Rosenqvist M, Bergfeldt L, Aili H, Mathé A A
Department of Cardiology, Karolinska Institute, at Karolinska Hospital, Stockholm, Sweden.
Br Heart J. 1993 Oct;70(4):371-5. doi: 10.1136/hrt.70.4.371.
Lithium has occasionally been reported to cause symptomatic sinus node bradyarrhythmias. The prevalence and mechanism of these arrhythmias during long-term treatment are unknown. The aims of this study were (a) to evaluate the systemic effects of lithium treatment on cardiac conduction in individuals who were free from cardiovascular disorders; (b) to assess the prevalence of lithium treatment in a group of patients with pacemakers; and (c) to evaluate the interaction between the parasympathetic limb of the autonomous nervous system and the sinus node cells during long-term lithium treatment.
45 patients who had been treated with lithium for > 12 months were investigated in a long-term electrocardiography study. Only patients without cardiovascular disease, or concomitant chronotropic medication, or metabolic disorders known to cause rhythm disturbances were included. An age-stratified population was used as a reference group. 21 patients also underwent analysis of carotid sinus pressure and sinus cycle length before and after atropine to clarify whether neural mechanisms were involved. The prevalence of lithium treated patients was determined in 650 patients with pacemakers.
(a) Signs of moderate sinus node dysfunction (sinus arrest > 1.5 s, minimum heart rate < 50 beats/min) were found in 56% and 78% respectively in the lithium-treated group compared with 30% and 30% respectively in the reference group (p < 0.01). Severe sinus node dysfunction was equally common in both groups. (b) The prevalence of chronic lithium treatment in the pacemaker population was 0.46%. (c) Sinus cycle variations were abnormal in the basal state in three (14%) patients and in 11 (52%) patients after atropine despite signs of intact and normal parasympathetic innervation.
Depressed sinus node function was significantly more common in a lithium-treated population than in an age-stratified reference group. Clinically significant dysfunction, however, was uncommon. The effect of lithium on the sinus node seemed to be intrinsic and was not caused by increased parasympathetic tone.
锂偶尔会被报道可引起有症状的窦房结缓慢性心律失常。长期治疗期间这些心律失常的发生率及机制尚不清楚。本研究的目的是：(a)评估锂治疗对无心血管疾病个体心脏传导的全身影响；(b)评估一组起搏器患者中锂治疗的发生率；(c)评估长期锂治疗期间自主神经系统副交感神经分支与窦房结细胞之间的相互作用。
在一项长期心电图研究中对45例接受锂治疗超过12个月的患者进行了调查。仅纳入无心血管疾病、无同时使用的变时性药物或已知可引起节律紊乱的代谢紊乱的患者。将一个按年龄分层的人群用作参照组。21例患者还在使用阿托品前后进行了颈动脉窦压力和窦房结周期长度分析，以明确是否涉及神经机制。在650例起搏器患者中确定了接受锂治疗患者的发生率。
(a)锂治疗组分别有56%和78%出现中度窦房结功能障碍的体征（窦性停搏>1.5秒，最低心率<50次/分钟），而参照组分别为30%和30%（p<0.01）。严重窦房结功能障碍在两组中同样常见。(b)起搏器人群中慢性锂治疗的发生率为0.46%。(c)尽管有完整且正常的副交感神经支配的体征，但在基础状态下3例（14%）患者的窦房结周期变化异常，使用阿托品后11例（52%）患者异常。
锂治疗人群中窦房结功能减退明显比按年龄分层的参照组更常见。然而，具有临床意义的功能障碍并不常见。锂对窦房结的作用似乎是内在的，并非由副交感神经张力增加所致。
