This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sivasubramonian, S. Articles by Rosenthal, E. Search for Related Content PubMed PubMed Citation Articles by Sivasubramonian, S. Articles by Rosenthal, E. Related Collections Arrhythmias, clinical electrophysiology, drugs

(Circulation. 2004;109:938-939.)
© 2004 American Heart Association, Inc.

Images in Cardiovascular Medicine

Fatal Bidirectional and Polymorphic Ventricular Tachycardia With Terminal Depolarization Abnormality in a Child

Sivasankaran Sivasubramonian, MD, DM; Eric Rosenthal, MD, FRCP

From Paediatric Cardiology, Guy’s Hospital, London, United Kingdom.

Correspondence to Dr Eric Rosenthal, MD, FRCP, Consultant Paediatric Cardiologist, Department of Congenital Heart Disease, 11th Floor, Guy’s Hospital, St Thomas St, London SE1 9RT, UK. E-mail eric.rosenthal@kcl.ac.uk

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

A 14-year-old boy was admitted after resuscitation from cardiac arrest that occurred while chasing a ball at school. An initial ECG showed incessant bidirectional and polymorphic ventricular tachycardia (Figure 1). ECG taken during the short periods of sinus rhythm attained with intravenous lignocaine infusions showed subtle depolarization abnormalities at the J point in the inferolateral leads that were accentuated by amiodarone (Figure 2).

View larger version (82K): [in this window] [in a new window]   Figure 1. Twelve lead ECG and rhythm strip showing bidirectional and polymorphic ventricular tachycardia.

View larger version (124K): [in this window] [in a new window]   Figure 2. Twelve lead electrocardiograms in sinus rhythm after lignocaine and amiodarone showing subtle terminal depolarization abnormalities in the inferolateral leads highlighted by the small circles. After amiodarone infusion, the J point abnormalities were accentuated in leads III, aVL, V5, and V6, mimicking fresh axis deviation

The boy was normothermic at admission and required multiple attempts at cardioversion, along with intravenous amiodarone and magnesium and dual-chamber pacing to control the electrical storm. Because of the evidence of severe anoxic damage sustained during the initial cardiac arrest, mechanical cardiopulmonary support was not initiated. A limited autopsy confirmed normal coronary artery anatomy and caliber, a structurally normal heart, and evidence for myocardial necrosis consistent with prolonged hypoxia and catecholamine use. Polymer-ase chain reaction studies ruled out myocarditis of viral origin.

The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of . . . [Full Text of this Article]