Premature ventricular contractions during apneic events showed significantly different turbulence onset (21.75% vs 31.96%, p<0.0008) and slope on a per-PVC basis compared to normal breathing.
Observational (n=11)
Do premature ventricular contractions during apneic events result in different heart rate turbulence metrics compared to those during normal breathing in patients with obstructive sleep apnea?
Nocturnal PVCs mediate quantifiably different disruptions in heart rate turbulence depending on whether they occur during apneic events or normal breathing in patients with OSA.
Absolute Event Rate: 21.75% vs 31.96%
p-value: p=<0.0008
Obstructive Sleep Apnea (OSA) affects an estimated 18 million individuals in the U.S. adult population. Numerous research findings indicate that OSA has significant adverse effects on the cardiac health. Current method of assessing the severity of OSA using apnea hypopnea index (AHI) which is the average count of apneic events per hour of sleep does not reflect how OSA affects the cardiovascular system health. In this study, we investigate the possibility of analyzing the nocturnal Electrocardiography (ECG) signal to assess the adverse impact of sleep apnea events on the heart. Our approach focuses on determining whether nocturnal cardiac arrhythmia is different depending on whether they occur during apneic events or during periods of normal breathing. We utilized the ECG recordings that are routinely made during full-night (6-8 hr) polysomnography to compute two metrics that are inspired by standard measures of heart rate turbulence (HRT): turbulence onset (TO), and turbulence slope (TS). Eleven volunteers (9M, 2F, 52±8 yrs., BMI 34.07±7.25 kg/m2) who were either previously diagnosed as having obstructive sleep apnea or were suspected of having OSA and referred to our accredited sleep laboratory for diagnosis participated in the study. The volunteers exhibited AHI with 60.80±26.84 range of 18.3 to 105.4. The TS values obtained from averaged tachograms of premature ventricular contractions (PVCs) that occurred during apneic events and normal breathing were 16.11±10.36 ms/RR and 8.77±7.96 ms/RR, respectively and had no significant different means (p>0.08). The corresponding averaged TO were 13.41%±20.87% for PVCs during apneic events and 12.06%±21.02% for PVCs during normal breathing intervals did not significantly different mean either (p>0.8). However, the TO values computed for each PVC during apnea events had a different mean (21.75%±33.00%) compared with TO mean (31.96%±33.24%) for PVCs during normal breathing (p<0.0008). Similar analysis for TS values (72.01±97.84 ms/RR for apneic events and 52.29±73.02 ms/RR for normal breathing) showed that they also have significantly different means (p<0.007). The results of this study suggest that nocturnal PVCs appear to mediate quantifiably different disruptions in the heart sinus depending on whether they occur during normal breathing or during apneic events.
Askari et al. (Wed,) conducted a observational in Obstructive Sleep Apnea (n=11). Apneic events vs. Normal breathing periods was evaluated on Turbulence onset (TO) computed for each premature ventricular contraction (p=<0.0008). Premature ventricular contractions during apneic events showed significantly different turbulence onset (21.75% vs 31.96%, p<0.0008) and slope on a per-PVC basis compared to normal breathing.