| Autor: |
Vondrova, Dana, Basrawala, Hussain, Reddy, Pavan, Valladares, Edwin, Patel, Krishan, Allam, Shamili, Konecny, Jan, Khoo, Michael C, Doshi, Rahul N, Grbach, Vincent X, Hammond, Terese, Borok, Zea, Castriotta, Richard J, Konecny, Tomas |
| Zdroj: |
Circulation (Ovid); November 2019, Vol. 140 Issue: Supplement 1 pA15043-A15043, 1p |
| Abstrakt: |
Introduction:Obstructive sleep apnea/hypopnea syndrome (OSA) has been associated with nocturnal sudden cardiac death, and prolongation in QTc has been suggested as a potential mechanistic link. Traditional scoring of OSA does not reflect how OSA episodes influence QTc.Hypothesis:To describe which characteristics of OSA episodes lead to the greatest QTc prolongation.Methods:Sleeping patients with mild-moderate OSA without cardiac medications were studied during overnight polysomnography by signal-averaged 8-lead ECG recording. Acute changes in ventricular repolarization were measured during isolated OSA episodes, and the characteristics of OSA episodes (type, duration, oxygen desaturation) that induced the greatest ECG changes were identified.Results:We studied 144 isolated OSA episodes in 11 patients (5 women, age 59.1 ? 4.5 years, apnea hypopnea index 13.5 ? 1.0). QTc increased from 442?62 (pre-episode baseline) to 460?50 (during OSA release, p<0.0001). Maximum increase in QTc was significantly greater during apneas vs hypopneas (48?49 vs 24?36; p=0.001), and this difference remained significant in a multi-variate analysis (p=0.002) after accounting for OSA episode length, acute oxygen desaturation, pre-episode oxygen level, and sleep stage.Conclusion:Characterization of OSA episodes with greater versus lesser influence on QTc opens the possibility of a weighted, more individualized score of OSA severity which would be more closely aligned with proposed pathophysiological links between OSA and sudden death. |
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