Hofstra L, Liem I H, Dumont E A, Boersma H H, van Heerde W L, Doevendans P A, De Muinck E, Wellens H J, Kemerink G J, Reutelingsperger C P, Heidendal G A
Department of Cardiology, University Hospital Maastricht, The Netherlands.
Lancet. 2000 Jul 15;356(9225):209-12. doi: 10.1016/s0140-6736(00)02482-x.
In-vivo visualisation and quantification of the extent and time-frame of cell death after acute myocardial infarction would be of great interest. We studied in-vivo cell death in the hearts of patients with an acute myocardial infarction using imaging with technetium-99m-labelled annexin-V-a protein that binds to cells undergoing apoptosis.
Seven patients with an acute myocardial infarction and one control were studied. All patients were treated by percutaneous transluminal coronary angioplasty (six primary and one rescue), resulting in thrombolysis in myocardial infarction (TIMI) III flow of the infarct-related artery. 2 h after reperfusion, 1 mg annexin-V labelled with 584 MBq Tc-99m was injected intravenously. Early (mean 3.4 h) and late (mean 20.5 h) single-photon-emission computed tomographic (SPECT) images of the heart were obtained. Routine myocardial resting-perfusion imaging was also done to verify infarct localisation.
In six of the seven patients, increased uptake of Tc-99m-labelled annexin-V was seen in the infarct area of the heart on early and late SPECT images. No increased uptake was seen in the heart outside the infarct area. All patients with increased Tc-99m-labelled annexin-V uptake in the infarct area showed a matching perfusion defect. In a control individual, no increased uptake in the heart was seen.
Increased uptake of Tc-99m-labelled annexin-V is present in the infarct area of patients with an acute myocardial infarction, suggesting that programmed cell death occurs in that area. The annexin-V imaging protocol might allow us to study the dynamics of reperfusion-induced cell death in the area at risk and may help to assess interventions that inhibit cell death in patients with an acute myocardial infarction.
急性心肌梗死后细胞死亡范围和时间框架的体内可视化及定量研究具有重要意义。我们利用锝-99m标记的膜联蛋白V(一种与凋亡细胞结合的蛋白质)成像技术,对急性心肌梗死患者心脏中的细胞死亡进行了体内研究。
研究了7例急性心肌梗死患者和1例对照者。所有患者均接受经皮冠状动脉腔内血管成形术治疗(6例为直接PCI,1例为补救性PCI),梗死相关动脉达到心肌梗死溶栓(TIMI)Ⅲ级血流。再灌注2小时后,静脉注射1mg用584MBq锝-99m标记的膜联蛋白V。获取心脏的早期(平均3.4小时)和晚期(平均20.5小时)单光子发射计算机断层扫描(SPECT)图像。还进行了常规心肌静息灌注成像以确认梗死定位。
7例患者中有6例在早期和晚期SPECT图像上,心脏梗死区域可见锝-99m标记的膜联蛋白V摄取增加。梗死区域以外的心脏未见摄取增加。所有梗死区域锝-99m标记的膜联蛋白V摄取增加的患者均显示出匹配的灌注缺损。在对照个体中,心脏未见摄取增加。
急性心肌梗死患者梗死区域存在锝-99m标记的膜联蛋白V摄取增加,提示该区域发生了程序性细胞死亡。膜联蛋白V成像方案可能使我们能够研究危险区域再灌注诱导的细胞死亡动态,并可能有助于评估抑制急性心肌梗死患者细胞死亡的干预措施。