Exercise-Induced Repolarization Changes in Patients With Stable Coronary Artery Disease

Exercise is a classic trigger of ventricular arrhythmias in the setting of coronary artery disease (CAD). The aim of this study was to examine the changes of novel indexes of repolarization in patients with stable CAD who underwent exercise stress testing. Sixty-seven consecutive patients (mean age 62 +/- 9 years, 60 men) who underwent treadmill exercise stress testing according to the Bruce protocol and completed the test without evidence of ischemia were enrolled. Baseline clinical and demographic characteristics were recorded, and indexes of repolarization such as corrected QT (QTc) interval, T peak-to-end (Tpe) interval, and Tpe/QT ratio were assessed at baseline and at peak exercise. A similar group of control subjects without CAD (n = 68, mean age 60 +/- 11 years, 52 men) were also studied. All participants successfully completed the test. In the patient group, the QTc interval significantly increased from baseline to peak exercise (median 385 ms [25th percentile 357 ms, 75th percentile 407 ms] vs 418 ms [381 ms, 447 ms], p < 0.001). The Tpe interval and the Tpe/QT ratio were also significantly increased at peak exercise (42 ms [36 ms, 60 ms] vs 78 ms [60 ms, 84 ms], p < 0.001; and 0.17 [0.14, 0.22] vs 0.21 [0.16, 0.25], p = 0.015). In the control group, the QTc interval did not change significantly, the Tpe interval decreased at peak exercise (62 ms [41 ms, 80 ms] vs 48 ms [40 ms, 78 ms], p = 0.05), and the Tpe/QT ratio did not show a significant change (0.18 [0.12, 0.22] vs 0.16 [1.14, 0.21], p = 0.39). In patients with stable CAD and normal treadmill exercise stress test results, the QTc interval, the Tpe interval, and the Tpe/QT ratio increased during exercise. In conclusion, it is reasonable to assume that despite the absence of inducible ischemia, the spatial dispersion of repolarization is increased during exercise, exposing these patients to increased arrhythmic risk. (c) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;107: 37-40)