The effect of mental stress on the non-dipolar components of the T wave

Mental or emotional stress-induced ventricular arrhythmias and sudden cardiac death are thought to be mediated by the autonomic nervous system and ischemia. In the absence of ischemia, increased inhomogeneity of repolarization is thought to be important. We tested the hypotheses that in the absence of ischemia, mental stress may modulate repolarization by changing autonomic balance; and mental relaxation induced by hypnosis may offset the potentially adverse effects of stress on the cardiac electrophysiology. METHODS: Twelve healthy volunteers (6 male, age 18-35, mean 25 years) experienced a series of different emotions intended to induce a wide range of autonomic response (42 test epochs) on two separate occasions, with and without hypnosis, with continuous electrocardiogram recording. Low- (LF) and HF (high-frequency) heart rate variability was measured and ventricular repolarization was assessed using the relative T-wave residua (proportion of nondipolar components of the T wave) calculated for the T-onset - T peak (TWR-peak T), T peak -T end (TWR-end T), and the whole T wave (TWR). RESULTS: Emotionally induced changes in LF and LF/HF ratio correlated with changes in TWR, e.g., (R = 0.51, p < .001; R = 0.59, p < .0001; and R = 0.59, p < .0003, for LF/HF versus TWR, TWR-Peak T, and TWR-end T, respectively. Mental relaxation induced by hypnosis increased LF power (1,205 ms2) versus 624 ms2, p < .003 for hypnotized versus nonhypnotized state), HF power (1,619 ms2 versus 572 ms2), p < .0004), and reduced LF/HF ratio (1.0 versus 1.5, p = .052) and was associated with a marked reduction in the changes in repolarization in response to emotion, e.g., 10.7 x 10(-6) versus 5.0 x10(-6), p < .03 for TWR. CONCLUSIONS: a) Mental stress in the absence of ischemia altered repolarization inhomogeneity via change in the autonomic balance. b) Mental relaxation induced by hypnosis greatly reduced the effect of mental stress on repolarization. c) These findings may have implications for arrhythmogenesis.

Department of Cardiology, The Hatter Institute and Centre for Cardiology, University College London Hospitals, Grafton Way, London WC1E 6DB, UK. peter.taggart@uclh.org