Hypertensive stress increases dispersion of repolarization.

Research paper by Bart Hooft BH Van Huysduynen, Cees A CA Swenne, Henk J Ritsema HJ Van Eck, Jan A JA Kors, Anna L AL Schoneveld, Hedde H Van De Vooren, Piet P Schiereck, Martin J MJ Schalij, Ernst E EE Van Der Wall

Indexed on: 23 Dec '04Published on: 23 Dec '04Published in: Pacing and Clinical Electrophysiology


Several electrocardiographic indices for repolarization heterogeneity have been proposed previously. The behavior of these indices under two different stressors at the same heart rate (i.e., normotensive gravitational stress, and hypertensive isometric stress) was studied. ECG and blood pressure were recorded in 56 healthy men during rest (sitting with horizontal legs), hypertensive stress (performing handgrip), and normotensive stress (sitting with lowered legs). During both stressors, heart rates differed <10% in 41 subjects, who constituted the final study group. Heart rate increased from 63 +/- 9 beats/min at rest to 71 +/- 11 beats/min during normotensive, and to 71 +/- 10 beats/min during hypertensive stress (P < 0.001). Systolic blood pressure was 122 +/- 15 mmHg at rest and 121 +/- 15 mmHg during normotensive stress, and increased to 151 +/- 17 mmHg during hypertensive stress (P < 0.001). The QT interval was larger during hypertensive (405 +/- 27) than during normotensive stress (389 +/- 26, P < 0.001). QT dispersion did not differ significantly between the two stressors. The mean interval between the apex and the end of the T wave (Tapex-Tend) of the mid-precordial leads was larger during hypertensive (121 +/- 17 ms) than during normotensive stress (116 +/- 15 ms, P < 0.001). The singular value decomposition T wave index was larger during hypertensive (0.144 +/- 0.071) than during normotensive stress (0.089 +/- 0.053, P < 0.001). Most indices of repolarization heterogeneity were larger during hypertensive stress than during normotensive stress. Hypertensive stressors are associated with arrhythmogeneity in vulnerable hearts. This may in part be explained by the induction of repolarization heterogeneity by hypertensive stress.