Jordan J L, Yamaguchi I, Mandel W J
Circulation. 1978 Feb;57(2):217-23. doi: 10.1161/01.cir.57.2.217.
The intrinsic heart rate (IHR) was determined in 17 patients with symptomatic sinus bradycardia by administering atropine 0.04 mg/kg and propranolol 0.2 mg/kg, i.v. In this way, sick sinus (SSS) patients with intrinsic sinus node (SN) dysfunction could be distinguished from those patients with disturbed autonomic regulation of SN function. Sick sinus syndrome patients with normal corrected sinus node recovery time (SNRTC), adjusted for the magnitude and direction of autonomic chronotrophy, consistently had normal IHRs and therefore abnormalities of autonomic regulation. Sick sinus syndrome patients with abnormal adjusted SNRTC consistently had abnormal IHRs and therefore abnormalities of intrinsic SN function. We conclude that more than one pathophysiologic mechanism can produce the clinical manifestations of sick sinus syndrome and that abnormal prolongation of SNRTC is dependent upon the underlying mechanism of sinus node dysfunction.
通过静脉注射0.04mg/kg阿托品和0.2mg/kg普萘洛尔,测定了17例有症状性窦性心动过缓患者的固有心率(IHR)。通过这种方式,可以将患有固有窦房结(SN)功能障碍的病态窦房结(SSS)患者与那些自主神经对SN功能调节紊乱的患者区分开来。校正窦房结恢复时间(SNRTC)正常、经自主神经变时性大小和方向调整后的病态窦房结综合征患者,其IHR始终正常,因此存在自主神经调节异常。校正后SNRTC异常的病态窦房结综合征患者,其IHR始终异常,因此存在固有SN功能异常。我们得出结论,不止一种病理生理机制可产生病态窦房结综合征的临床表现,且SNRTC的异常延长取决于窦房结功能障碍的潜在机制。