Role of autonomic regulatory mechanism in sinoatrial conduction and sinus node automaticity in sick sinus syndrome.

To assess the role of autonomic regulatory mechanisms on sinoatrial conduction and automaticity in patients with clinical evidence of sick sinus syndrome, electrophysiologic studies were conducted in 12 male patients, mean age 64 4 7 years. Heart rate, sinus node recovery time (SNRT) and sinoatrial conduction time (SACT) were determined before and after autonomic blockade with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). The mean sinus cycle length was 1033 ± 208 msec (4 SD) before autonomic blockade and 1016 4 188 msec after autonomic blockade. The observed intrinsic heart rate (1HRo) after autonomic blockade was abnormal in nine of 12 patients. The mean corrected SNRT before autonomic blockade was 606.5: 432 msec and was abnormal (< 450 msec) in six of 12 patients (50%). After autonomic blockade the mean SNRT was 661.8 + 604.8 msec and was abnormal (> 450 msec) in eight of 12 (67%). Six of nine patients (66%) with an abnormal intrinsic observed HR had an abnormal SNRTc before autonomic blockade. After autonomic blockade, eight of these nine (88%) had an abnormal SNRTc. SACT was estimated by continuous pacing and by premature stimulation. The mean SACT estimated by continuous pacing before autonomic blockade was 190.3 ± 99.6 msec and decreased significantly after autonomic blockade (140.6 ± 53.4 msec, p < 0.05). The mean SACT estimated by premature stimulation before autonomic blockade was 218 ± 87.6 msec and decreased significantly after autonomic blockade (143.7 ± 49.9 msec, p < 0.01). The coefficient of correlation between the two methods was 0.8 before autonomic blockade and 0.85 after autonomic blockade. SACT was abnormally prolonged (> 206 msec) in five of 12 patients (41%) during control studies and in two of 12 patients (16%) after autonomic blockade. SAC by either method decreased in eight of 12 patients (67%) and increased in four of 12 patients (33%) after autonomic blockade. Changes in SACT after autonomic blockade could not be predicted from symptoms, electrocardiographic findings or determination of intrinsic HR. In conclusion, assessment of IHR, SNRT and SACT after autonomic blockade can differentiate patients with sick sinus syndrome, whether due to intrinsic or extrinsic abnormality of sinus node automaticity or conduction. The significant decrease in SACT in most patients with sick sinus syndrome after autonomic blockade suggests enhanced basal parasympathetic tone and normal intrinsic conduction in the perinodal region. The increase in SACT in a minority of patients after autonomic blockade suggests that enhanced basal sympathetic tone can mask an underlying intrinsic abnormality of sinoatrial conduction.