Mitral Valve Prolapse and Ventricular Arrhythmias: Observations in a Patient with a 20‐Year History

• Published in: Journal of cardiovascular electrophysiology Vol. 8; no. 3; pp. 307 - 316
• Main Authors: WILDE, ARTHUR A.M., DÜREN, DONALD R., HAUER, RICHARD N.W., BAKKER, JACQUES M.T., BAKKER, PATRICIA F.A., BECKER, ANTON E., JANSE, MICHIEL J.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.03.1997
• Subjects: Adult; delayed afterdepolarization; Electrocardiography; electrophysiology; Exercise Test; Flunarizine; Heart Valve Prosthesis; Humans; Male; Mitral Valve - surgery; Mitral Valve Prolapse - complications; Mitral Valve Prolapse - physiopathology; Mitral Valve Prolapse - surgery; Tachycardia, Ventricular - complications; Tachycardia, Ventricular - physiopathology; Tachycardia, Ventricular - prevention & control; triggered activity; ventricular fibrillation; Ventricular Fibrillation - complications; Ventricular Fibrillation - physiopathology; Ventricular Fibrillation - prevention & control; Ventricular Premature Complexes - complications; Ventricular Premature Complexes - physiopathology; ventricular tachycardia
• ISSN: 1045-3873; 1540-8167
• DOI: 10.1111/j.1540-8167.1997.tb00793.x

Ventricular Arrhythmias in MVP. Introduction: Ventricular arrhythmias are a common feature in patients with mitral valve prolapse. In an attempt to determine the origin and underlying electrophysiologic mechanism, we describe a patient with ventricular fibrillation, exercise‐induced ventricular tachycardia (VT), and, at the time of diagnosis, prolapse of the posterior mitral valve leaflet without mitral regurgitation. Methods and Results: Treatment with β‐blockade and diphenyihydantoin prevented the occurrence of malignant ventricular arrhythmias for more than 17 years. Discontinuation of the therapy resulted in an immediate reappearance of the VT, which, despite the marked enlargement of the left ventricle (secondary to development of severe mitral valve regurgitation), had a strikingly similar morphology. For hemodynamic reasons, the patient was finally selected for valve replacement. Detailed pre‐, peri‐, and postoperative studies were performed, including administration of flunarizine, body surface mapping, construction of perioperative epicardial and endocardial maps, and studies of the excised muscles in vitro. Conclusions: Delayed afterdepolarization‐induced triggered activity is the mechanism of VT in this mitral valve prolapse patient. The trigger is provided by Isolated ventricular premature complexes elicited by a different electrophysiologic mechanism, possibly reentry, which is related to stretch and presumably to fibrosis of the papillary muscles.