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

本研究旨在探讨靶向重离子照射(TIR)对心肌梗死(MI)犬心脏电机械性能的纵向影响。4只犬在心肌梗死后2周接受TIR(12C6r，15Gy；日本理研)治疗。信号平均的ECG和超声心动图是在一年多的时间里纵向获得的。观察MI后1年大鼠致死性室性快速性心律失常(VT/VF)的诱发率及左心室组织连接蛋白43(Cx43)的免疫标记。在非缺血区和缺血区，免疫标记的Cx43显著增加。过滤后QRS在心肌梗死后增加2W，在没有THIR的狗的1年内保持不变，而在有THIR的狗恢复到基线。心肌梗死后RMS40降低2W，然后仅在有THIR的犬恢复到基线水平。有THIR者1/4可诱发VT/VFS，而无THIR者有4/4可诱发VT/VFS。心肌梗死后2周时，左心室收缩功能受到抑制，而三氢叶酸二氢叶酸显著促进1年恢复。

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.