Effects of low-dose radiation produced during radiofrequency ablation guided by 3D mapping on mitochondrial apoptosis in diabetic cardiomyocytes.

Abstract

Background: Three-dimensional (3D) mapping has been widely used in the clinical radiofrequency ablation of arrhythmia; however, the dose of intraoperative radiation exposure has not been determined. Moreover, whether a single instance of intraoperative radiation exposure has an effect on myocardial tissue or exacerbates diabetic heart injury remains uncertain.

Methods and results: In this study, we evaluated the dose of intraoperative radiation generated during radiofrequency ablation via 3D mapping. ELISA, Western blot, flow cytometry, and oxygen consumption rate detection were used to identify the effects of the intraoperative radiation dose on cardiomyocyte apoptosis via the mitochondrial pathway and its specific mechanism. These results indicated that the exposure radiation used in radiofrequency ablation guided by 3D mapping for all types of arrhythmia was low-dose radiation (LDR; the doses were all less than 200 mGy). Although LDR (50, 100 and 200 mGy) had no significant effect on the mitochondrial apoptosis of normal cardiomyocytes, the 200 mGy radiation dose reduced the mitochondrial apoptosis of cardiomyocytes subjected to high glucose and high lipid (HG/HL) treatment. Mechanistically, an LDR of 200 mGy improved the expression of IL-10, reversed the accumulation of IL-6, ROS, disruption of Δψm, and the impairment of mitochondrial function caused by HG/HL. Additionally, 200 mGy radiation promoted the expression of Bcl-xl while reducing the expression of Bax in cardiomyocytes treated with HG/HL.

Conclusion: In summary, this study demonstrated that the exposure radiation dose used in radiofrequency ablation guided by 3D mapping was low-dose radiation (LDR), which had no effect on the mitochondrial apoptosis pathway in normal cardiomyocytes and even had a protective effect on cardiomyocytes treated with HG/HL via increased IL-10 levels and the suppression of IL-6, ROS, and mitochondrial damage induced by HG/HL.