Background Depression is a risk factor for coronary heart disease (CHD), but less is known whether genetic susceptibility to CHD or regional-level social indicators modify this association.
Methods Risk factors of CHD including a Polygenic Risk Score (PRS) were measured for 19 999 individuals residing in Finland in 1997, 2002, 2007 and 2012 (response rates 60%–75%). During the register-based follow-up until 2015, there were 1381 fatal and non-fatal incident CHD events. Unemployment rate, degree of urbanisation and crime rate of the municipality of residence were used as regional level social indicators. HRs were calculated using register-based antidepressant purchases as a non-reversible time-dependent covariate.
Results Those having depression and in the highest quartile of PRS had somewhat higher CHD risk than predicted only by the main effects of depression and PRS (HR for interaction 1.53, 95% CI 0.95 to 2.45). Depression was moderately associated with CHD in high crime (HR 1.51, 95% CI 1.20 to 1.90) and weakly in low crime regions (HR 1.07, 95% CI 0.86 to 1.33; p value of interaction=0.087). Otherwise, we did not found evidence for interactions.
Conclusions Those having both depression and high genetic susceptibility need a special attention in healthcare for CHD.
- chd/coronorary heart
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Contributors KS drafted the manuscript. KK conducted the statistical analyses. AH, SR and VS collected the data. KS, KK, HL and PM designed the study. KK, HL, AJ, AH, SR, VS, GDS and PM revised the manuscript for important intellectual content. All authors participated in interpretation of the data, have approved the submitted version of the manuscript and agree to be accountable for all aspects of the work.
Funding PM was supported by grants 1308247 and 1294861 from the Academy of Finland, and a HORIZON 2020 research and innovation action award number 667661 from the European Commission MINDMAP project versus was supported by the Finnish Foundation for Cardiovascular Research. GDS works in the Medical Research Council Integrative Epidemiology Unit at the University of Bristol MC_UU_00011/1. AH was supported by the Academy of Finland (grant 321356).
Competing interests VS reports personal fees from Novo Nordisk and Sanofi for consulting and grants from Bayer outside this work.
Provenance and peer review Not commissioned; externally peer reviewed.
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