Smoking Accelerates Atrioventricular Conduction in Humans Concordant with Increased Dopamine Release.
Smoking Accelerates Atrioventricular Conduction in Humans Concordant with Increased Dopamine Release.
复制标题
吸烟与多巴胺释放增加的人类一致的人类室传导加速。
DOI：
10.1007/s12012-020-09610-5
复制
发表时间：
2021-03
影响因子：
3.2
通讯作者：
Carll AP
中科院分区：
文献类型：
--
作者：
Irfan AB;Arab C;DeFilippis AP;Lorkiewicz P;Keith RJ;Xie Z;Bhatnagar A;Carll AP
吸烟与心律失常、中风、心力衰竭和心脏骤停有关，所有这些都可能是由于交感神经对心脏传导系统的影响增加和心室复极改变。然而，吸烟对室上性传导的影响以及交感神经系统在其中的作用的知识仍然不完整。测量中-高心血管疾病风险的参与者的尿儿茶酚胺和可替宁，测量12导联心电图（ECG）的心房和房室传导时间，包括P持续时间，PR间期和PR段（II导联），通过广义线性模型分析与可替宁的相关性。统计调解分析，然后用于测试是否有任何显着的可替宁和房室传导之间的关联介导的儿茶酚胺。ECG终点和尿代谢产物包括来自总共136名窦性心律的参与者。吸烟者（n=53）和非吸烟者（n=83）之间的心房和房室传导无显著差异。未校正和模型校正的线性回归显示，可替宁与PR间期和PR段显著负相关，但与P持续时间无关。多巴胺、去甲肾上腺素和肾上腺素均与PR间期呈负相关，而只有多巴胺与PR段呈负相关（p<0.05）。多巴胺和去甲肾上腺素（但不是肾上腺素）也与可替宁呈正相关。多巴胺介导可替宁与PR间期的关系，以及可替宁与PR段的关系。吸烟与房室传导加速和尿多巴胺和去甲肾上腺素升高有关。吸烟可能通过增加多巴胺的产生加速房室结传导。房室传导的心电图标志物（PR间期和PR段）对肾上腺素能刺激特别敏感，可预测全因和心血管死亡率。我们的研究结果表明，香烟烟雾暴露通过增加多巴胺加速房室传导。这些观察确定了吸烟可能增加心血管发病率和死亡率风险的途径，以及潜在的治疗靶点。
Smoking is associated with cardiac arrhythmia, stroke, heart failure, and sudden cardiac arrest, all of which may derive from increased sympathetic influence on cardiac conduction system and altered ventricular repolarization. However, knowledge of the effects of smoking on supraventricular conduction, and the role of the sympathetic nervous system in them, remains incomplete. Participants with intermediate-high cardiovascular disease risk were measured for urinary catecholamines and cotinine, and 12-lead electrocardiograms (ECGs) were measured for atrial and atrioventricular conduction times, including P duration, PR interval, and PR segment (lead II), which were analyzed for associations with cotinine by generalized linear models. Statistical mediation analyses were then used to test whether any significant associations between cotinine and atrioventricular conduction were mediated by catecholamines. ECG endpoints and urinary metabolites were included from a total of 136 participants in sinus rhythm. Atrial and atrioventricular conduction did not significantly differ between smokers (n=53) and non-smokers (n=83). Unadjusted and model-adjusted linear regressions revealed cotinine significantly and inversely associated with PR interval and PR segment, but not P duration. Dopamine, norepinephrine, and epinephrine all inversely associated with PR interval, whereas only dopamine was also inversely associated with PR segment (p<0.05). Dopamine and norepinephrine (but not epinephrine) also associated positively with cotinine. Dopamine mediated the relationship between cotinine and PR interval, as well as the relationship between cotinine and PR segment. Smoking is associated with accelerated atrioventricular conduction and elevated urinary dopamine and norepinephrine. Smoking may accelerate atrioventricular nodal conduction via increased dopamine production. The electrocardiographic markers of atrioventricular conduction (PR interval and PR segment) are particularly sensitive to adrenergic stimulation and predictive of all-cause and cardiovascular mortality. Our study findings suggest that cigarette smoke exposure accelerates atrioventricular conduction by augmenting dopamine. These observations identify a pathway by which smoking may increase risk for cardiovascular morbidity and mortality, and a potential for therapeutic target.
登录
查看更多内容
影响因子：
3.7
作者：
Launay JM;Del Pino M;Chironi G;Callebert J;Peoc'h K;Mégnien JL;Mallet J;Simon A;Rendu F
通讯作者：
Rendu F
影响因子：
3.4
作者：
Fowler, JS;Logan, J;Volkow, ND
通讯作者：
Volkow, ND
DOI：
10.1016/s0735-1097(84)80344-7
发表时间：
1984-01-01
影响因子：
24
作者：
KLEIN, LW;AMBROSE, J;TEICHHOLZ, LE
通讯作者：
TEICHHOLZ, LE
DOI：
10.1016/j.jchromb.2006.07.029
发表时间：
2006-12-05
影响因子：
3
作者：
Man, Che Nin;Gam, Lay-Harn;Awang, Rahmat
通讯作者：
Awang, Rahmat
影响因子：
5.5
作者：
Nielsen, Jonas Bille;Pietersen, Adrian;Holst, Anders Gaarsdal
通讯作者：
Holst, Anders Gaarsdal