19ДЄ small number of studies have quantified the risk of incident CVD associated with duration of symptoms of psychological distress, finding that longer-term symptoms are associated with elevated CVD risk. The direction and magnitude of bias are difficult to predict because they depend on whether the misclassification is differential with respect to other characteristics of the respondents. 17 These findings indicate that using single assessments to indicate longer-term symptoms of distress is likely to result in a degree of misclassification, potentially biasing estimates of the distressвЂ“CVD association. 16вЂ“18 One study found that while three-quarters of people reported either consistently low (73%) or consistently high (3%) symptoms of depression over a 12-year period, a quarter had either decreasing (11%), remitting (5%) or increasing (8%) symptoms. Studies describing change in symptoms find that symptoms of distress are broadly stable over time however, a proportion of people do show variability. Whether this assumption is valid is unclear. 13вЂ“15 Given that symptoms of distress experienced for short periods are unlikely to cause disease, an implicit assumption in studies using single time-point assessments is that they can be used as proxies for the longer-term experience of symptoms. However, the course of depression and anxiety is variable: symptoms can remit, reoccur or become chronic, including with fluctuating patterns of severity. Single time-point assessments of distress are practical in large-scale cohort studies.

9вЂ“12 Most studies quantifying the distressвЂ“incident CVD association assess symptoms of distress once, with measures assessing symptoms in the previous 4вЂ‰weeks. One limitation to the current evidence relates to the way distress is measured. 8 However, whether a direct relationship exists remains uncertain, 9 at least in part due to methodological limitations to the evidence. Multiple linking mechanisms have been proposed, including genetic pleiotropy, reverse causality, a behaviour-related (eg, poor diet) pathway and a direct relationship, potentially mediated by biological changes resulting from ongoing cognitive factors (eg, excessive worry). Reasons for the elevated rates of CVD among people with distress are currently unclear. The incidence of ischaemic heart disease (IHD) and stroke is elevated by around 50% 5 6 and CVD mortality is elevated by 72% 7 in those with high compared with low levels of distress. 3 4 Given that symptoms of depression and anxiety commonly co-occur, they are often studied together and collectively referred to as psychological distress. 1 2 The burden of CVD is disproportionately high among people who experience symptoms of depression and anxiety. IntroductionД¬ardiovascular disease (CVD) is a leading contributor to fatal and non-fatal burden of disease internationally and in Australia. Our sample was restricted to participants who completed two questionnaires, and we cannot rule out that loss to follow-up biased our estimates. Using questionnaires linked to administrative data allowed for assessment of sociodemographic and health behaviours with virtually complete and objectively measured cardiovascular disease outcomes.Дespite a large sample size, we observed small numbers of outcome events in some exposure groups, limiting the precision of our estimates. We were able to use questionnaire data collected at two time-points, allowing us to ascertain a longer-term measure of psychological distress. We used data from a large-scale prospective study of people aged 45 years and over living in the general community.

Half life 2 missing information