使用线性回归，每降低 1°C 再灌注温度，IS 减少预测值为 6.7%（AAR）和 2.1%（LV）。
结论
与 35°C 和对照组相比，中度（32°C）治疗性低温显示出更好和近乎完全的心脏保护作用，值得进一步研究其临床应用。
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