Neuss H, Conrad A, Mitrovic V, Schlepper M
J Cardiovasc Pharmacol. 1986;8 Suppl 11:S167-70. doi: 10.1097/00005344-198511001-00030.
The acute electrophysiologic effects of 10 mg bisoprolol (B, given intravenously) were evaluated during an electrophysiological study in 10 patients with a history of paroxysmal tachycardia. Drug administration resulted in a significant decrease of sinus rate (Control [C]; 70.8/min; B: 59.4), and in an increase in sinus node recovery time (+20%). AV-nodal depression was marked at high heart rates during incremental atrial pacing. A second-degree AV-block occurred at a pacing cycle length (CL) of 329 ms (182/min) before and at a CL of 378 ms (158/min) after drug administration. Depression of AV-nodal conduction was negligible at low heart rates; the AH-interval at sinus rhythm was not affected (C: 84 ms, B: 86 ms); and functional and effective refractory periods of the AV-node were only slightly prolonged. Conduction intervals and refractory periods on atrial and ventricular level did not change. In 5 of 6 patients with accessory AV-pathways, circus movement tachycardia (CMT) could be elicited prior to as well as after B. Due to AV-nodal delay, CMT CL was slightly prolonged after B. Echozone and refractoriness of accessory pathways were not affected. In 1 of 2 patients with ectopic atrial tachycardia, B prevented the induction of paroxysms. In one patient with paroxysmal atrial fibrillation, the ventricular response decreased from 128/min to 94/min. The findings suggest that the electrophysiologic effects of B are due to a selective beta-adrenergic antagonism. Therapeutic efficacy is only to be expected if an increased adrenergic drive is a prerequisite for induction and continuation of a tachycardia.
在一项电生理研究中,对10例有阵发性心动过速病史的患者静脉注射10毫克比索洛尔(B),评估其急性电生理效应。给药后窦性心率显著降低(对照[C]:70.8次/分钟;B:59.4次/分钟),窦房结恢复时间增加(+20%)。在递增心房起搏时,高心率下房室结抑制明显。给药前起搏周期长度(CL)为329毫秒(182次/分钟)时出现二度房室传导阻滞,给药后CL为378毫秒(158次/分钟)时出现。低心率时房室结传导抑制可忽略不计;窦性心律时AH间期未受影响(C:84毫秒,B:86毫秒);房室结的功能和有效不应期仅略有延长。心房和心室水平的传导间期和不应期未改变。6例有房室旁路的患者中,5例在给予B之前和之后均可诱发折返性心动过速(CMT)。由于房室结延迟,给予B后CMT的CL略有延长。旁路的回声区和不应期未受影响。2例异位房性心动过速患者中,1例B可预防阵发性发作。1例阵发性心房颤动患者的心室率从128次/分钟降至94次/分钟。这些发现提示B的电生理效应是由于选择性β肾上腺素能拮抗作用。只有当肾上腺素能驱动增加是心动过速诱发和持续的前提条件时,才有望获得治疗效果。