Tsenov I, Urumov G, Belov Iu
Vutr Boles. 1981;20(4):73-84.
Intracardial electrophysiological examination was conducted in 50 patients with suspicious or confirmed data about disturbed function of sinus node--namely: short-term auricular stimulation for determination of sinoatrial time (SAT) and long-term auricular stimulation with increasing frequency with analysis of the phenomena in the post-stimulation period--time of sinus node recovery (TSNR), corrected recovery time of sinus node (CRTSN=TSNR minus the basal cycle of auricle before stimulation), emerging of ectopic rhythm leaders and secondary pauses. The following data were obtained in the two groups of patients formed: Group I--26 patients with ECG data about disturbed function of sinus node (periods of sinus bradycardia under 40 beats (minute and/or sinus pauses over 1800 msec): SAT identical to 375 +/- 168; TSNR = 2714 +/- 562; CRTSN = 1684 +/- 347; SAT over 400 msec was found in 8 out of 22 patients; TSNR over 1400 msec in 20 out of 26 patients, CRTSN over 550 msec in 20 out of 26 patients. Ectopic rhythm leader occurred in the poststimulation interval in 5 out of 26 patients and in 4 patients--secondary pauses over 1800 msec were observed; Group II--24 patients, with no data about disturbed function of sinus node (according to the upper criteria): SAT = 254 +/- 91; TSNR +/- 1082 +/- 168; CRTSN = 326 +/- 108; SAT over 400 msec was observed in none of the patients from that group. TSNR over 1400 msec (but under 1700 msec) was found in one patient, CRTSN in the same patient and in the rest of that group was under 550 msec. No ectopic rhythm leaders and secondary pauses over 1200 msec were found in that group of patients during the poststimulation interval. SAT, TSNR and CRTSN were shortened with a statistical significance in both the patient groups after the administration of atropine--I mg intravenously and the reexamination but in 5 patients from group I TSNR, CRTSN were paradoxically lengthened and became pathological. The electrophysiological methods for the studies on sinus node and the electrophysiological parameters, obtained via them, could contribute to the characterization and assessment of the functional potentialities of sinus node as well as to a better understanding of the mechanism of its injury.
对50例有窦房结功能紊乱可疑或确诊数据的患者进行了心内电生理检查，具体如下：进行短期心房刺激以测定窦房时间（SAT），并进行频率递增的长期心房刺激，同时分析刺激后阶段的现象，包括窦房结恢复时间（TSNR）、窦房结校正恢复时间（CRTSN = TSNR减去刺激前心房的基础周期）、异位节律领先者的出现和继发性停搏。在形成的两组患者中获得了以下数据：第一组——26例有窦房结功能紊乱心电图数据的患者（窦性心动过缓周期低于40次/分钟和/或窦性停搏超过1800毫秒）：SAT为375±168；TSNR = 2714±562；CRTSN = 1684±347；22例患者中有8例SAT超过400毫秒；26例患者中有20例TSNR超过1400毫秒，26例患者中有20例CRTSN超过550毫秒。26例患者中有5例在刺激后间期出现异位节律领先者，4例患者观察到继发性停搏超过1800毫秒；第二组——24例无窦房结功能紊乱数据的患者（根据上述标准）：SAT = 254±91；TSNR = 1082±168；CRTSN = 326±108；该组患者中无一例SAT超过400毫秒。1例患者TSNR超过1400毫秒（但低于1700毫秒），该患者及该组其他患者的CRTSN低于550毫秒。在该组患者的刺激后间期未发现异位节律领先者和超过1200毫秒的继发性停搏。静脉注射1毫克阿托品并重新检查后，两组患者的SAT、TSNR和CRTSN均有统计学意义地缩短，但第一组中有5例患者的TSNR和CRTSN反而延长并变得病理性。用于研究窦房结的电生理方法以及通过这些方法获得的电生理参数，有助于表征和评估窦房结的功能潜力，以及更好地理解其损伤机制。
