Narula J, Nicol P D, Southern J F, Pieri P, O'Donnell S M, Guererro J L, Nossiff N D, Newell J B, Strauss H W, Khaw B A
Division of Nuclear Medicine, Massachusetts General Hospital, Boston.
J Nucl Med. 1994 Jun;35(6):1076-85.
Antimyosin antibody is a specific marker of myocardial necrosis that is based on the loss of integrity of the sarcolemmal membrane. Because antimyosin can be labeled with several different radiotracers, gamma imaging performed with antimyosin labeled with two different radionuclides can be used to quantify infarct size before and after an intervention such as reperfusion.
Twelve open-chested anesthetized dogs were evaluated both at the end of 1.5 hr of occlusion of the left anterior descending coronary artery and following reperfusion. Antimyosin Fab radiolabeled with either 123I or 111In was injected by intracoronary administration over 3 min at the end of the occlusion interval, and the coronary sinus was drained continuously for 7 min to prevent recirculation of the antibody. One hour after reperfusion, a second injection of antimyosin Fab (labeled with a different isotope from the first) was administered as before. Six dogs were given intracoronary trifluoperazine (150 micrograms/kg of body weight) simultaneously with reperfusion, and another six dogs received saline as the control. The infarct size in grams before and after reperfusion was assessed by antimyosin antibody uptake in ex vivo images of 1-cm thick slices of the hearts. The mean infarct sizes before (W1) and after (W2) reperfusion were then calculated as the percent of infarcted myocardium/ventricular myocardial mass.
There was a significant increase in the mean percent infarct size after reperfusion in the control group (W2 = 16.73 +/- 4.0, W1 = 14.92 +/- 3.88; p = 0.029). The mean infarct size was uniformly smaller with trifluoperazine intervention (W2 = 12.33 +/- 2.03, W1 = 16.34 +/- 2.78; p = 0.004). The difference between the mean change in the infarct sizes in the two groups was highly significant (p = 0.002).
Dual imaging of the extent of myocardial necrosis before and after an intervention (reperfusion) in the same animal demonstrated the utility of antimyosin imaging to document changes in the extent of necrosis.
抗肌球蛋白抗体是心肌坏死的一种特异性标志物,其基于肌膜完整性的丧失。由于抗肌球蛋白可用几种不同的放射性示踪剂进行标记,因此用两种不同放射性核素标记的抗肌球蛋白进行的γ成像可用于在诸如再灌注等干预前后定量梗死面积。
对12只开胸麻醉的犬在左前降支冠状动脉闭塞1.5小时结束时和再灌注后进行评估。在闭塞间隔结束时,通过冠状动脉内给药在3分钟内注射用123I或111In标记的抗肌球蛋白Fab,并持续引流冠状窦7分钟以防止抗体再循环。再灌注1小时后,像之前一样第二次注射抗肌球蛋白Fab(用与第一次不同的同位素标记)。6只犬在再灌注时同时给予冠状动脉内三氟拉嗪(150微克/千克体重),另外6只犬接受生理盐水作为对照。通过心脏1厘米厚切片的离体图像中抗肌球蛋白抗体摄取情况评估再灌注前后梗死面积(以克为单位)。然后将再灌注前(W1)和再灌注后(W2)的平均梗死面积计算为梗死心肌/心室心肌质量的百分比。
对照组再灌注后平均梗死面积百分比显著增加(W2 = 16.73±4.0,W1 = 14.92±3.88;p = 0.029)。三氟拉嗪干预后平均梗死面积一致较小(W2 = 12.33±2.03,W1 = 16.34±2.78;p = 0.004)。两组梗死面积平均变化之间的差异非常显著(p = 0.002)。
在同一只动物中对干预(再灌注)前后心肌坏死范围进行双成像证明了抗肌球蛋白成像记录坏死范围变化的实用性。