INVASIVE ELECTROPHYSIOLOGICAL EVALUATION OF PATIENTS WITH SLEEP APNEA-ASSOCIATED VENTRICULAR ASYSTOLE - METHODS AND PRELIMINARY-RESULTS

Twelve patients (aged 48 +/- 12 y) with ventricular asystole of >3 s d ue to complete atrioventricular (AV) block (n = 8), sinoatrial (SA) bl ock or sinus node arrest (n = 3) or both (n = 1) associated with obstr uctive sleep apnoea underwent invasive electrophysiological evaluation of sinus node function and AV conduction properties before and after administration of atropine (0.02 mgkg(-1)). Ventricular asystole laste d for 5.9 +/- 12.8 s (range 3.1-13 s). Sinus node function was assesse d by measurement of sinus node recovery time, sinoatrial conduction ti me, and the response of sinus rate to atropine. Parameters of AV-condu ction assessment included AH- and HV-intervals, AV- and VA-Wenckebach periods, and effective refractory period of the AV node before and aft er atropine. Sinus node function was normal in 11 of the 12 study pati ents and moderately abnormal in 1 patient. AV-nodal function was norma l in 8 patients and moderately abnormal in 4 patients. A slightly prol onged HV-interval (59-63 ms) was present in 6 patients. Intra- or infr a His block was not observed in any patient. In conclusion, normal or only moderately abnormal electrophysiological findings in patients wit h sleep apnoea-associated ventricular asystole suggest that a neurally mediated cardioinhibitory reflex may cause ventricular asystole in th ese patients. This sleep apnoea-triggered 'vasovagal' reflex may unmas k pre-existing mild to moderate structural abnormalities of the AV con duction system.