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The patient is a 58-year-old white male cardiologist who first came to attention in 2004 at the age of 53 years, with a history of paroxysmal atrial fibrillation (PAF) dating to 1982. The episodes, which were often precipitated by recumbency and alcohol, occurred 2 to 3 times per year and lasted only minutes. His ECG (Figure 1) while in normal sinus rhythm was normal.Figure 1. ECG taken when the patient was not using flecainide.His PAF was not rapid and did not cause hemodynamic or ischemic symptoms. During 2003 to 2004, the PAF increased in frequency to several times per week and lasted longer, for which he began flecainide 50 mg bid with success for 6 months. Thereafter, however, they recurred with a progressive increase in frequency to several times per day, despite increasing the flecainide to 100 mg bid and then 150 mg bid and thereafter while trying sotalol up to 160 mg bid instead. A stress-echo was normal aside from a left atrial diameter of 4.5 cm (an increase from 10 years earlier). There was no family history of any dysrhythmia, syncope, seizure disorder, or sudden death and no other personal medical history of any relevance aside from simvacor-controlled hyperlipidemia (including no personal or family history of syncope or sudden death). His physical examination was entirely normal. All routine laboratory studies were normal, as was his 12-lead ECG and chest radiography. While taking flecainide, his PAF recurred as typical atrial flutter. The QRST pattern on his 12-lead ECG did not change during the flecainide or sotalol administration. Catheter ablation was recommended.While considering ablation and proceeding to schedule it, the patient took a trip out of the country, during which, while on a cruise, a protracted episode recurred. At that time he was again taking flecainide 50 mg bid …

Does a Brugada Pattern ECG Precipitated by Excessive-Dose Flecainide Provide a Diagnosis of a Brugada Syndrome Patient and/or Contraindicate Its Use?