PLoS ONE (Jan 2022)

Inter-sleep stage variations in corrected QT interval differ between obstructive sleep apnea patients with and without stroke history.

  • Serajeddin Ebrahimian,
  • Saara Sillanmäki,
  • Salla Hietakoste,
  • Brett Duce,
  • Antti Kulkas,
  • Juha Töyräs,
  • Timo Leppänen,
  • Jukka A Lipponen,
  • Samu Kainulainen

DOI
https://doi.org/10.1371/journal.pone.0278520
Journal volume & issue
Vol. 17, no. 12
p. e0278520

Abstract

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Obstructive sleep apnea (OSA) is related to the progression of cardiovascular diseases (CVD); it is an independent risk factor for stroke and is also prevalent post-stroke. Furthermore, heart rate corrected QT (QTc) is an important predictor of the risk of arrhythmia and CVD. Thus, we aimed to investigate QTc interval variations in different sleep stages in OSA patients and whether nocturnal QTc intervals differ between OSA patients with and without stroke history. 18 OSA patients (apnea-hypopnea index (AHI)≥15) with previously diagnosed stroke and 18 OSA patients (AHI≥15) without stroke history were studied. Subjects underwent full polysomnography including an electrocardiogram measured by modified lead II configuration. RR, QT, and QTc intervals were calculated in all sleep stages. Regression analysis was utilized to investigate possible confounding effects of sleep stages and stroke history on QTc intervals. Compared to patients without previous stroke history, QTc intervals were significantly higher (β = 34, p<0.01) in patients with stroke history independent of age, sex, body mass index, and OSA severity. N3 sleep (β = 5.8, p<0.01) and REM sleep (β = 2.8, p<0.01) increased QTc intervals in both patient groups. In addition, QTc intervals increased progressively (p<0.05) towards deeper sleep in both groups; however, the magnitude of changes compared to the wake stage was significantly higher (p<0.05) in patients with stroke history. The findings of this study indicate that especially in deeper sleep, OSA patients with a previous stroke have an elevated risk for QTc prolongation further increasing the risk for ventricular arrhythmogenicity and sudden cardiac death.