Secondhand smoke and atrial fibrillation: Data from the Health eHeart Study
Introduction
Atrial fibrillation (AF) affects millions of Americans and is growing in incidence and prevalence.1 It nearly doubles mortality and is one of the most common causes of stroke.2, 3 Though the mechanism of AF remains largely unknown, observational analyses have identified age, male sex, white race, hypertension (HTN), heart failure, diabetes, obesity, and alcohol consumption as risk factors for AF.4, 5 An emerging risk factor for AF is cigarette smoking, which has been linked to the development of AF in both current and former smokers.6, 7
Though no studies have been published examining the effect of secondhand smoke (SHS) on AF, SHS exposure is associated with increased cardiovascular disease and mortality.8 It is estimated that SHS exposure increases nonsmokers’ coronary artery disease (CAD) risk by 25%–30%,9 and the vast majority of deaths in the United States attributed to SHS are from heart disease.10 Protection from SHS through the implementation of smoke-free legislation is rapidly followed by reductions in hospital admissions for acute myocardial infarctions, stroke, and other cardiac events.11, 12, 13 Despite progress in reducing smoking prevalence and the resultant SHS exposure, SHS remains a significant hazard in the United States and worldwide.14 Current hypotheses regarding the mechanism by which SHS leads to cardiac disease include induction of an inflammatory state,15 direct effects of nicotine on atrial structural remodeling,16, 17 and effects on autonomic function.18, 19 Each of these mechanisms has also been implicated in the pathogenesis of AF.4, 20
Up to 30% of all AF occurs in patients without any clear risk factors.21 While some “lone AF” patients may have an inherited component, the majority do not,22, 23 suggesting that some as-yet-unknown environmental exposure may be important. Given the increasing burden of AF and the need to identify effective prevention strategies, we examined the possible relationship between SHS exposure and the prevalence of AF, hypothesizing that SHS exposure increases the risk of AF.
Section snippets
Study design
We performed a cross-sectional analysis of data obtained between March 8, 2013 (enrollment initiation) and November 13, 2014 from consecutive participants enrolled in the Health eHeart Study. The Health eHeart Study is an internet-based, longitudinal, cardiovascular cohort study.
English-speaking adults worldwide with a working e-mail address were eligible for participation. Participants were recruited from the University of California, San Francisco (UCSF) cardiology and general medicine
Results
At the time of this analysis, there were 6863 participants enrolled in the study, of whom 4976 had completed the baseline SHS exposure and medical conditions questionnaires. Of these participants, 593 (11.9%) reported having AF, of whom 271 (45.7%) reported persistent AF and 275 (46.4%) reported paroxysmal AF. Of the 42 Health eHeart participants with medical records at UCSF who provided electronic HIPAA consent, 25 indicated having AF. Of those, 100% had AF documented by a physician in their
Discussion
We found that SHS, particularly when present during development and early childhood, was statistically significantly associated with the presence of AF. This relationship was particularly strong in the absence of known AF risk factors, suggesting a direct connection between SHS in early life and AF pathophysiology.
Past research on tobacco and AF has focused on the effects of active smoking, providing the foundation for the hypothesis tested in the current study. The Rotterdam Study, a
Conclusions
In our study of nearly 5000 Health eHeart participants, SHS exposure during gestational development and during childhood were both associated with having AF later in life. Furthermore, this association was even stronger in the absence of established risk factors for AF. These findings indicate that SHS may be an important, potentially modifiable risk factor for the development of AF, operating outside of known mechanisms for the arrhythmia. Finally, this research suggests that parental
References (33)
- et al.
Increasing prevalence of atrial fibrillation and flutter in the United States
Am J Cardiol
(2009) - et al.
Epidemiology and natural history of atrial fibrillation: clinical implications
J Am Coll Cardiol
(2001) - et al.
Smoking and incidence of atrial fibrillation: results from the Atherosclerosis Risk in Communities (ARIC) study
Heart Rhythm
(2011) - et al.
Cigarette smoking and risk of atrial fibrillation: the Rotterdam Study
Am Heart J
(2008) Passive smoking as a cause of heart disease
J Am Coll Cardiol
(1994)- et al.
Cardiovascular effect of bans on smoking in public places: a systematic review and meta-analysis
J Am Coll Cardiol
(2009) - et al.
Secondhand smoke exposure among never-smoking youth in 168 countries
J Adolesc Health
(2015) - et al.
Lone atrial fibrillation: does it exist?
J Am Coll Cardiol
(2014) - et al.
A first-degree family history in lone atrial fibrillation patients
Heart Rhythm
(2008) - et al.
ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society
Circulation
(2006)
The clinical profile and pathophysiology of atrial fibrillation: relationships among clinical features, epidemiology, and mechanisms
Circ Res
Incident atrial fibrillation among Asians, Hispanics, blacks, and whites
Circulation
Committee on Secondhand Smoke Exposure and Acute Coronary Events IoM. Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence
Cardiology Rx for Change: improving clinical attention to tobacco use and secondhand smoke exposure in cardiology
Clin Cardiol
Declines in acute myocardial infarction after smoke-free laws and individual risk attributable to secondhand smoke
Circulation
Association between smoke-free legislation and hospitalizations for cardiac, cerebrovascular, and respiratory diseases: a meta-analysis
Circulation
Cited by (52)
Aging and atrial fibrillation: A vicious circle
2024, International Journal of CardiologyThe underlying mechanism of PM2.5-induced ischemic stroke
2022, Environmental PollutionCitation Excerpt :Interestingly, atrial fibrillation has been related to repeated exposure to second hand tobacco smoke (SHS). Longitudinal data from the Framingham Heart and Offspring Study, and the Health eHeart Study, both suggest that SHS exposure is a risk factor for atrial fibrillation (Dixit et al., 2016; Groh et al., 2019). An Israeli study on the risk of atrial fibrillation among women indicated that SHS was associated with an increased risk of atrial fibrillation, with adjusted odds ratio (OR) of 3.81 (95% CI: 2.02–7.18) (Regev-Avraham et al., 2020).
Secondhand tobacco smoke exposure, urine cotinine, and risk of incident atrial fibrillation: The multi-ethnic study of atherosclerosis
2022, Progress in Cardiovascular DiseasesSecondhand smoke exposure is associated with abnormal P-wave axis
2022, Public HealthSocial Risk Factors and Atrial Fibrillation
2021, Cardiac Electrophysiology ClinicsPhysical activity and atrial fibrillation: Data from wearable fitness trackers
2020, Heart RhythmCitation Excerpt :Comorbid health conditions were identified via patient-administered surveys using the HeH online platform. Although it is possible that these data are less reliable than data obtained from direct medical examination or chart analysis, previous analyses have shown a high accuracy between HeH participant self-report and primary medical record review.16 Furthermore, to result in a false-positive finding, misclassification of these comorbidities would need to correlate with step count.
Dr Marcus has received research support from the NIH, PCORI, SentreHeart, Medtronic, and Pfizer and is a consultant for and holds equity in InCarda. This research was made possible in part by the Clinical and Translational Research Fellowship Program, a program of the University of California, San Francisco’s (UCSF) Clinical and Translational Science Institute (CTSI) that is sponsored in part by the National Center for Advancing Translational Sciences, National Institutes of Health (NIH), through UCSF-CTSI Grant Number TL1 TR000144 and the Doris Duke Charitable Foundation (DDCF). The contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH, UCSF, or the DDCF.