Toivonen L, Helenius K, Viitasalo M
Division of Cardiology, Helsinki University Central Hospital, Finland.
J Am Coll Cardiol. 1997 Sep;30(3):774-9. doi: 10.1016/s0735-1097(97)00222-2.
The present study aimed to characterize the electrocardiographic features of cardiac repolarization during an arousal reaction in healthy subjects.
Electrocardiographic ST segments and T waves may indicate the activity of cardiac autonomic nervous control. Abnormal dynamics of repolarization are considered to reveal susceptibility to cardiac arrhythmias. Responses in normal subjects may help to understand the effects on patients' arrhythmias.
Ambulatory electrocardiography was performed in 30 healthy physicians during emergency calls while they were on duty in the hospital. Samples were taken before and during the 1st 30 s after the calls. Polarity of the T wave and ST segment depression were determined. The QT interval and the cardiac cycle length (CL) were measured, and their relation (QT/CL slope) was calculated. For comparison, the QT interval was also measured in stable conditions at specified heart rates of 60 to 110 beats/min.
During arousal, the T wave was inverted in 19 subjects (63%) and the ST segment depressed > or = 0.1 mV in 10 (33%). The proportional duration of the terminal T wave also varied. The time course of these alterations followed the change in heart rate. During the strongest arousal reaction, the heart rate increased from 55 +/- 7 to 112 +/- 18 beats/min (mean +/-SD) and reached maximum at 17s on average. The QT interval shortened only slightly and was on average 59 to 67 ms longer (p < 0.001) than that at similar heart rates during stable conditions. The QT/CL slope was almost horizontal, 0.085 +/- 0.061, during arousal and much steeper, 0.168 +/- 0.055 (p < 0.001), during stable conditions.
Derangements in the T wave and ST segment as signs of sympathetic overactivity are common during arousal and are associated with marked inertia in QT interval adaptation. These modifications of ventricular repolarization may mediate the generation of stress-provoked arrhythmias in electrically unstable hearts.
