Psychological distress and medication use for secondary prevention of cardiovascular events: Evidence from a large-scale population-based cohort study

Objective: Cardiac patients with psychological distress have a poorer prognosis than patients without distress, potentially reflecting differences in preventive care. We aimed to examine distress-related variation in guideline-recommended medication use for secondary prevention of cardiovascular disease (CVD). Methods: Baseline questionnaire data from the 45 and Up Study (collected 2006–2009) were linked to hospitalisation, pharmaceutical dispensing and death records (to exclude those who died). Among participants hospitalised with myocardial infarction, angina, stroke/transient ischaemic attack in the six years before the questionnaire, Modified Poisson regression was used to estimate relative risks (RR) for distress (Kessler 10 scores: low[10- < 12], mild[12- < 16], moderate[16- < 22] and high[22–50]) and use of both blood pressure- and lipid-lowering medications, and use of neither medication in the three months following the questionnaire, adjusting for sociodemographic and health characteristics. Results: Among 7598 participants, 34.0% had low, 35.4% mild, 18.3% moderate and 12.3% high psychological distress. Around two-thirds (63.4%) were using both medications and the proportion declined with increasing levels of distress: RRs were 1.01(95%CI:0.97–1.05), 0.95(0.90–1.00) and 0.91(0.86–0.97) for mild, moderate and high compared to low distress, respectively (p(trend) = 0.001). The proportion using neither medication was 9.1% and increased with increasing distress: RRs for mild, moderate and high compared to low distress were 0.99(0.82–1.19), 1.30(1.06–1.59) and 1.60(1.28–1.98), respectively (p(trend) < 0.001). Conclusion: Patients with psychological distress may need more support to optimise their use of secondary CVD prevention medications. Increasing the use of these medications for distressed patients may improve prognosis for patients with distress and improve population-level secondary prevention of CVD more broadly.