LAUSR

After more than 50 years of empirical research, there is substantial evidence that psychosocial risk factors (PSRFs) contribute both to the risk of onset of coronary heart disease (CHD) and a worse prognosis with respect to quality of life and cardiac events. Factors such as low socioeconomic status, social isolation and lack of social support, acute and chronic stress related to both the environmental and social situation, and symptoms like depression, inappropriate anxiety or other mental disorders have been shown to increase the relative risk for cardiac events and mortality from 1.2 to 2.0. Several mechanisms have been identified that link PSRFs to increased risk in CHD: first, unhealthy lifestyles such as smoking, sedentary behaviour and unhealthy food choices are much more prevalent in people at risk and CHD patients, affected by PSRFs. Second, people and patients with PSRFs are more resistant to behaviour change, which also includes low adherence to prescribed medication. Third, several psychobiological mechanisms have been identified that may increase risk even when controlling for ‘classical’ risk factors. These mechanisms include alterations in autonomic function, in the hypothalamic–pituitary axis and in other endocrine markers, which affect haemostatic and inflammatory processes, endothelial function and myocardial perfusion. Notably, PSRFs tend to cluster in individuals and groups, which may even enhance risk. For example, the retrospective, controlled INTERHEART study on survivors of a first myocardial infarction (MI) has shown that a cluster of PSRFs (i.e. social deprivation, stress at work or in family life, and depression) was strongly associated with increased risk for incident MI (relative risk 3.5 for women and 2.3 for men). The so called ‘population attributable risk’ (a certain statistical analysis on the impact of one risk factor on the incidence of an event, controlled for other risk factors) of that cluster of PSRFs was 40% in women and 25% in men, which means that 40% and 25%, respectively, of all MIs could possibly be avoided if one could completely eliminate PSRFs. Some of the aforementioned aspects have also been shown in a substudy of the EUROASPIRE III survey (2006–2007), which included more than 8000 patients in 22 European countries, and was published in this journal. This study evaluated the impact of depressive and anxious symptoms on risk factor control six months after hospitalization for CHD. In that highly representative population, prevalence of depressive symptoms varied from 8% to 62%; anxious symptoms were assessed in 12–64% of CHD patients (depending on sex – women were nearly twice as often affected as men – and country). In general, depressive and anxious symptoms were associated with less frequent lifestyle change. In patients with depression, also higher body mass index, waist circumference and fasting glucose were observed. In this issue of the EJPC, Pogosova and coworkers report contemporary data from the EUROASPIRE IV survey, which was carried out in 2012–2013. In a subgroup of more than 7000 patients from 24 European countries, they reevaluated the prevalence of depressive and anxious symptoms, their associations with other risk factors, and treatment of depressive or anxious disorders, around 1.4 years after hospitalization for CHD. Their results replicate the high prevalence of depressive and anxious symptoms found in the EUROASPIRE III survey: depressive symptoms were assessed in 31% of women and 20% of men, anxious symptoms were found in 39% of women and 22% of men. Again, especially depression was associated with current smoking, central obesity and self-reported diabetes. In addition to the EUROASPIRE III survey, the authors for the first time also assessed treatment for depression and anxiety, which resulted in very low rates in antidepressant or anxiolytic medication at discharge from