Development of new treatment for fatal ventricular tachyarrhythmias using heavy ion irradiation

本研究的目的是研究靶向重离子照射（THIR）对心肌梗死（MI）犬心脏机电性能的纵向变化。4只犬在MI后2 W接受THIR（12 C6 r，15 Gy; RIKEN，Japan）治疗。信号平均心电图和超声心动图获得纵向超过1年。心肌梗死后1年，研究了致命性室性快速性心律失常（VT/VF）的诱导和左心室组织连接蛋白43（Cx 43）的免疫标记。免疫标记的Cx43在THIR犬的非缺血区和缺血边缘区均显著增加。滤波QRS在MI后2 W增加，在没有THIR的狗中保持不变，而在THIR的狗中恢复到基线。RMS 40在MI后2 W降低，然后仅在THIR犬中恢复至基线。THIR组1/4例出现VT/VF，而非THIR组4/4例出现VT/VF。心肌梗死后2 W左室收缩功能受到抑制，但THIR可显著促进心肌梗死后1年的恢复。

The aim of this study is to investigate longitudinal changes in electromechanical performance of myocardial infarction (MI) dog hearts by targeted heavy ion irradiation (THIR). Four dogs were treated with THIR (12C6r, 15Gy; RIKEN,Japan) 2W after MI. Signal-averaged ECGs and echocardiograms were obtained longitudinally over 1 yr. Inducibility of fatal ventricular tachyarrhythmias (VT/VF) and connexin 43(Cx43) immunolabeling of the left ventricular tissues were studied 1 yr after MI. Immunolabeled Cx43 were significantly increased in dogs with THIR at non-ischemic zone and ischemic-border zone. Filtered-QRS increased 2W after MI and remained unchanged up to 1 yr in dogs without THIR, while returned toward baseline in dogs with THIR. RMS40 reduced 2W after MI, and then returned toward baseline only in dogs with THIR. VT/VFs were induced in 1/4 with THIR, whereas in 4/4 without THIR. LV systolic function inhibited 2W after MI, however 1 yr recovery was significantly enhanced by THIR.