Ito Arisa, Miyoshi Shunichiro, Kimura Takehiro, Takatsuki Seiji, Fukumoto Kotaro, Fukuda Keiichi, Arai Tsunenori
School of Fundamental Science and Technology, Graduate School of Science and Technology, Keio University, Hiyoshi, Kohoku-ku, Yokohama, Japan.
Lasers Surg Med. 2011 Dec;43(10):984-90. doi: 10.1002/lsm.21136. Epub 2011 Nov 22.
This study proposes photosensitization reaction for non-thermal cardiac ablation in arrhythmia therapy. Acute and chronic phase experiments were conducted in exposed porcine hearts to demonstrate the photosensitization reaction-induced myocardial electrical conduction block in vivo.
STUDY DESIGN/MATERIALS AND METHODS: The porcine left atrial appendage was exposed under an open-chest procedure. Then, a water-soluble chlorin photosensitizer, NPe6, was injected into the pigs intravenously at 5 or 10 mg/kg. About 15 or 30 minutes after the injection, a 663-nm continuous-wave diode laser was irradiated on the surface of the atrial appendage through a silica optical fiber. The laser energy was delivered to the tissue point by point at an energy density of 50-208 J/cm(2).
Acute and chronic tissue damages as a result of the photosensitization reaction were determined by electrophysiology and histology, respectively. The change in the myocardial conduction time between two electrodes was measured immediately after the completion of the 35-mm irradiation line between the electrodes. The conduction delay of 35.5 milliseconds might be due to the change in the conduction pathway induced by transmural acute conduction block with the photosensitization reaction. The tissue temperature increase in the irradiated area was approximately 12.8°C. Azan-staining revealed about 1-mm transmural fibrosis of the atrial appendage at 2 weeks after the irradiation (50 J/cm(2)).
The results suggest that the photosensitization reaction might induce acute and chronic myocardial electrical conduction block. Cardiac ablation with the photosensitization reaction might be a non-temperature-mediated methodology for arrhythmia therapy.
本研究提出将光致敏反应用于心律失常治疗中的非热心脏消融。在暴露的猪心脏上进行了急性期和慢性期实验，以证明光致敏反应在体内诱导的心肌电传导阻滞。
研究设计/材料与方法：在开胸手术下暴露猪的左心耳。然后，以5或10mg/kg的剂量给猪静脉注射水溶性二氢卟吩光致敏剂NPe6。注射后约15或30分钟，通过石英光纤将663nm连续波二极管激光照射于心耳表面。激光能量以50-208J/cm²的能量密度逐点传递至组织。
分别通过电生理学和组织学确定光致敏反应导致的急性和慢性组织损伤。在电极间35mm照射线完成后，立即测量两个电极之间心肌传导时间的变化。35.5毫秒的传导延迟可能是由于光致敏反应引起的透壁急性传导阻滞导致传导途径改变所致。照射区域的组织温度升高约12.8°C。偶氮染色显示照射后2周（50J/cm²）心耳有大约1mm的透壁纤维化。
结果表明光致敏反应可能诱导急性和慢性心肌电传导阻滞。光致敏反应心脏消融可能是一种用于心律失常治疗的非温度介导方法。
