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Published on: July 3, 2014
C-reactive protein predicts hematoma growth in intracerebral hemorrhage
Mario Di Napoli1, Adrian R Parry-Jones, Craig J Smith
1From the Neurological Service, San Camillo de' Lellis General Hospital, Rieti, Italy (M.D.N.); Neurological Section, SMDN-Center for Cardiovascular Medicine and Cerebrovascular Disease Prevention, Sulmona, L'Aquila, Italy (M.D.N., F.P.); Vascular and Stroke Centre, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Salford, United Kingdom (A.R.P.-J., C.J.S., S.J.H.); SBCHS, Manchester Metropolitan University, Manchester, United Kingdom (M.S.); Institut Català de Ciències Cardiovasculars Hospital de la Santa Creu i Sant Pau, Pavelló del Convent Sant Antoni Maria Claret, Barcelona, Spain (M.S.); Department of Internal Medicine, Cecina Hospital, Cecina, Italy (L.M.); Central Laboratory, Sanatorio Pasteur, Catamarca, Argentina (V.C.); Molecular Genetics Laboratory, Department of Human Genetics, Punjabi University, Patiala, India (P.S.); Research Center for Microscopic Morphology and Immunology & Chair of Biochemistry, University of Medicine and Pharmacy of Craiova, Craiova, Romania (A.P.-W.); Molecular Psychiatry, Department of Psychiatry, Medical University Rostock, Rostock, Germany (A.P.-W.); Department of Neurology, University of Medicine and Pharmacy, Craiova, Romania (V.T.); and Neurocritical Care Unit, Sanatorio Pasteur, and Intensive Care Unit, San Juan Bautista Hospital, Catamarca, Argentina (D.A.G.).
Background And Purpose:
Early hematoma growth (EHG) occurs in about one third of patients with spontaneous intracerebral hemorrhage. The main aim of this study was to investigate the potential of plasma C-reactive protein (CRP) for predicting EHG after acute spontaneous intracerebral hemorrhage.
Methods:
Plasma CRP was measured within 6 hours of onset (median, 120 minutes) in 399 patients with primary or vitamin K antagonist-associated spontaneous intracerebral hemorrhage and without recent infection. Computed tomography brain scans were performed at baseline and repeated within 24 hours (median, 22 hours). The primary outcome was EHG, defined as absolute growth>12.5 cm3 or relative growth>33%. Secondary outcomes included early neurological worsening (ENW) using the Glasgow Coma Scale and 30-day mortality. Multivariable regression analyses were used to evaluate associations of CRP concentration and outcomes. Kaplan-Meier analysis was used for survival.
Results:
EHG occurred in 25.8%, ENW in 19.3%, and mortality was 31.8% at 30 days. Thirty-day mortality was significantly higher in patients with ENW (hazard ratio, 3.21; 95% confidence interval, 2.00-5.17; P<0.0001) and in patients with EHG (hazard ratio, 2.13; 95% confidence interval, 1.42-3.18; P<0.0001, log-rank test). Median CRP was 12 mg/L (interquartile range, 10-17) in the EHG group and 7 mg/L (interquartile range, 4-12.1) in those without EHG (P<0.0001). In multivariable analyses, plasma CRP>10 mg/L independently predicted EHG (odds ratio, 4.71; 95% confidence interval, 2.75-8.06; P<0.0001) and ENW (odds ratio, 2.70; 95% confidence interval, 1.50-4.84; P=0.0009).
Conclusions:
CRP>10 mg/L is independently predictive of EHG and ENW, both of which are associated with increased mortality. Inflammation may be important in contributing to EHG and warrants further investigation.
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