Two Cases of Pilsicainide Intoxication showing the Brugada-type Electrocardiographic Findings and Incessant Wide QRS Tachycardia

Abstract

We have experienced two patients with the Brugada-type electrocardiographic abnormalities and incessant wide QRS tachycardia (presumed ventricular tachycardia) induced by intoxication of a class IC antiarrhythmic drug pilsicainide. They were elderly men with impaired renal function. Plasma concentration of pilsicainide was elevated to a toxic level in both patients. After cessation of pilsicainide, incessant wide QRS tachycardia spontaneously subsided and intraventricular conduction delay with coved type ST segment elevation in V1 and V2 disappeared. In the elderly or patients with renal dysfunction, we should be very careful regarding dose adjustment of pilsicainide or it may be better to avoid using this drug. Pilsicainide, classified as a class IC drug, has a strong sodium channel blocking effect which depresses conduction in various regions of the heart. 1) Pilsicainide can unmask or aggravate the Brugadatype electrocardiogram (ECG) in patients with latent Brugada syndrome. 2,3) We have experienced 2 patients with the Brugada-type ECG abnormalities and incessant wide QRS tachycardia, presumed ventricular tachycardia (VT), induced by intoxication of pilsicainide. Case PresentationCase 1: A 73-year-old man was referred to our hospital for loss of consciousness. He had suffered from hypertension and diabetes since he was 30-year-old, and he had blood dialysis regularly in a local clinic for chronic renal failure since he was 65. He had been taking flecainide (50 mg per day) for 3 years because of paroxysmal atrial fibrillation (AF). However, two months ago, another clinic gave him an additional prescription of pilsicainide 150 mg per day (50 mg t.i.d.) for recurrent AF. On May 10, 2005, he had an episode of polymorphic wide QRS tachycardia with loss of consciousness during hemodialysis. The 12-lead ECG showed a regular wide QRS rhythm of 80 beats/min without visible P waves and marked coved-type ST segment elevation in V1 and V2 (Figure 1, left). He was transferred to our hospital to treat his presumed Brugada syndrome. On admission, physical examination was unremarkable. Chest X-ray revealed cardiomegaly