Subarachnoid haemorrhage induces an inflammatory response followed by a delayed persisting increase in asymmetric dimethylarginine

Abstract Objective. Subarachnoid haemorrhage (SAH) is associated with an inflammatory systemic response and cardiovascular complications. Asymmetric dimethyl arginine (ADMA), an endogenous inhibitor of nitric oxide synthase, mediates vasoconstriction and might contribute to cerebral vasoconstriction and cardiovascular complications after SAH. ADMA is also involved in inflammation and induces endothelial dysfunction. The aim of this study was to evaluate whether and how CRP (marker for systemic inflammation) and ADMA increased in patients during the acute phase (first week) after SAH. The ADMA level was also assessed in the patients in a non-acute phase (three months), and in healthy controls. Methods. A prospective study of 20 patients with aneurysmal SAH. ADMA and CRP were followed daily during the first week after SAH and a follow up sample for ADMA was obtained 3 months later. A single blood sample for ADMA was collected from age- and sex-matched healthy controls (n = 40, two for each case). Results. CRP increased significantly from day 2; 16 (Confidence interval (CI) 10-23) mg/L to day 4; 84 (CI 47-120) mg/L, (p < 0.01). ADMA increased significantly from day 2; 0.22 (CI 0.17-0.27) μmol/L, to day 7; 0.37 (CI 0.21-0.54) μmol/L, p < 0.01. ADMA remained elevated at a 3-month follow-up: 0.36 (CI 0.31-0.42) μmol/L. ADMA in the first sample from the patients (day 1-3); 0.25 (CI 0.19-0.30) μmol/L, was not different from ADMA in matched healthy controls; 0.25 (CI 0.20-0.31), p > 0.05. Conclusion. After SAH, CRP and ADMA in serum increased significantly during the first week and ADMA remained elevated 3 months later.