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Elevated C-reactive protein and long-term mortality after ischaemic stroke: relationship with markers of endothelial
Insights
Elevated C-reactive protein (CRP) levels predict long-term mortality after ischemic stroke. This association may be linked to inflammation-induced endothelial dysfunction and platelet activation, not solely traditional risk factors.
Area of Science:
- Biomedical research
- Cardiovascular science
- Inflammation and thrombosis
Background:
- Investigates the predictive value of C-reactive protein (CRP) and complement C3 for long-term mortality following acute ischemic stroke.
- Analyzes CRP and C3 levels in 394 ischemic stroke survivors with a median follow-up of 7.4 years.
Discussion:
- CRP levels were significantly higher in non-survivors compared to survivors.
- Complement C3 levels did not show a significant difference between survivors and non-survivors.
- CRP's predictive power for mortality was independent of conventional risk factors but diminished after adjusting for markers of endothelial dysfunction and platelet activation.
Key Insights:
- C-reactive protein (CRP) is a significant predictor of long-term mortality post-ischemic stroke.
- The predictive relationship between CRP and mortality appears to be mediated by inflammation-induced endothelial cell dysfunction and platelet activation.
- Complement C3 is not a significant predictor of mortality in this cohort.
Outlook:
- Further research into the interplay between inflammation, endothelial function, and platelet activation is warranted for stroke outcome prediction.
- Exploring therapeutic strategies targeting inflammation and platelet activation could potentially reduce post-stroke mortality.
- Validation of these findings in larger, diverse stroke populations is essential.
Background And Purpose:
Inflammatory biomarkers predict development of atherothrombotic events. In the present study we examined the relationships between C-reactive protein (CRP), complement C3, and long-term mortality after acute ischemic stroke.
Methods:
CRP and C3 were analyzed by in-house enzyme-linked immunosorbent assay in 394 subjects with acute ischemic stroke who survived for >30 days, followed-up for a median of 7.4 years.
Results:
CRP was higher in subjects who died (10.8 mg/L; 95% CI, 9.1-12.8) compared with survivors (3.8 mg/L; 95% CI, 3.1-4.7), whereas C3 was similar in both groups (P=0.26). CRP remained predictive for mortality after adjusting for conventional clinical and demographic risk factors (the adjusted hazard ratio for those with CRP in the highest compared with the lowest quartile was 2.0; 95% CI, 1.3-3.1). However, CRP was no longer independently predictive of mortality after additionally adjusting for beta-thromboglobulin or von Willebrand factor.
Conclusions:
Our data suggest that the relationship between CRP and poststroke mortality may in part reflect inflammation-induced endothelial cell dysfunction and platelet activation.
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