Our study involved several interrelated components (Fig 1). First, we constructed separate PRSs for CHD and stroke, using methods previously described [16,17]. Second, we calculated measures of risk discrimination and reclassification to quantify the incremental predictive gain with these PRSs on top of conventional risk factors. Third, to estimate the potential for disease prevention in a general population setting, we adapted (i.e., recalibrated) our findings to the context of a primary prevention population eligible for CVD screening, using incidence rates from contemporary computerised records from general practices in the UK. Fourth, we modelled the clinical implications of initiating statin therapy as recommended by current guidelines, comparing a ‘blanket’ approach (i.e., assessment of PRSs in all individuals eligible for CVD primary prevention) with a ‘targeted’ approach (i.e., focusing PRSs assessment only in people judged to be at intermediate 10-year risk of CVD after initial screening with conventional risk predictors alone). Fifth, to help contextualise the potential population health gains afforded by assessing PRSs, we compared them in the same dataset with gains afforded by assessment of CRP.

CHD, coronary heart disease; PRS, polygenic risk score.

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