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Abstract Background Obesity is a global issue with a major impact on cardiovascular health. This study explores how obesity influences nocturnal cardiac electrophysiology in suspected obstructive sleep apnea (OSA) patients. Methods We randomly selected 12 patients from each of the five World Health Organization body mass index (BMI) classifications groups (ntotal = 60) while keeping the group's age and sex matched. We evaluated 1965 nocturnal electrocardiography (ECG) samples (10 s) using modified lead II recorded during normal saturation conditions. R‐wave peaks were detected and confirmed using dedicated software, with the exclusion of ventricular extrasystoles and artifacts. The duration of waves and intervals was manually marked. The average electric potential graphs were computed for each segment. Thresholds for abnormal ECG waveforms were P‐wave > 120 ms, PQ interval > 200 ms, QRS complex > 120 ms for, and QTc > 440 ms. Results Obesity was significantly (p

Abstract Background Obstructive sleep apnea (OSA) is associated with vascular diseases from which stroke and sudden cardiac death are the most significant ones. It is known that disturbances of the autonomic nervous system and electrocardiographic changes are seen in patients with a previous cerebrovascular event. However, the pathophysiological cascade between breathing cessations, autonomic regulation, and cardiovascular events is not fully understood. Methods We aimed to investigate the acute effect of desaturation on repolarisation in OSA patients with a previous stroke. We retrospectively analysed heart-rate corrected QT (QTc) intervals before, within, and after 975 desaturations in OSA patients with a stroke history and at least moderate sleep apnea (apnea–hypopnea index ≥ 15 events/h, n = 18). For the control population (n = 18), QTc intervals related to 1070 desaturation were analysed. Desaturations were assigned to groups according to their length and duration. Groupwise comparisons and regression analyses were further executed to investigate the influence of desaturation features on repolarization. Results In the stroke population the QTc prolonged at least 11 ms during 27.1% of desaturations, and over 20 ms during 12.2% of desaturations. QTc was significantly prolonged during longer (> 30 s, p 7%, p 45 s desaturations and 7.4 ms during > 9% deep desaturations. In the control population, QTc prolongation was observed but to a significantly lesser extent than in stroke patients. In addition, desaturation duration was found to be an independent predictor of QTc prolongation (β = 0.08, p 30 s) and deeper (> 7%) desaturations prolong QTc in patients with stroke history. A significant proportion of desaturations produced clinically relevant QTc prolongation. As it is known that a long QTc interval is associated with lethal arrhythmias, this finding might in part explain the pathophysiological sequelae of cardiovascular mortality in OSA patients with a history of stroke.