Szatmáry L, Barnay C, Medvedowsky J L, Torresani J, Jouve A
Acta Cardiol. 1982;37(6):427-40.
To study the diagnostic possibility and the mechanisms involved in sinus node dysfunction, 23 patients with sick sinus syndrome were evaluated by the basic electrophysiological method (recovery times, secondary postpacing phases, sinoatrial conduction times) before and after pharmacologic autonomic blockade with i.v. propranolol 0.2 mg/kg and atropine 0.04 mg/kg, and by continuous rhythm monitoring. Patient groups of normal (I) and pathological (II) intrinsic heart rate (IHR) were compared. In group I (no. 15) prolonged recovery time (2/15), postpacing sinoatrial-block (1/15) and chaotic postextrasystolic patterns (5/15) ceased after autonomic blockade; we obtained normal intrinsic recovery time, gradual return to the stable intrinsic sinus cycle length in the secondary phase, and a normal intrinsic sinoatrial conduction time. In group II (no. 8) during the control study only 50% of patients had pathological electrophysiological parameters before, and 100% after the drug test (no gradual postpacing return to the intrinsic heart rate, abnormal recovery times, abnormal sinoatrial conduction times or chaotic postextrasystolic patterns). Holter monitoring revealed significant differences between the minimal heart rate during sleeping (group I: 48 +/- 10 bpm, mean +/- SD group II: 32 +/- 4 bpm, probability less than 0.001) as well as in the average sinus cycle length for 24 hours (group I: 848 +/- 88 ms, group II: 1254 +/- 136 ms, P less than 0.001) with a very characteristic histogram. In the patients with pharmacologically and electrophysiologically documented abnormal intrinsic rhythmicity (group II), the first 24 hour Holter monitoring revealed positive ECGs for sinus node dysfunction. In patients with normal intrinsic electrophysiological sinus node properties (group I) repeated continuous rhythm recordings revealed severe sinus bradycardia (1 patient), sinoatrial-block (1 patient), tachybrady syndrome (1 patient) and sinus-arrest (2 patients, up to 29 120 ms in waking period). These findings suggest that 1) IHR is the best and simplest diagnostic method of intrinsic sinus node dysfunction (in patients of abnormal low IHR we found positive electrophysiological and Holter parameters), and 2) in autonomic sinus node dysfunction electrophysiological parameters are essentially negative showing normal intrinsic sinus node function; in these patients systematically repeated Holter monitoring is the most valuable diagnostic method.
为研究窦房结功能障碍的诊断可能性及相关机制,对23例病态窦房结综合征患者在静脉注射0.2mg/kg普萘洛尔和0.04mg/kg阿托品进行药物自主神经阻滞前后,采用基本电生理方法(恢复时间、继发性起搏后阶段、窦房传导时间)进行评估,并进行连续心律监测。比较了正常固有心率(IHR)(I组)和病理性固有心率(II组)的患者群体。在I组(15例)中,自主神经阻滞后,延长的恢复时间(2/15)、起搏后窦房阻滞(1/15)和早搏后混乱模式(5/15)消失;我们获得了正常的固有恢复时间,在继发性阶段逐渐恢复到稳定的固有窦性周期长度,以及正常的固有窦房传导时间。在II组(8例)中,在对照研究期间,只有50%的患者在用药前有病理电生理参数,而在药物试验后100%的患者有病理电生理参数(无逐渐起搏后恢复到固有心率、异常恢复时间、异常窦房传导时间或早搏后混乱模式)。动态心电图监测显示,睡眠期间的最低心率(I组:48±10次/分钟;II组:32±4次/分钟,概率小于0.001)以及24小时的平均窦性周期长度(I组:848±88毫秒;II组:1254±136毫秒,P小于0.001)之间存在显著差异,且有非常典型的直方图。在药理学和电生理学记录的固有节律异常的患者(II组)中,首次24小时动态心电图监测显示窦房结功能障碍的心电图阳性。在固有窦房结电生理特性正常的患者(I组)中,重复的连续心律记录显示严重窦性心动过缓(1例)、窦房阻滞(1例)、快慢综合征(1例)和窦性停搏(2例,清醒期长达29120毫秒)。这些发现表明:1)固有心率是固有窦房结功能障碍的最佳和最简单的诊断方法(在固有心率异常低的患者中,我们发现了阳性的电生理和动态心电图参数);2)在自主神经源性窦房结功能障碍中,电生理参数基本为阴性,显示固有窦房结功能正常;在这些患者中,系统地重复动态心电图监测是最有价值的诊断方法。