Prevention & lipidsCohort study
Autoantibodies against the chemokine receptor 3 predict cardiovascular risk
- Prospective cohort study
- population-based
- preclinical validation in ApoE(-/-) mice
Authors' conclusion
In individuals free of autoimmune disease, anti-CXCR3 aAbs were abundant, related to CV end-organ damage, and predicted all-cause death as well as cardiac morbidity and mortality in conjunction with the acceleration of experimental atherosclerosis.
Study context
- Population
- Participants of the population-based Gutenberg Health Study, free of autoimmune disease, immunomodulatory medication, acute infection and history of cancer4,195 analysed
- Participants
- 5,000 participants
- Exposure
- Anti-CXCR3 aAbs above vs below the 75th percentile
- Outcome
- All-cause mortality, cardiac death, HF and major adverse cardiac events (incident CAD, MI, cardiac death)
Main finding
As reported in the abstract
All-cause death and cardiac death (age- and sex-adjusted)
Anti-CXCR3 aAbs >75th percentile vs Anti-CXCR3 aAbs ≤75th percentileHRP value
all-cause death
1.25(95% CI 1.02–1.52)
P = 0.029cardiac death
2.51(CI 1.21–5.22)
P = 0.014Observational data: associations, not effects.
Further findings
| Outcome | HR (CI) | P value | |
|---|---|---|---|
| Major adverse cardiac events · trend | 1.42 (1.0–2.0) | P = 0.05 | |
| Incident HF · per SD increase | 1.26 (1.02–1.56) | P = 0.03 | |
| 0.512Hazard ratio (log scale) |
Cardiovascular (CV) end-organ damage
- Increasing anti-CXCR3 aAbs associated with higher intima-media thickness, LV mass and NT-proBNP, independent of age, sex, renal function and traditional CV risk factors
Experimental atherosclerosis in ApoE(-/-) mice
- Mice immunized against CXCR3 had increased anti-CXCR3 aAbs and higher atherosclerosis burden vs non-immunized controls
Original publication
Autoantibodies against the chemokine receptor 3 predict cardiovascular risk. Eur Heart J. Published 6 November 2023. doi:10.1093/eurheartj/ehad666
Summarised from the published abstract; every number is checked against it