Abstract

Introduction: Sleep-disordered breathing (SDB) is a prevalent condition associated with adverse cardiovascular events, including nocturnal arrhythmias and sudden cardiac death, but the underlying mechanism is unclear. Hypothesis: Ventricular repolarization instability increases in those who develop SDB. Methods: For the participants of the Sleep Heart Health Study (SHHS), the percentage of sleep time with oxygen saturation levels < 90% (T90) was measured. We identified participants who did not have SDB (T90 < 0.22% = median of the SHHS cohort) during the initial study but developed SDB (T90 > 10%) by the time of the 5-year follow-up. A comparator group was identified as those who matched the first group on age, sex, BMI, and race but had T90 < 0.22% during both the initial and the follow-up sleep studies. Each group consisted of 25 (8 M and 17 F) participants, none of whom had any diagnosed comorbidities or prescriptions that could affect cardiac repolarization. Heart rate (HR), heart rate variability (SDNN), and QT variability index (QTVI, a measure of ventricular repolarization instability) were calculated from one-lead ECG recordings. Paired sample t- test was used to assess statistical associations. Results: The respiratory disturbance index (RDI) for the study group increased from 2.57 ± 0.74 events/hr at baseline to 14.8 ± 3.72 events/hr at follow-up (P = 0.001), while the RDI was not different for the comparators (3.08 ± 0.71 events/hr at baseline, 3.65 ± 0.68 events/hr at follow-up, P = 0.599). In those who developed SDB, HR and SDNN did not change between baseline and follow-up, but QTVI increased from -1.25 ± 0.15 to -0.85 ± 0.15 (P = 0.013). None of the measured electrocardiographic parameters differed between baseline and follow-up in comparators. Conclusion: Over a five-year follow-up, the development of SDB was associated with an increase in QT variability comparable to symptomatic heart failure. Hypoxemia appears to be the main underlying mechanism.

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