AIMS: Radiofrequency catheter ablation is a successful treatment for cardiac arrhythmias, but may lead to major complications such as permanent coronary damage. Irreversible electroporation (IRE) is a new non-thermal ablation modality, but its effect on coronary arteries is still unknown. METHODS AND RESULTS: In a porcine model, epicardial IRE lesions were created at the base of the left ventricle in four hearts (group A) and directly on the left anterior descending artery (LAD) in five hearts (group B). After 3 weeks, coronary arteries inside IRE lesions and in apparently undamaged myocardium next to the lesions were (immuno-)histologically studied. Two untreated hearts served as controls. Coronary damage was defined as intimal hyperplasia. Left anterior descending artery angiograms were obtained before ablation, directly after ablation, and before termination in group B. In group A, 103 arterial branches were studied. Of these, 5 of 56 arterial branches inside lesions and 1 of 47 outside lesions showed intimal hyperplasia, but all had <50% area stenosis. Targeted LADs (group B) did not reveal intimal hyperplasia and angiograms showed no signs of stenosis. Expression of connective tissue growth factor was observed in the scar tissue, but not in the fibrotic tissue directly around the arteries, confirming that the arteries are indeed spared from tissue damage and remodelling. CONCLUSION: Coronary arteries remain free of clinically relevant damage 3 weeks after epicardial IRE ablation, even amid very large myocardial lesions. This suggests that IRE ablation can be applied safely near or even on coronary arteries. With IRE ablation, arterial blood flow does not appear to affect lesion formation.
AIMS: Radiofrequency catheter ablation is a successful treatment for cardiac arrhythmias, but may lead to major complications such as permanent coronary damage. Irreversible electroporation (IRE) is a new non-thermal ablation modality, but its effect on coronary arteries is still unknown. METHODS AND RESULTS: In a porcine model, epicardial IRE lesions were created at the base of the left ventricle in four hearts (group A) and directly on the left anterior descending artery (LAD) in five hearts (group B). After 3 weeks, coronary arteries inside IRE lesions and in apparently undamaged myocardium next to the lesions were (immuno-)histologically studied. Two untreated hearts served as controls. Coronary damage was defined as intimal hyperplasia. Left anterior descending artery angiograms were obtained before ablation, directly after ablation, and before termination in group B. In group A, 103 arterial branches were studied. Of these, 5 of 56 arterial branches inside lesions and 1 of 47 outside lesions showed intimal hyperplasia, but all had <50% area stenosis. Targeted LADs (group B) did not reveal intimal hyperplasia and angiograms showed no signs of stenosis. Expression of connective tissue growth factor was observed in the scar tissue, but not in the fibrotic tissue directly around the arteries, confirming that the arteries are indeed spared from tissue damage and remodelling. CONCLUSION: Coronary arteries remain free of clinically relevant damage 3 weeks after epicardial IRE ablation, even amid very large myocardial lesions. This suggests that IRE ablation can be applied safely near or even on coronary arteries. With IRE ablation, arterial blood flow does not appear to affect lesion formation.
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