The QT and Tp-e intervals in left and right chest leads: comparison between patients with systemic and pulmonary hypertension

Thinn Hlaing, Donglin Guo, Xiaojing Zhao, Tara DiMino, Lee Greenspon, Peter R Kowey, Gan-Xin Yan
Journal of Electrocardiology 2005, 38 (4 Suppl): 154-8

BACKGROUND: Action potential duration in the right ventricle is normally shorter than that in the left. We tested the hypothesis that there may be intrinsic differences in the QT and Tp-e (an interval from the peak to the end of the T wave) intervals between the left and right chest leads that can be exaggerated by systemic hypertension but attenuated by pulmonary hypertension in humans.

METHODS: Electrocardiograms in the left (V4L-V6L) and right (V4R-V6R) chest leads were obtained in 40 healthy individuals, 29 patients with systemic hypertension and left ventricular hypertrophy, and 15 patients with pulmonary hypertension.

RESULTS: In healthy individuals, the corrected QT (QTc) and corrected Tp-e [T(p-e)c] intervals were 421+/-5 and 86+/-3 milliseconds in V4L through V6L, respectively, significantly longer than those recorded from V4R through V6R (383+/-5 and 62+/-4 milliseconds, respectively; P<.01). Left ventricular hypertrophy prolonged the QTc interval in V4L through V6L (456+/-5 milliseconds), exaggerating the difference in the QTc interval between the left and right chest leads (61+/-4 vs 40+/-3 milliseconds in healthy control subjects; P<.01). Left ventricular hypertrophy also resulted in a small but significant increase in the T(p-e)c interval in V4L through V6L (97+/-3 vs 86+/-3 milliseconds in control subjects; P<.05) but exerted no significant effect on the T(p-e)c interval in the right. In contrast, pulmonary hypertension lengthened the QTc interval in the right chest leads, reducing the difference in the QTc interval between the left and right chest leads (3+/-8 vs 40+/-3 milliseconds in control subjects; P<.01).

CONCLUSIONS: There are intrinsic differences in the QT and Tp-e intervals between V4L-V6L and V4R-V6R that are significantly amplified by systemic hypertension but markedly attenuated by pulmonary hypertension.

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