Morbid obesity influences the nocturnal electrocardiogram wave and interval durations among suspected sleep apnea patients.

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 < .05) associated with prolonged conduction times. Compared to the normal weight (18.5 ≤ BMI < 25) group, the morbidly obese patients (BMI ≥ 40) had a significantly longer P-wave duration (101.7 vs. 117.2 ms), PQ interval (175.8 vs. 198.0 ms), QRS interval (89.9 vs. 97.7 ms), and QTc interval (402.8 vs. 421.2 ms). We further examined ECG waveform prolongations related to BMI. Compared to other patient groups, the morbidly obese patients had the highest number of ECG segments with PQ interval (44% of the ECG samples), QRS duration (14%), and QTc duration (20%) above the normal limits. CONCLUSIONS: Morbid obesity predisposes patients to prolongation of cardiac conduction times. This might increase the risk of arrhythmias, stroke, and even sudden cardiac death.

Obstructive Sleep Apnea Patients With Atrial Arrhythmias Suffer From Prolonged Recovery From Desaturations.

OBJECTIVE: We aimed to investigate how acute and long-term effects of atrial arrhythmias affect the desaturation severity and characteristics determined from the oxygen saturation signal in obstructive sleep apnea (OSA) patients. METHODS: 520 suspected OSA patients were included in retrospective analyses. Eight desaturation area and slope parameters were calculated from blood oxygen saturation signals recorded during polysomnographic recordings. Patients were grouped based on whether they had previously diagnosed atrial arrhythmia (i.e., atrial fibrillation (AFib) or atrial flutter) or not. Furthermore, patients with a previous atrial arrhythmia diagnosis were sub-grouped based on whether they had continuous AFib or sinus rhythm during the polysomnographic recordings. Empirical cumulative distribution functions and linear mixed models were utilized to investigate the connection between diagnosed atrial arrhythmia and the desaturation characteristics. RESULTS: Patients with previous atrial arrhythmia diagnosis had greater desaturation recovery area when the 100% oxygen saturation baseline reference was considered (ß = 0.150--0.127, p ≤ 0.039) and more gradual recovery slopes (ß = -0.181 to -0.199, p < 0.004) than patients without a previous atrial arrhythmia diagnosis. Furthermore, patients with AFib had more gradual oxygen saturation fall and recovery slopes than patients with sinus rhythm. CONCLUSION: Desaturation recovery characteristics in the oxygen saturation signal contains essential information about the cardiovascular response to hypoxemic periods. SIGNIFICANCE: More comprehensive consideration of the desaturation recovery section could provide more detailed information about OSA severity, for example when developing new diagnostic parameters.

QTc prolongation is associated with severe desaturations in stroke patients with sleep apnea.

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 (ß = 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.