Perivalvular fibrosis and monomorphic ventricular tachycardia: toward a unifying hypothesis in nonischemic cardiomyopathy.

The 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.