C-reactive protein and prospective cardiometabolic risk: observational and Mendelian randomization study of ischemic stroke and all-cause death
Authors' conclusion
In this observational and one- and two-sample Mendelian randomization study, we found that elevated CRP concentrations above the population median of 1.4 mg/L predicted risk of ischemic stroke and all-cause death. There was no causal genetic effect of C-reactive protein on risk of stroke or all-cause death.
Study context
- Population
- General population: Copenhagen City Heart Study and Copenhagen General Population Study; two-sample MR in up to 575,531 individuals from CHARGE CIWG, UKBB, FinnGen and MEGASTROKE
- Participants
- 113,491 individuals
- Exposure
- Higher vs lower plasma C-reactive protein (CRP) concentrations
- Outcome
- Ischemic stroke and all-cause death
Methodological detailsone-sample Mendelian randomization, two-sample Mendelian randomization
- One-sample Mendelian randomization
- Two-sample Mendelian randomization
Main finding
As reported in the abstract
Higher CRP associated with stepwise higher risk of ischemic stroke; highest HR
1.51 (1.34, 1.71) (95% CI)
Higher CRP associated with stepwise higher risk of all-cause death; highest HR
1.69 (1.60, 1.79) (95% CI)
Observational data: associations, not effects.
Further findings
Cumulative incidence, CRP ≥ 2 mg/L vs < 2 mg/L
- Ischemic stroke at age 72: higher with CRP ≥ 2 mg/L
- 57% higher
- All-cause death at age 80: higher with CRP ≥ 2 mg/L
- 62% higher
Causal effect of CRP (one- and two-sample MR, studies combined)
- Ischemic stroke, OR (95% CI); no causal effect supported
- 1.01 (0.98, 1.05)
- All-cause death, OR (95% CI); no causal effect supported
- 1.01 (0.98, 1.05)
Original publication
Composed by AI from the published abstract and checked against it. How Briefs are made →