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Clinical Investigations: SLEEP AND BREATHING |

Corrected QT Dispersion and Cardiac Sympathetic Function in Patients With Obstructive Sleep Apnea-Hypopnea Syndrome*

Takaya Nakamura, MD, PhD; Kazuo Chin, MD, PhD; Ryohei Hosokawa, MD, PhD; Kenichi Takahashi, MD; Kensuke Sumi, MD; Motoharu Ohi, MD, PhD; Michiaki Mishima, MD, PhD
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*From the Departments of Respiratory Medicine (Drs. Nakamura, Takahashi, Sumi, and Mishima) and Cardiovascular Medicine (Dr. Hosokawa), Graduate School of Medicine, and the Department of Physical Therapeutics (Dr. Chin), Kyoto University Hospital, Kyoto University, Kyoto, Japan; and Osaka Kaisei Hospital (Dr. Ohi), Osaka, Japan.

Correspondence to: Kazuo Chin, MD, PhD, Department of Physical Therapeutics, Kyoto University Hospital, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan; e-mail: chink@kuhp.kyoto-u.ac.jp



Chest. 2004;125(6):2107-2114. doi:10.1378/chest.125.6.2107
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Study objectives: Hypoxemia increases corrected QT dispersion (QTcD), which is the difference between the maximum and minimum QT intervals and is a strong risk factor for cardiovascular mortality. The aim of this study was to investigate the QTcD in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), and the relationship between the QTcD and 123I-metaiodobenzylguanidine (MIBG) cardiac imaging, which reflects cardiac sympathetic activity.

Setting: A university hospital.

Patients: Forty-eight OSAHS patients without cardiac diseases (mean [± SD] age, 45.9 ± 10.8 years; apnea-hypopnea index [AHI] 51.9 ± 18.5 events per hour) who underwent polysomnography before treatment and on the first night of nasal continuous positive airway pressure (nCPAP) treatment.

Methods: Before and after nCPAP treatment was started, we measured the QTcD with computer software, before, during, and after sleep, as well as the washout rate of the MIBG administered for cardiac imaging. As a control, QTcD was also measured in the morning from 26 healthy subjects.

Results: Before treatment, the mean QTcD during sleep (65.0 ± 14.6 ms) was greater than that before sleep (57.0 ± 13.5 ms; p < 0.0001). Meanwhile, after 1 night of nCPAP therapy, the QTcD during sleep (50.6 ± 11.4 ms) decreased from that before treatment (p < 0.0001) and was smaller than the QTcD before sleep (56.2 ± 13.3 ms; p = 0.003). Before treatment, the QTcD during sleep correlated with the AHI (r = 0.38; p = 0.009) and the percentage of time that Sao2 was < 90% (Sao2 < 90% time) [r = 0.34; p = 0.018]. The QTcD did not correlate with the body mass index or the washout rate of MIBG. However, the washout rate of MIBG correlated with the AHI and the Sao2 < 90% time.

Conclusions: Nocturnal QTcD is increased in OSAHS patients but is decreased by nCPAP therapy independently of cardiac sympathetic function.

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