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Work-related stress increases risk of CHD

occupational stress has often been linked to heart disease and some would consider stress an independent risk factor for CHD. Indeed, ‘stress' is often a patient's favourite suspect when faced with unexpected cardiac events.

There can be no doubt that smoking, hyperlipidaemia, hypertension, diabetes, family history and obesity increase coronary risk, but the association with stress has been more elusive. The Whitehall II study1 has now provided a clear link between chronic work stress and CHD among a population of working age. It is the first population study to show such a link.

The INTERHEART2 study, published in 2004, also found evidence of a link, but this case-control study did not attempt to explore the possible mechanisms.

The Whitehall II study was designed to assess the effect of work-related stress on CHD and provide a plausible mechanism for any observed association.

There have been many theories as to how stress could influence cardiovascular events but probably the most robust is that it involves the interplay of both biological and behavioural mechanisms. The key element to this theory is that increased and cumulative exposure to stress results in adverse neuroendocrine activation and concomitant adverse lifestyle changes, such as smoking, lack of exercise and poor diet, which in turn lead to an increased risk of cardiovascular morbidity and mortality.

The Whitehall II study recruited 10,308 London-based civil servants aged 35-55 between 1985 and 1988. Self-reported work stress was measured and standardised using the job-strain questionnaire3 on two occasions during the first five years of the study. The study population was then followed up until 2004.

Outcomes measured included behavioural risk factors, the metabolic syndrome, heart rate variability, morning rise in cortisol and incidence of CHD-related death, non-fatal MI or definite angina. The mean duration of follow-up was 12 years.

Results were adjusted for age, sex, employment grade, hypertension, total cholesterol and smoking.

The study found that chronic work stress increased the incidence of CHD, with the strongest association in those aged under 50 years at baseline (hazard ratio 1.68, 95% CI 1.17–2.42, P= <0.01). There was an increased risk in those aged 50 or over, but this was not statistically significant (hazard ratio 1.13, 95% CI 0.79-1.63, P= 0.47). Work stress was also associated with low physical activity, poor diet, the metabolic syndrome (and its individual components), lower heart rate variability and a higher morning rise in cortisol.

Overall, a third of the effect of work stress on CHD risk was attributable to its effect on health behaviours and the metabolic syndrome. However, adjusting for adverse health behaviours did not change the association between work stress and low heart rate variability, suggesting a direct effect on the autonomic nervous system and neuroendocrine function, rather than indirect effects through health behaviour.

The observed lack of a significant effect of stress on CHD risk in those aged 50 or over at baseline was attributed to a healthy worker survivor bias, retirement during follow-up and an increase in the incidence of other age-related causes of CHD.

Although we have become accustomed to looking at randomised controlled trials and meta-analyses of these to provide the most robust evidence, the value of longitudinal population-based studies must not be ignored. This was a large study and not only established a link between stress and coronary disease but also proposed that this is primarily mediated through effects on health behaviour and neuroendocrine stress pathways.

Finally, it is worth considering that people in other occupations may be exposed to even greater work-related stress and therefore, possibly, to a greater risk of CHD.


Dr Peter Savill
GPwSI Cardiology, Southampton

Chronic work stress increased the incidence of CHD, with the strongest association in those aged under 50 years

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