Volume 27, Issue 12 pp. 1603-1609

Hypertensive Stress Increases Dispersion of Repolarization

BART HOOFT VAN HUYSDUYNEN

BART HOOFT VAN HUYSDUYNEN

Cardiology Department, Leiden University Medical Center, Leiden

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CEES A. SWENNE

CEES A. SWENNE

Cardiology Department, Leiden University Medical Center, Leiden

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HENK J. RITSEMA VAN ECK

HENK J. RITSEMA VAN ECK

Department of Medical Informatics, Erasmus University Medical Center, Rotterdam

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JAN A. KORS

JAN A. KORS

Department of Medical Informatics, Erasmus University Medical Center, Rotterdam

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ANNA L. SCHONEVELD

ANNA L. SCHONEVELD

Cardiology Department, Leiden University Medical Center, Leiden

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HEDDE VAN DE VOOREN

HEDDE VAN DE VOOREN

Cardiology Department, Leiden University Medical Center, Leiden

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PIET SCHIERECK

PIET SCHIERECK

Department of Medical and Sports Physiology, University Medical Center, Utrecht, the Netherlands

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MARTIN J. SCHALIJ

MARTIN J. SCHALIJ

Cardiology Department, Leiden University Medical Center, Leiden

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ERNST E. VAN DER WALL

ERNST E. VAN DER WALL

Cardiology Department, Leiden University Medical Center, Leiden

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First published: 10 December 2004
Citations: 5
Address for reprints: Cees A. Swenne, PhD, Cardiology Dept., Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, the Netherlands. Fax: +31-84-221-8904; e-mail: [email protected]

Supported in part by the Netherlands Heart Foundation (grant 2001.177). Subject expenses were reimbursed by the Leiden Foundation for ECG Analysis SEAL. Mortara Rangoni Europe, S. Giorgio di Piano, Italy, provided the signal recording equipment.

Abstract

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.

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