Related Experiment Videos
C-reactive protein and outcome after ischemic stroke
1Acute Stroke Unit, University Department of Medicine, Department of Immunology, Glasgow, Scotland. k.muir@clinmed.gla.ac.uk
Insights
Elevated C-reactive protein (CRP) levels after ischemic stroke predict worse survival. Higher CRP indicates increased mortality risk, suggesting inflammation plays a role in stroke outcomes and future cardiovascular events.
Area of Science:
- Neuroscience
- Cardiology
- Inflammation Research
Background:
- Elevated C-reactive protein (CRP) is linked to ischemic cardiac events.
- Inflammation may destabilize cardiovascular disease.
- The role of CRP in acute ischemic stroke outcomes requires investigation.
Purpose of the Study:
- To examine the relationship between C-reactive protein (CRP) concentration and patient outcomes following acute ischemic stroke.
- To determine if CRP levels predict mortality after ischemic stroke.
Main Methods:
- Prospective observational study in a University Hospital Acute Stroke Unit.
- Survival time and cause of death analyzed for up to 4 years post-stroke.
- Cox proportional hazards regression used to relate CRP concentration (within 72 hours) to mortality, considering age and stroke severity.
Main Results:
- Higher CRP concentration (>10.1 mg/L) was significantly associated with worse survival (P=0.00009).
- CRP level independently predicted mortality (HR 1.23 per log unit; P=0.02), alongside age and stroke severity.
- Cardiovascular disease was the primary cause of death in both high and low CRP groups.
Conclusions:
- C-reactive protein concentration is an independent predictor of survival after ischemic stroke.
- Findings support a role for inflammation in acute ischemic stroke.
- Elevated CRP may predict future cardiovascular mortality.
Background And Purpose:
Elevated concentrations of the acute-phase reactant C-reactive protein (CRP) predict ischemic cardiac events in both hospital- and population-based studies and may signify a role for inflammation in the destabilization of cardiovascular disease. We examined the relationship between CRP and outcome after acute ischemic stroke.
Methods:
This was a subgroup analysis from a prospective observational study based in a University Hospital Acute Stroke Unit serving a population of approximately 260 000. Survival time and cause of death for up to 4 years after the index stroke were determined and related to CRP concentration within 72 hours of stroke and known prognostic variables by a Cox proportional hazards regression model.
Results:
Ischemic stroke was diagnosed in 228 of 283 consecutive admissions. Median follow-up was 959 days. Geometric mean CRP concentration was 10.1 mg/L. Survival in those with CRP >10.1 mg/L was significantly worse than in those with CRP 10.1 mg/L and 63% of deaths in those with CRP
Conclusions:
CRP concentration is an independent predictor of survival after ischemic stroke. These findings are consistent with a role for inflammation in acute ischemic stroke, as well as with the hypothesis that elevated CRP may predict future cardiovascular mortality.