Psychosocial stressors at work, including high job strain and effort-reward imbalance, may be associated with an increased risk of incident atrial fibrillation over an 18-year period, according to a prospective cohort study.
The study, published in the Journal of the American Heart Association, investigators recruited 5,926 white-collar workers (51% women with a mean age of 45.3 years) in Quebec, Canada who were free of cardiovascular disease at baseline.
At the end of the follow-up period, the mean age was 63.5 years. Nearly half (47%) of participants had a university education, 34% were sedentary, 17% were current smokers, 14% had hypertension, 2% had diabetes, and 27% had hypercholesterolemia.
Job strain, defined as high psychological demands combined with low decision latitude, was present in 19% of the participants. Effort-reward imbalance, indicating high efforts coupled with low rewards, affected 25%.
Over a mean follow-up of 18.4 years (108,952 person-years), 186 incident atrial fibrillation cases were identified through linked medical databases, yielding an incidence rate of 1.71 per 1,000 person-years. Among these cases, 34% (n = 63) of them had been diagnosed with coronary heart disease or heart failure prior to the atrial fibrillation event.
In fully adjusted Cox proportional hazards models, job strain was associated with an 83% higher risk of atrial fibrillation (hazard ratio [HR] = 1.83, 95% confidence interval [CI] = 1.14–2.92) compared with low strain. Effort-reward imbalance conferred a 44% increased risk (HR = 1.44, 95% CI = 1.05–1.98). The risk nearly doubled (HR = 1.97, 95% CI = 1.26–3.07) with combined exposure to both job strain and effort-reward imbalance. Associations remained significant after controlling for sociodemographic factors, lifestyle habits, and clinical risk factors.
Cumulative incidence curves revealed a slightly higher atrial fibrillation incidence among workers younger than 60 years exposed to either stressor. The incidence associated with combined exposure increased more steeply, reaching a similar progression after age 60.
Subgroup analyses found no statistically significant associations between passive jobs (HR = 1.12, 95% CI = 0.73–1.73) or active jobs (HR = 1.17, 95% CI = 0.76–1.82) and atrial fibrillation compared with low strain jobs.
Sensitivity analyses excluding atrial fibrillation cases in the first 5 years slightly attenuated the associations for job strain and combined exposure, but not effort-reward imbalance. Censoring at retirement yielded slightly higher point estimates. Excluding atrial fibrillation preceded by coronary heart disease or heart failure generally strengthened the associations.
Key study strengths included the prospective design, high participation rate, validated exposure assessment, and 18-year follow-up. Limitations included exposure measurement at a single timepoint and potential underdetection of atrial fibrillation using administrative data. The findings may not generalize to blue-collar workers.
The investigators discussed potential pathophysiological mechanisms linking work stress to atrial fibrillation, including autonomic nervous system activation; hypothalamic-pituitary-adrenal axis and renin-angiotensin-aldosterone system stimulation; and increased risk of hypertension, diabetes, and arterial stiffness.
"Workplace prevention strategies targeting these psychosocial stressors at work may be effective to reduce the burden associated with atrial fibrillation," the study authors concluded.
The authors declared having no competing interests.
