991-71 Electrophysiologic Findings in Patients with Obstructive Sleep Apnea Associated Ventricular Asystole

Abstract

Fourteen patients (47 ± 11 years) with ventricular asystole of 5.6 ± 2.7 sec (range: 3.1–13.6 sec) due to complete atrioventricular (AV) block (n = 8), sinoatrial (SA) block or sinus node (SN) arrest (n = 5) or both (n = 1) occurring exclusively during sleep apnea episodes as documented by cardiorespiratory polysomnography underwent conventional electrophysiologic study: evaluation of sinus node function included rate corrected SN recovery time (CSNRT), sinoatrial conduction time (SACT, Narula method), and sinus rate (SR) response to atropine (0.02 mg/kg). CSNRT of <550 ms, SACT of <125 ms, and SR increase after atropin to >90 bpm were considered to be normal. Assessment of AV-conduction included AH- and HV-intervals. AV-Wenckebach periods, and AV nodal effective refractory periods (ERPs) before and after atropine. None of the 14 pts received digitalis, beta-blockers or verapamil during polysomnography or EP study. 6 pts (42%) had hypertensive heart disease, 1 pt (8%) had coronary disease, and 7 pts (50%) showed no evidence of structural heart disease. SN function was normal in 12 of 14 pts (86%). Two pts had slightly prolonged SACTs (160 and 165 ms respectively). CSNRT and SR response to atropine was normal in all pts. AV nodal function was normal in 8 of 14 pts (57%) and abnormal in 4 pts (43%): 2 pts had prolonged AH-intervals of 135 and 143 ms, and 2 pts had AV-Wenckebach points at 520 and 730 ms and AV nodal ERPs of 500 and 700 ms respectively. AV-nodal function normalized after administration of atropine in all 4 pts. His-Purkinje system function was normal in 8 pts (57%), and 6 pts (43%) had slightly prolonged HV-Intervals (range: 59–63 ms). Intra- or infra His block was not observed in any pt. In conclusion , normal or only slightly abnormal electrophysiologic findings in most patients with sleep apnea associated ventricular asystole support the hypothesis that ventricular asystole is due to a neurally mediated cardioinhibitory reflex. However, it remains unsolved, why sleep apnea associated prolonged ventricular asystole does occur in some pts and does not occur in other pts despite severe obstructive sleep apnea.