Study | Population screened (cardiovascular events) | Risk assessment | Detection rate (%) | False positive rate (%) | No of patients prescribed statin | Cardiovascular events above cut-off value | Events prevented | Number needed to genotype |
Sun et al26 | 100 000 (7997) | Conventional risk factors | 60 | 24 | 26 722 | 4783 | 957 | — |
Conventional risk factors+polygenic risk score | 61 | 23 | 26 445 | 4870 | 974 | 5882 | ||
Riveros et al5 | 186 451 (4247) | QRISK3 | 81 | 42 | 79 754 | 3450 | 690 | — |
QRISK3+polygenic risk score | 84 | 41 | 78 092 | 3557 | 711 | 8879 |
Values are based on data from Sun et al26 and Riveros-Mckay et al.5 Both studies used data from UK Biobank. Sun et al developed a conventional risk factor model and examined the effect of adding polygenic risk scores for coronary artery disease (Polygenic Score Catalog identifier PGS000018) and stroke (PGS000039) on the prediction of subsequent coronary artery disease and stroke events. Sun et al used a 10 year risk cut-off value of 10% for prescribing treatment with statins. Riveros-McKay et al5 modelled screening performance in 186 451 participants based on the cardiovascular risk score, QRISK3, also with a 10% risk cut-off value for prescription of statins. Data on events reported by Riveros-Mackay et al5 were for coronary artery disease only rather than coronary artery disease and stroke. Calculations assume that all those exceeding the specified risk cut-off value receive a statin, 100% adherence, and that statin treatment produces a 20% reduction in relative risk. Counts were used to calculate number needed to genotype: number of individuals that need to be genotyped (and have a polygenic risk score calculated) to detect or prevent one additional cardiovascular event (see text).