Intracranial plaque characteristics on high-resolution MRI and high-sensitivity C-reactive protein levels: association and clinical relevance in acute cerebral infarction

To investigate the association between intracranial plaque characteristics and high-sensitivity C-reactive protein (hs-CRP) levels, and their combined effects on the occurrence of acute cerebral infarction (ACI).One hundred and forty-three patients with recent ischaemic events in the territory of middle cerebral artery or basilar artery were enrolled and divided into the ACI group (n=93) and non-ACI group (n=50) according to clinical data and diffusion-weighting imaging (DWI) results. All recruited patients underwent high-resolution magnetic resonance imaging (MRI) to assess intracranial plaque characteristics, including plaque enhancement, standardised wall index, stenosis ratio, T1 hyperintense component, remodelling pattern, plaque area, plaque burden, and maximum wall thickness. hs-CRP levels were further grouped into the low group (<1 mg/l), the intermediate group (1-3 mg/l), and the high group (≥3 mg/l). Multivariate logistic regression and receiver operating characteristic curve were constructed to evaluate the association between intracranial plaque characteristics and hs-CRP levels, as well as their synergistic effects on determining the occurrence of ACI.High hs-CRP levels were associated with strong plaque enhancement (p<0.001, odds ratio [OR] = 7.497). Strong plaque enhancement (p=0.002, OR=2.109) and high hs-CRP levels (p=0.009, OR=3.893) were independently associated with the occurrence of ACI after adjustments for sex, age, and other traditional atherosclerotic risk factors. The combination of hs-CRP levels and strong plaque enhancement provided incremental information to determine ACI with an AUC of 0.823, which was significantly higher than that of strong plaque enhancement (0.711) and hs-CRP levels (0.686), respectively.High hs-CRP levels were associated with strong plaque enhancement. The synergistic effects of hs-CRP levels and strong plaque enhancement provided incremental effects on the occurrence of ACI.