Parental smoking increases AF risk in offspring
Childhood Tobacco Smoke Exposure and Risk of Atrial Fibrillation in AdulthoodLiterature - Groh CA, Vittinghoff E, Benjamin EJ et al., - J Am Coll Cardiol 2019: 74(13). DOI: 10.1016/j.jacc.2019.07.060
Introduction and methods
Several large epidemiological studies have described an association between cigarette smoking and incident atrial fibrillation (AF), with estimates that up to 7% of all AF can be attributed to smoking [1-3]. The authors of the current study have previously published that exposure to cigarette smoke while in utero or as a child may increase AF risk later in life . If true, these findings may form a motivation for smokers to quite and for potential smokers not to start. Moreover, findings may point to new mechanistic pathways involved in AF pathogenesis. The study mentioned relied on self-reported cigarette smoke exposure, thus recall bias may have been at play.
This study therefore used data from the multi-generational Framingham Heart Study [5,6] to test the hypothesis that parental smoking predicts offspring AF. To this end, data of all Framingham Offspring cohort participants with at least 1 parent in the Original cohort with a known smoking status at any point until the offspring turned 18 years old, were used. The Offspring cohort was started in 1971. The Original cohort was evaluated approximately every 2 to 4 years and the Offspring cohort every 4 to 8 years. During interexam periods, participants were under routine surveillance for CV outcomes through review of outside medical records and physician visits. The most recent examination period for both cohorts concluded in 2014. Parental smoking ascertainment data was available for 2816 (out of 5124) participants in the Offspring cohort, of whom 82% was exposed to secondhand smoke at some point during childhood.
- Median number of parental cigarettes smoked daily in the exposed group was 0.5 packs (IQR: 0.07 – 1 pack/day), which is similar to 10 cigarettes/day.
- 404 (14.3%) Of Offspring participants developed AF during a median follow-up of 40.5 years (IQR: 33.3 to 41.9 years). Overall incidence rate was 4.02 per 1000 person-years.
- The cumulative incidence curves showed higher adjusted AF rates with higher smoke exposure. After multivariable adjustment, an 18% higher AF incidence in Offspring was seen for every pack/day increase in parental smoking.
- After adjusting for AF risk factors, parental smoking was associated with a significantly higher odds of smoking in offspring (AdjOR: 1.34, 95%CI: 1.17-1.54, P<0.001). Also, smoking in offspring was associated with 32% higher AF incidence (AdjHR: 1.32, 95%CI: 1.11-1.56, P=0.002).
- Adjusting the indirect pathway of exposure to parental smoke for offspring smoking, showed an attenuated association between parental smoking and offspring AF (HR: 1.15, 95%CI: 0.98-1.35, P=0.10), and offspring smoking mediated 17% (95%CI: 1.5% to 103.3%) of this relation.
This analysis in the Original and Offspring Cohorts of the Framingham Study shows that parental smoking is associated with a higher risk of AF in offspring. Part of this relation seems to be mediated by a greater propensity for offspring to smoke themselves, after having been exposed to smoke in childhood.
Alanna Chamberlain  sees a unique advantage in the design of this analysis in the linkage of smoking data in the parents until the offspring reached 18 years of age, and extensive follow-up of the offspring for ascertainment of AF events. A limitation is that 45% of participants in the Offspring cohort, data on parental smoking status were missing, and these participants were excluded from the analysis. The authors explain that smoking ascertainment was not performed between 1948 and 1955, when there was no awareness of the harmful effects of smoking. Indeed, temporal trends in behaviour and attitudes about smoking, and the amount and type of cigarettes smoked could affect risk over time, and may have affected these results. The findings also raise the question how either direct or secondhand exposure to other tobacco products influences AF risk.
Chamberlain notes that more smoking cessation may have downstream effects on smoking initiation in offspring, as the study showed that offspring are more likely to smoke if their parents did. Clinicians should therefore not miss an opportunity to discuss the harms of both tobacco use and of secondhand smoke with their smoking and non-smoking patients. The current study emphasizes the importance of managing modifiable risk factors, which includes secondhand smoke, to reduce the risk of AF.