Author + information
- Received July 21, 2015
- Revision received September 18, 2015
- Accepted October 6, 2015
- Published online January 5, 2016.
- Ofer Havakuk, MD and
- Sami Viskin, MD∗ ()
- Tel Aviv Sourasky Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
- ↵∗Reprint requests and correspondence:
Dr. Sami Viskin, Tel Aviv Medical Center, Department of Cardiology, Weizman 16, Tel Aviv 64239, Israel.
The Brugada syndrome (BrS) and long-QT syndrome (LQTS) present as congenital or acquired disorders with diagnostic electrocardiograms (ST-segment elevation and prolonged QT interval, respectively) and increased risk for malignant arrhythmias. Our understanding of the 2 disease forms (congenital vs. acquired) differs. A female patient on quinidine for atrial fibrillation who develops ventricular fibrillation is diagnosed with “acquired LQTS” and is discharged with no therapy other than instructions to avoid QT-prolonging medications. In contrast, an asymptomatic male patient who develops a Brugada electrocardiogram on flecainide is diagnosed with “asymptomatic BrS” and could be referred for an electrophysiological evaluation that could result in defibrillator implantation. The typical patient undergoing defibrillator implantation for BrS is asymptomatic but has a Brugada electrocardiogram provoked by a drug. The authors describe how the histories of LQTS and BrS went through the same stages, but in different sequences, leading to different conclusions.
Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 21, 2015.
- Revision received September 18, 2015.
- Accepted October 6, 2015.
- American College of Cardiology Foundation