T he basis for arrhythmogenesis in patients with nonischemic cardiomyopathy and ventricular tachycardia (VT) needs further elucidation. Cardiac arrest and/or nonsustained VT are common arrhythmia presentations in the setting of nonischemic cardiomyopathy, with sustained monomorphic VT being relatively uncommon. 1,2 Importantly, bundlebranch reentrant VT is identified as the VT mechanism in a significant percentage of patients with monomorphic VT in the setting of nonischemic cardiomyopathy. 3,4 However, even in patients with nonischemic left ventricular (LV) or right ventricular (RV) cardiomyopathy, the majority of VT appears to originate from the myocardium and is not due to bundlebranch reentry. 4 -11 Detailed substrate, activation, and entrainment mapping has begun to provide some valuable clues related to the mechanism and pathophysiology of scar-based VT in the setting of nonischemic cardiomyopathy resulting from a variety of causes. 4 -11 Although not focusing on VT after valve surgery, these data have been helpful in identifying likely regions of origin for VT and facilitating ablative therapy in other nonischemic settings.
Article p 2005
Lessons Learned From Ablation of VT After Valve SurgeryWhen dealing with uncommon disease processes, one looks to centers with sizable clinical experience to review their results and provide important insight. In this issue of Circulation, the report by Eckart and colleagues 12 answers that charge. Six years of clinical experience with VT ablation resulted in the identification of 20 patients who developed VT after prior cardiac valve surgery and underwent catheter ablative therapy. Importantly, most of the patients demonstrated mildly to moderately depressed LV function with a median LV ejection fraction of 45%. Characterization of the substrate, mechanism, and outcome of ablative therapy provides important insight in terms of pathogenesis. Such detailed information should be compared with findings at the time of VT ablation in a variety of other nonischemic cardiomyopathies to attempt to identify common and potentially important pathophysiological links. 4 -11 Indeed, the study by Eckart and colleagues is modestly handicapped by its retrospective study design. Details of the preoperative status of LV function and the surgical intervention were unavailable, making it difficult to determine whether some abnormalities preceded or were created by surgical incisions, venting, or the like. The timing of the "late" onset of VT as it relates to the surgery also is probably much shorter than the described 12 years for the second mode of presentation timing. Of note, 12 of the 16 patients who underwent ablation late after surgery because of VT in the present report already had an implantable cardioverterdefibrillator in place for a median of 4.5 years, presumably for a documented arrhythmia episode in most. 12 Nevertheless, a distinction between early, Ͻ1 month, and late, Ͼ1 to 20 years, is valid and somewhat similar to the bimodal distribution of VT after myocardial infarct...