Wu D L, Yeh S J, Lin F C, Wang C C, Cherng W J
Department of Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan.
J Am Coll Cardiol. 1992 Feb;19(2):355-64. doi: 10.1016/0735-1097(92)90492-6.
Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 +/- 2.8 s (mean +/- SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional sinoatrial block. Group II consisted of 22 patients with either 1:1 sinoatrial conduction (group IIa = 13 patients) or second degree sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to greater than 14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 +/- 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 +/- 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patients with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 +/- 1,121). Thus, abnormalities in both sinus node automaticity and sinoatrial conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive sinoatrial exit block plays a major role in producing posttachycardia pauses.
对38例有严重症状性病态窦房结综合征患者进行了记录窦房结电图的电生理研究。38例患者中,32例有阵发性快速心律失常,17例有晕厥表现。临床记录的窦性或房性停搏为5.6±2.8秒(均值±标准差)。根据电生理检查结果将患者分为三组。第一组包括9例完全性窦房阻滞患者。在长间歇发作期间记录窦房结电图。7例有单向传出阻滞,房性冲动能够逆向传入窦房结导致窦性自律性受抑制;2例有双向窦房阻滞。第二组包括22例在自发窦性心律时呈1:1窦房传导(IIa组 = 13例患者)或二度窦房传出阻滞(IIb组 = 9例患者)的患者。在起搏后间歇期间观察到窦房传出阻滞,范围为1至超过14个窦性搏动,起搏后间歇为1650至37000毫秒(平均7286±6989)。最大窦房结恢复时间为770至5580毫秒(平均3004±1686),5例正常,17例延长。第三组包括7例无法记录到窦房结电图的患者,这反映了技术失败或窦房活动静止。这7例患者的窦房结恢复时间为1190至4260毫秒(平均2949±1121)。因此,病态窦房结综合征中窦性或房性长间歇是由窦房结自律性和窦房传导异常共同导致的。然而,可出现完全性窦房传出阻滞并导致严重心动过缓及逸搏心律;反复性窦房传出阻滞在心动过速后间歇的产生中起主要作用。