Atrial fibrillation: An additional cardiovascular detrimental effect of stress at work?

More and more evidence accumulates on the association between job strain – work stress – and cardiovascular diseases (CVDs). The cumulative meta-analysis of cohort studies published up to 2014 indicates a risk excess of 33% for coronary heart disease (CHD) and of 24% for ischaemic stroke among high strain versus non-high strain workers.1 The hazard ratio of high strain versus non-high strain increases up to 1.81 (95% confidence interval (CI): 1.21–2.69) when the analysis is restricted to salaried manual and non-manual workers.2 Moreover, when the psychosocial work environment is investigated using both the demand–control and the imbalance between effort and reward models, the first referring to the content of the work tasks and the second to its recognition, the CHD excess risk increases to 41% when both stressors are present together on the same subject.3 Finally, the two major stress-related work organization conditions, that is, long working hours and shift work, are also independently associated with CHD and ischaemic stroke risk.1,3 In this issue of the European Journal of Preventive Cardiology, Eleonore Fransson and colleagues, using a large Swedish longitudinal cohort, the SLOSH study, find ‘an almost 50% increased risk of atrial fibrillation’ again when high versus non-high job strain subjects are compared.4 The excess risk reduces somewhat when adjusting for multiple CVD risk factors, but, as we know, this may represent an over-adjustment as job strain is related to some of them, in particular type II diabetes mellitus1 and hypertension.5 The paper, combining the results of other two Swedish studies,6,7 using a fixed-effect meta-analysis, estimates a pooled hazard ratio of 1.37 (95% CI: 1.13–1.67) for atrial fibrillation when comparing high versus non-high job strain. The adaptation of humans to psychological stress involves the reactions of the hypothalamic–pituitary–adrenal axis, with increased release of cortisol, and of the autonomous nervous system (ANS), with increased sympathetic activity in healthy patients8 and in patients with cardiovascular diseases.9 The mechanisms linking psychological stress to increased atrial fibrillation risk have not been thoroughly investigated so far.10 It has been hypothesized that the alterations of the ANS can induce the atrial arrhythmogenesis either through a lack of cardiac control, due to an increased sympathetic tone and decreased vagal tone that can trigger atrial fibrillation,11 or through focal ectopic firing and vulnerable substrates that can maintain the re-entry.11 In this context, prolonged job strain has been found to produce persisting modifications of time- and frequency-domains of heart rate variability: alterations of the high- and low-frequency powers inducing a reduction in the vagal control of the heart rate that may play an intermediate role in the relation between work stress and the cardiovascular system.12 Further pathways linking stress to atrial fibrillation can be represented by the inflammatory state, commonly detected among workers exposed to prolonged stress,13 which may lead to structural remodelling of the atria and hence to atrial fibrillation progression and persistence.14 Finally, hypertension, a possible outcome of prolonged stress conditions, can promote the onset and the maintenance of atrial fibrillation through structural and electrical atrial remodelling.15 Conversely, it has been shown that hypertensive control reduces the onset of atrial fibrillation.16 Finally, it is worth mentioning that when using the non-high strain category as reference to estimate the risk excess of high strain subjects, the results are likely biased to the null. In fact, the non-high strain group combines workers with low job strain (low demand and high control at work), but also people with only one strain condition of the two dimensions of the Karasek’s job content questionnaire: active (high psychological job demand) and passive (poor control) workers. In our study linking job strain and CHD in manual and non-manual workers of diverse job titles, the high strain group in comparison with the low strain group showed a hazard ratio of 2.94. The same results were obtained by the study of Fransson et al., with atrial fibrillation as the endpoint.4 Therefore, the choice of non-high as the reference category may determine an underestimate of the detrimental effects of work stress on the cardiovascular system.2 In conclusion, more and more evidences are accumulating showing that work stress and working conditions, including job strain, effort–reward imbalance, long working hours and shift and night work, are main life-threatening risk factors for different CVD outcomes in the working population. Further researches are needed to explore the attractive theory that the same pathways involved in work stress may produce, in differently susceptible individuals, specific phenotypical consequences on the cardiovascular system. In this line, mental stress inducing left ventricular dysfunction has shown an association with adverse outcomes in CHD patients.17 The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The author(s) received no financial support for the research, authorship, and/or publication of this article.