Abstract
In this issue of HeartRhythm, Hayase et al1 present a case report of a human ventricular fibrillation (VF) rotor that was localized to ablation sites for scar-mediated monomorphic ventricular tachycardia (VT). A growing body of evidence from animal models, computer models, and human myocardium in vitro supports an important role of rotors as drivers of fibrillation.2–6 However, identifying culprit rotors in vivo is in its infancy. Moving beyond surgical epicardial recording techniques, new software has recently been used to study rotors in atrial fibrillation from the endocardial surface using basket catheters.
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