Smoking Accelerates Atrioventricular Conduction in Humans Concordant with Increased Dopamine Release
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Smoking Accelerates Atrioventricular Conduction in Humans Concordant with Increased Dopamine Release Affan B. Irfan1,2,3 · Claudia Arab3,4 · Andrew P. DeFilippis3,5,6 · Pawel Lorkiewicz3,5,6 · Rachel J. Keith3,5,6 · Zhengzhi Xie3,5,6 · Aruni Bhatnagar3,5,6 · Alex P. Carll1,3,5,6 Received: 25 June 2020 / Accepted: 1 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract 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 18 years of age) with intermediate to high CVD risk were recruited from the University of Louisville Hospital and affiliated clinic system between October 2009 and March 2011 as described previously [13]. All accessible patients visiting the clinics during this time period were pre-screened through a review of medical records prior to recruitment to exclude individuals that did not meet the enrollment criteria. In addition, persons unwilling or unable to provide informed consent or with significant and/or severe comorbidities were excluded. Exclusion criteria included: significant chronic lung, liver, kidney, hematological, or neoplastic disease, chronic neurological or psychiatric illness, chronic infectious disease such as HIV or hepatitis, severe coagulopathies, drug/substance abuse, and chronic cachexia. Pregnant women, prisoners, and other vulnerable populations were also excluded from the study. Patients who met the enrollment criteria and gave written consent were consented and administered a questionnaire to provide demographic information and baseline characteristics. Medical records were reviewed for past medical history, vital signs and medication history. To reduce selection b
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