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(Circulation. 2007;116:1998-2001.)
© 2007 American Heart Association, Inc.

Editorial

Perivalvular Fibrosis and Monomorphic Ventricular Tachycardia

Toward a Unifying Hypothesis in Nonischemic Cardiomyopathy

Francis E. Marchlinski, MD

From the Cardiovascular Division, Department of Medicine, Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia.

Correspondence to Francis Marchlinski, MD, 9 Founders Pavilion, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104. E-mail francis.marchlinski@uphs.upenn.edu

Key Words: Editorials • ablation, catheter • cardiomyopathies • tachycardia • cardiac valves • ventricles

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
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, bundle-branch 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 bundle-branch 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 Surgery

 
When 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 colleagues¹² 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, . . . [Full Text of this Article]

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