Ischaemic stroke polygenic risk score and recurrent cardiac and cerebrovascular events after coronary artery revascularization

Le résumé fourni par la source

Ischaemic stroke is a major cause of global morbidity and mortality and is a heritable condition influenced by both non-modifiable and lifestyle related risk factors, some of which have genetic components. Genome wide association studies have identified multiple loci associated with ischaemic stroke, enabling the development of a polygenic risk score for ischaemic stroke (PRS IS) that captures cumulative genetic susceptibility.1 Despite guideline directed medical therapy, patients with coronary artery disease (CAD) undergoing coronary artery revascularization continue to face substantial residual risk. Ischaemic stroke occurs in ∼2% to 5% of patients after percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), and 10 year all-cause mortality approaches 20% to 25%.2,3 We therefore evaluated whether higher PRS IS could serve as a potential secondary prevention marker associated with increased risks of cardio-cerebrovascular outcomes among patients with established severe CAD requiring index revascularization. All participants were drawn from the UK Biobank (UKB). Among 501 092 individuals enrolled between 13 March 2006, and 12 June 2023, those who underwent coronary artery revascularization with PCI or CABG were included. Identification of revascularization procedures was based on International Classification of Diseases, Tenth Revision (ICD-10) diagnostic codes and Office of Population Censuses and Surveys Classification of Interventions and Procedures, version 4 (OPCS-4) procedural codes. Participants were stratified into low (≤20th percentile), intermediate (21st−80th percentile), and high (≥80th percentile) PRS IS (PGS002724) groups. Outcomes included non-fatal ischaemic stroke, cardiovascular death, all-cause mortality, and repeat coronary artery revascularization. Baseline characteristics were compared using analysis of variance for continuous variables and chi squared tests for categorical variables. Time-to-event analyses used Fine Gray competing risk regression for non-fatal ischaemic stroke, cardiovascular death, and repeat coronary artery revascularization, with death as a competing event, and Cox proportional hazards regression for all-cause mortality. All models were adjusted for age at index coronary artery revascularization, sex, and genetic background using the top 10 principal components. Cumulative incidence curves accounting for competing non-cardiovascular death were generated for all non-fatal and cardiovascular outcomes.

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