Ciavolella M, Greco C, Tavolaro R, Tanzilli G, Scopinaro F, Campa P P
2nd Department of Cardiology and the Institute of Nuclear Medicine, University La Sapienza, Rome, Italy.
J Nucl Cardiol. 1998 Mar-Apr;5(2):128-33. doi: 10.1016/s1071-3581(98)90195-7.
Trimetazidine is an antiischemic drug protecting the myocardium from ischemic damage through the preservation of mitochondrial oxidative metabolism, without any hemodynamic effect. 99mTc-sestamibi is accumulated by myocytes according to mitochondrial function. As mitochondrial metabolism is thought to be present in hibernating myocardium, the aim of the study was to investigate trimetazidine effects on infarcted and eventually hibernating myocardial areas by means of 99mTc-sestamibi perfusional scintigraphy, comparing them to postoperative recovery of wall motion.
Twelve patients with previous myocardial infarction underwent 2 perfusion imaging tomographic studies at rest with 99mTc-sestamibi, receiving placebo or trimetazidine (60 mg orally), and subsequently underwent revascularization procedures. An echocardiographic study was carried out before and >3 months after revascularization. At polar map analysis of placebo scan, infarcted vascular territories (wall motion score index: 2.65 +/- 0.31) showed 73.7% +/- 10.4% of the territory with activity <2.5 SD from the mean of normals, for a severity (expressed as the sum of the standard deviations below average normal values in all abnormal pixels) of 833.8 +/- 345.7. Polar map analysis of the trimetazidine scan showed tracer uptake increased significantly in 11 of them, by 8.2% +/- 3.0% (p < 0.001) and by 180.3 +/- 111.0 SD (p < 0.001), respectively. Postoperative wall motion score index improved significantly in 9 of these territories (-0.9 +/- 0.4, p < 0.001).
Trimetazidine-associated increase in 99mTc-sestamibi uptake in infarcted but viable myocardial areas is probably related to an improvement in mitochondrial oxidative metabolism that is essential to 99mTc-sestamibi retention. Additionally, coupling trimetazidine administration to 99mTc-sestamibi perfusional scintigraphy may represent a means of detecting viable myocardium.
曲美他嗪是一种抗缺血药物,通过维持线粒体氧化代谢保护心肌免受缺血损伤,且无任何血流动力学效应。99mTc-甲氧基异丁基异腈根据线粒体功能在心肌细胞中蓄积。由于认为冬眠心肌存在线粒体代谢,本研究旨在通过99mTc-甲氧基异丁基异腈灌注闪烁显像研究曲美他嗪对梗死及最终冬眠心肌区域的影响,并将其与术后室壁运动恢复情况进行比较。
12例既往有心肌梗死的患者接受了2次静息状态下的99mTc-甲氧基异丁基异腈灌注断层显像研究,分别服用安慰剂或曲美他嗪(口服60 mg),随后接受血运重建手术。在血运重建术前及术后3个月以上进行了超声心动图研究。在安慰剂扫描的极坐标图分析中,梗死血管区域(室壁运动评分指数:2.65±0.31)显示,该区域73.7%±10.4%的活性低于正常均值2.5个标准差,严重程度(以所有异常像素低于正常均值的标准差总和表示)为833.8±345.7。曲美他嗪扫描的极坐标图分析显示,其中11例患者的示踪剂摄取显著增加,分别增加了8.2%±3.0%(p<0.001)和180.3±111.0个标准差(p<0.001)。这些区域中有9个区域的术后室壁运动评分指数显著改善(-0.9±0.4,p<0.001)。
曲美他嗪使梗死但存活心肌区域的99mTc-甲氧基异丁基异腈摄取增加,可能与线粒体氧化代谢改善有关,而线粒体氧化代谢对99mTc-甲氧基异丁基异腈滞留至关重要。此外,将曲美他嗪给药与99mTc-甲氧基异丁基异腈灌注闪烁显像相结合可能是检测存活心肌的一种方法。