Psychological distress and cardiovascular disease: An investigation into the epidemiological evidence
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2020
Authors
Welsh, Jennifer
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Cardiovascular disease (CVD) is a leading cause of death and a large contributor to disease burden globally. People with symptoms of depression and anxiety (referred to as psychological distress) have an elevated risk of developing CVD and poorer prognosis once it is present. However, the nature of this association remains poorly understood and contested. Therefore, the most effective points of intervention to reduce CVD burden for this group are also unclear.
This thesis had two broad aims. First, to contribute to the evidence regarding the independent association between distress and incident CVD by investigating the impact of two common sources of bias. Second, to quantify gaps in CVD preventive treatment to identify opportunities to reduce CVD incidence and improve outcomes for people with distress.
To address my first aim, I performed three longitudinal studies. First, I examined the extent to which confounding by physical morbidity overestimates the independent distress-incident CVD association using data from the 45 and Up Study linked to hospitalisation and death records. I found that when restricted to respondents with no or low levels of physical morbidity, the higher rate of CVD associated with higher distress attenuated substantially, suggesting at most, a weak independent distress-CVD association.
In studies two and three, I examined the extent to which assessment of distress at a single time point underestimates the independent distress-incident CVD association. I found broad agreement between measures of distress over time using biennial data covering 10-years from the Household, Income and Labour Dynamics of Australia Survey. Using linked 45 and Up Study data, I found that measures of longer-term high distress were associated with a similar elevation in CVD risk relative to single assessments of high distress. However, longer-term high distress was not associated with elevated incident CVD risk after considering personal, behavioural and physical health-related risk factors, also indicative of no, or only a weak, independent distress-CVD association.
To address my second aim, I undertook three studies. I examined gaps in primary prevention using data from the 2011-12 Australian Health Survey. The prevalence of high absolute primary CVD risk was higher in those with high compared to low distress, reflecting a poor CVD risk factor profile in this group. Treatment of high absolute risk was low overall, but did not vary in relation to distress.
The final two studies examined secondary prevention using 45 and Up Study data linked to hospital and pharmaceutical records. Among respondents admitted to hospital with incident diagnosis of ischaemic heart disease, rates of coronary procedures were generally lower in people with higher compared to lower levels of distress. Among participants with a history of ischaemic heart disease or ischaemic stroke, use of guideline-recommended medications for secondary CVD prevention was lower for those with higher psychological distress.
The evidence generated in this thesis suggests that psychological distress might best be considered a marker of CVD risk, rather than a risk factor. Furthermore, the observed gaps in preventive treatments represent opportunities to reduce the disproportionately high rate of CVD events among people with distress.
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