Hale Sharon L, Kloner Robert A
The Heart Institute of Good Samaritan Hospital, 1225 Wilshire Blvd, Los Angeles, CA, 90017, USA,
J Thromb Thrombolysis. 2015 Jan;39(1):50-4. doi: 10.1007/s11239-014-1098-x.
The no-reflow phenomenon occurs when an epicardial coronary artery is reopened following myocardial infarction, but portions of the intramural microvasculature fail to reperfuse. One potential mechanism for this is the presence of fibrin tactoids. In addition, some recent studies have suggested that dabigatran treatment may be associated with increased incidence of myocardial infarction. Our aim was to investigate the effect on myocardial infarct size and no-reflow in an acute model of ischemia/reperfusion. Anesthetized, open-chest rabbits were randomly assigned to receive dabigatran (Dab, 0.5 mg/kg bolus + infusion, 0.15 mg/kg/h, IV, n = 11) or vehicle (Veh, n = 11) 15 m before a 30-m coronary artery occlusion and during 2.5 h of the 3 h reperfusion procedure. At the end of the reperfusion period, infarct size (% risk zone) and no-reflow defect were measured. The ischemic risk zone (% of left ventricle) was similar in groups, 24 % in Dab and 25 % in Veh. Necrosis was neither reduced nor increased by Dab treatment; expressed as a percentage of the risk region, infarct size was 30 ± 4 % in Dab and 28 ± 5 % in Veh, p = 0.76. The extent of no-reflow was comparable, expressed either as a percent of the risk region (19 ± 3 %, Dab and 18 ± 3 %, Veh) or as a percent of the necrotic zone (67 ± 8 % Dab and 65 ± 10 % Veh). Dab treatment had no effect on heart rate or blood pressure. Dabigatran treatment did not prevent or ameliorate the no-reflow phenomenon, suggesting that fibrin does not play a major role in the development of microvascular obstruction. Dabigatran did not exacerbate myocardial infarct size.
无复流现象发生于心外膜冠状动脉在心肌梗死后重新开放时，但壁内微血管的部分区域未能再灌注。其一种潜在机制是存在纤维蛋白类晶体。此外，一些近期研究表明，达比加群治疗可能与心肌梗死发生率增加有关。我们的目的是在急性缺血/再灌注模型中研究其对心肌梗死面积和无复流的影响。将麻醉的开胸兔随机分为两组，在冠状动脉闭塞30分钟前15分钟及3小时再灌注过程中的2.5小时，一组接受达比加群（Dab，静脉推注0.5mg/kg + 输注，0.15mg/kg/h，n = 11），另一组接受赋形剂（Veh，n = 11）。在再灌注期结束时，测量梗死面积（%危险区）和无复流缺陷。两组的缺血危险区（左心室的%）相似，达比加群组为24%，赋形剂组为25%。达比加群治疗既未减少也未增加坏死；以危险区域的百分比表示，达比加群组梗死面积为30±4%，赋形剂组为28±5%，p = 0.76。无复流程度相当，以危险区域的百分比表示（达比加群组为19±3%，赋形剂组为18±3%）或以坏死区域的百分比表示（达比加群组为67±8%，赋形剂组为65±10%）。达比加群治疗对心率或血压无影响。达比加群治疗未预防或改善无复流现象，提示纤维蛋白在微血管阻塞的发生中不发挥主要作用。达比加群未加重心肌梗死面积。
