Sethi K K, Jaishankar S, Balachander J, Bahl V K, Gupta M P
Int J Cardiol. 1984 Jun;5(6):707-19. doi: 10.1016/0167-5273(84)90218-3.
Electrophysiologic studies were performed in 10 normals and 33 patients with sick sinus syndrome before and after total autonomic blockade with propranolol and atropine. In normals both corrected sinus node recovery time (SNRT) and sinoatrial conduction time (SACT) decreased significantly after autonomic blockade. In patients with sick sinus syndrome the corrected SNRT was abnormal (greater than 450 msec) in 16 (48.5%) cases before and 25 (76%) cases (greater than 285 msec) after autonomic ablation (P less than 0.02). Thirteen of 21 patients (62%) with normal intrinsic heart rate and all 12 cases with abnormally low intrinsic rate after autonomic blockade had abnormal corrected SNRT (greater than 285 msec). Mean SACT measured in 19 patients also shortened significantly following pharmacologic denervation. During control it was prolonged (greater than 226 msec) in 8 patients (44%). After autonomic blockade 2 of 13 patients with normal intrinsic heart rate and 3 of 6 with low intrinsic rate showed abnormal SACT (greater than 151 msec). The data suggest that the majority (76%) of patients with sick sinus syndrome have intrinsic abnormality of sinus node automaticity while in a minority (24%) disturbed autonomic regulation is the pathogenetic mechanism. Patients with normal intrinsic heart rate usually have normal intrinsic SACT, while a significant proportion of those with low intrinsic rate have abnormal perinodal conduction. Subjects with abnormal intrinsic heart rate have more severe disturbances of sinus node function than those with normal intrinsic rate.
对10名正常人和33例病态窦房结综合征患者在使用普萘洛尔和阿托品进行完全自主神经阻滞后进行了电生理研究。在正常人中,自主神经阻滞后校正窦房结恢复时间(SNRT)和窦房传导时间(SACT)均显著降低。在病态窦房结综合征患者中,校正SNRT在自主神经消融前16例(48.5%)异常(大于450毫秒),消融后25例(76%)异常(大于285毫秒)(P<0.02)。21例固有心率正常的患者中有13例(62%)以及自主神经阻滞后固有心率异常降低的所有12例患者校正SNRT均异常(大于285毫秒)。在19例患者中测量的平均SACT在药物去神经支配后也显著缩短。在对照期间,8例患者(44%)的SACT延长(大于226毫秒)。自主神经阻滞后,13例固有心率正常的患者中有2例以及6例固有心率低的患者中有3例SACT异常(大于151毫秒)。数据表明,大多数(76%)病态窦房结综合征患者存在窦房结自律性的内在异常,而少数(24%)患者自主神经调节紊乱是发病机制。固有心率正常的患者通常固有SACT正常,而固有心率低的患者中有相当一部分存在结周传导异常。固有心率异常的受试者比固有心率正常的受试者窦房结功能紊乱更严重。