ST segment elevation in the right precordial leads induced with Class IC antiarrhythmic drugs: Insight into the mechanism of Brugada syndrome

ST Segment Elevation by Class IC Drugs. We evaluated two patients without p revious episodes of syncope who showed characteristic ECG changes similar t o Brugada syndrome following administration of Class IC drugs, flecainide a nd pilsicainide, but not following Class IA drugs. Patient 1 had frequent e pisodes of paroxysmal atrial fibrillation resistant to Class IA drugs. Afte r treatment with flecainide, the ECG showed a marked ST elevation in leads V-2 and V-3, and the coved-type configuration of ST segment in lead V-2. A signal-averaged ECG showed late potentials that became more prominent after flecainide, Pilsicainide, a Class IC drug, induced the same ST segment ele vation as flecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation, Pilsicainide changed atrial fi brillation to atrial flutter with 2:1 ventricular response, and the ECG sho wed right bundle branch block and a marked coved-type ST elevation in leads V-1 and V-2. After termination of atrial flutter, ST segment elevation in leads V-1 and V-2 continued. In this patient, procainamide and quinidine di d not induce this type of ECG change. In conclusion, strong Na channel bloc king drugs induce ST segment elevation similar to Brugada syndrome even in patients without any history of syncope or ventricular fibrillation.