ABSTRACT
This patient was a 50-year-old man. Oral pilsicainide unmasked a Brugada-type ECG abnormality and self-terminating polymorphic VT was repetitively induced. The polymorphic VT always developed following a specific ventricular premature complex showing a left bundle branch block pattern suggesting a limited origin in the right ventricle.
Subject(s)
Bundle-Branch Block/complications , Death, Sudden, Cardiac , Ventricular Fibrillation/etiology , Ventricular Premature Complexes/complications , Bundle-Branch Block/physiopathology , Electrocardiography , Humans , Male , Middle Aged , Syndrome , Ventricular Fibrillation/physiopathology , Ventricular Premature Complexes/physiopathologyABSTRACT
A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.
