Rheumatoid arthritis (RA) is associated with an increased cardiovascular (CV) mortality risk; however, evidence to date suggests that the presence of traditional CV risk factors, prevalent in patients with RA, only partially accounts for the increased cardiac mortality risk1. In an effort to reduce the CV morbidity and mortality associated with RA, numerous novel risk factors have been sought and implicated, including myocardial repolarization abnormalities2, autonomic dysfunction3, and inflammation4. Given that RA is associated with a doubled risk of sudden cardiac death1, an arrhythmic mechanism would seem plausible. The QT interval marks the time from onset of ventricular depolarization to the completion of repolarization and can be measured using a 12-lead electrocardiogram (ECG) from the beginning of the Q wave to the end of the T wave. Prolongation of ventricular repolarization duration increases the risk of torsade de pointes, which can lead to ventricular fibrillation and sudden death. Prolongation of heart rate-corrected QT interval (QTc) independently predicts sudden death in the general population5 and …
Address correspondence to A.M. Adlan. E-mail: adlan.ahmed{at}gmail.com