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 < 0.04) and deeper (> 7%, p < 0.03) desaturations. Less severe desaturations didn't influence QTc. In median, QTc prolonged 7.5 ms during > 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 < 0.001) among all study patients. CONCLUSIONS: We demonstrated that longer (> 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.