INTRODUCTION: The use of catheter-based radiofrequency (RF) ablation for the treatment of ventricular tachyarrhythmias due to previous myocardial infarction has been steadily increasing. The histopathologic changes caused by this technique are not well described in humans. METHODS AND RESULTS: Three patients with hemodynamically tolerated ventricular tachycardias (VTs) due to previous myocardial infarction underwent endocardial mapping and catheter based RF ablation. All patients received between 5 and 11 RF lesions each of 60-second duration. One patient underwent myocardial resection of a left ventricular aneurysm 1 day following RF ablation, one expired 7 days after RF ablation, and one expired 9 months after RF ablation. None of the deaths occurred as a result of RF ablation. Pathologic specimens obtained early after RF ablation revealed areas of focal acute inflammation and fibrin deposition. Later specimens revealed several focal areas of fibrosis and granulation tissue. Specimens obtained late after RF ablation revealed a dense band of fibrosis, measuring 17 x 17 x 5 mm (1,250 mm3). CONCLUSION: Catheter-based RF ablation of ischemic VT in humans causes lesions that initially resemble coagulation necrosis. This is followed by the development of an inflammatory infiltrate and, finally, the development of fibrosis. Repeated application of RF ablation may result in much larger lesions than have been previously reported.
INTRODUCTION: The use of catheter-based radiofrequency (RF) ablation for the treatment of ventricular tachyarrhythmias due to previous myocardial infarction has been steadily increasing. The histopathologic changes caused by this technique are not well described in humans. METHODS AND RESULTS: Three patients with hemodynamically tolerated ventricular tachycardias (VTs) due to previous myocardial infarction underwent endocardial mapping and catheter based RF ablation. All patients received between 5 and 11 RF lesions each of 60-second duration. One patient underwent myocardial resection of a left ventricular aneurysm 1 day following RF ablation, one expired 7 days after RF ablation, and one expired 9 months after RF ablation. None of the deaths occurred as a result of RF ablation. Pathologic specimens obtained early after RF ablation revealed areas of focal acute inflammation and fibrin deposition. Later specimens revealed several focal areas of fibrosis and granulation tissue. Specimens obtained late after RF ablation revealed a dense band of fibrosis, measuring 17 x 17 x 5 mm (1,250 mm3). CONCLUSION: Catheter-based RF ablation of ischemic VT in humans causes lesions that initially resemble coagulation necrosis. This is followed by the development of an inflammatory infiltrate and, finally, the development of fibrosis. Repeated application of RF ablation may result in much larger lesions than have been previously reported.
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