# Association of CRP levels and clinical and radiological outcomes in patients with large-vessel occlusion stroke: A MR CLEAN Registry study

**Authors:** Yan Wang, Sven P R Luijten, Daniel Bos, Inge A Mulder, Manon Kappelhof, Willeke F Westendorp, Bart J Emmer, Stefan D Roosendaal, Yvo B W M Roos, Ido R van den Wijngaard, Robert J van Oostenbrugge, Diederik van de Beek, Jonathan M Coutinho

PMC · DOI: 10.1093/esj/23969873251357134 · European Stroke Journal · 2026-01-01

## TL;DR

This study found no link between CRP levels and outcomes in stroke patients treated with endovascular therapy.

## Contribution

The novel contribution is the first comprehensive analysis of CRP's role in outcomes for large-vessel stroke patients undergoing endovascular therapy.

## Key findings

- CRP levels above 3.0 mg/L were not associated with worse clinical outcomes in stroke patients.
- No significant association was found between CRP levels and radiological outcomes or mortality.
- Atrial fibrillation patients had higher CRP levels compared to other subgroups.

## Abstract

Inflammation is important in the pathogenesis of acute ischemic stroke (AIS). The association between CRP and outcomes in patients with large vessel occlusion (LVO) stroke receiving endovascular therapy (EVT) has not been fully elucidated.

We used data from the MR CLEAN Registry (2014–2017), including LVO-AIS patients with intracranial carotid atherosclerotic disease (ICAD), extracranial carotid atherosclerotic disease (ECAD) or atrial fibrillation (AF). The primary outcome was modified Rankin Scale (mRS) score at 90 days. Secondary outcomes included mRS ⩾3 at 90 days, all-cause mortality, successful recanalization, and symptomatic intracranial hemorrhages. CRP was analyzed both dichotomously (>3.0 vs ⩽3.0 mg/L) and continuously, using multivariable regression adjusted for potential confounders.

Among 865 included patients (ICAD: 286; ECAD: 154; AF: 425), median CRP level was 3.4 mg/L (IQR: 2.0–6.1) and 446 patients had elevated CRP (>3.0 mg/L). AF patients had higher CRP than ICAD and ECAD patients (4.0–3.0–3.2 mg/L, p = 0.002). CRP >3.0 mg/L was not associated with mRS in the full cohort (acOR 0.983, 95% CI (0.767, 1.260)) or in any etiological subgroups (ICAD: acOR = 0.968, 95% CI (0.626, 1.496), ECAD: acOR = 1.114, 95% CI (0.617, 2.012), AF: acOR = 0.937, 95% CI (0.653, 1.344)). There was also no association between CRP and any of the other outcomes. When analyzed as a continuous variable, CRP was also not associated with any other outcomes.

We did not observe an association between CRP levels and clinical and radiological outcomes after LVO stroke.

Graphical abstract

## Linked entities

- **Diseases:** atrial fibrillation (MONDO:0004981)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** intracranial hemorrhages (MESH:D020300), AIS (MESH:D000083242), Inflammation (MESH:D007249), AF (MESH:D001281), LVO (MESH:C536223), stroke (MESH:D020521), ECAD (MESH:D002340)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12866208/full.md

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Source: https://tomesphere.com/paper/PMC12866208