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(Circulation. 2002;106:176.)
© 2002 American Heart Association, Inc.

Clinician Update

Ventricular Tachycardia Associated With Myocardial Infarct Scar

A Spectrum of Therapies for a Single Patient

Kyoko Soejima, MD; William G. Stevenson, MD

From the Cardiovascular Division, Department of Internal Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Mass.

Correspondence to William G. Stevenson, MD, Cardiovascular Division, Brigham and Women’s Hospital 75 Francis St, Boston, MA 02115. E-mail wstevenson@partners.org

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

	Introduction

 
Case: A 73-year-old woman is referred for management of recurrent ventricular tachycardia (VT). She had suffered an inferior wall myocardial infarction in 1970. Fifteen years later, she presented with a wide QRS tachycardia, palpitations, and dizziness. Therapy with amiodarone was initiated but discontinued in 1997 because of toxicity, and she received an implantable cardioverter-defibrillator (ICD). She did well until July 2000, when she had several shocks from the ICD, all of which were preceded by syncope. Interrogation of the ICD confirmed 23 episodes of VT, 20 asymptomatic runs terminated by antitachycardia pacing (ATP), and 3 episodes requiring cardioversion from the ICD. Her left ventricular ejection fraction was 25%. Sotalol failed to prevent VT recurrences and mexiletine produced nausea and tremor.

She was referred for catheter ablation. An echocardiogram revealed akinesis of the inferior wall and no left ventricular thrombus. In the electrophysiology laboratory, programmed stimulation induced 5 different morphologies of VT (Figure 1) with rates ranging from 180 to 220 bpm. Because the induced VTs were unstable, producing hypotension and often changing from one VT to another, catheter mapping and ablation were performed largely during sinus rhythm, guided by electrogram characteristics and pacing during sinus rhythm (pace-mapping) that marked the location of the infarct scar and likely reentry paths in the subendocardium. After placement of lines of radiofrequency (RF) lesions through these abnormal regions, only ventricular flutter (280 bpm) was inducible; the slower VTs were no longer inducible. There have been no VT recurrences in the 18 months . . . [Full Text of this Article]

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