Abstract
Inflammation following ischemic brain injury is correlated with adverse outcome. Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. We hypothesized that early treatment with ASA + ER-DP will reduce levels of MCP-1 also in patients with ischemic stroke. The EARLY trial randomized patients with ischemic stroke or TIA to either ASA + ER-DP treatment or ASA monotherapy within 24 h following the event. After 7 days, all patients were treated for up to 90 days with ASA + ER-DP. MCP-1 was determined from blood samples taken from 425 patients on admission and day 8. The change in MCP-1 from admission to day 8 did not differ between patients treated with ASA + ER-DP and ASA monotherapy (p > 0.05). Comparisons within MCP-1 baseline quartiles indicated that patients in the highest quartile (>217–973 pg/mL) showed improved outcome at 90 days if treated with ASA + ER-DP in comparison to treatment with ASA alone (p = 0.004). Our data does not provide any evidence that treatment with ASA + ER-DP lowers MCP-1 in acute stroke patients. However, MCP-1 may be a useful biomarker for deciding on early stroke therapy, as patients with high MCP-1 at baseline appear to benefit from early treatment with ASA + ER-DP.
Highlights
Considering recent findings in experimental animals and stroke patients, the extent of the secondary inflammatory response that immediately follows ischemic brain injury, is suggested to be significantly accountable for the outcome in ischemic stroke [1,2,3,4,5]
We hypothesized that early treatment with ASA + ER-DP in patients with ischemic stroke or TIA will result in reduced levels of monocyte chemotactic protein-1 (MCP-1)
A total of 425 randomized patients (220 patients assigned to early ASA + ER-DP and 205 patients to early ASA alone) with TIA/stroke were included in this sub-study of the EARLY trial
Summary
Considering recent findings in experimental animals and stroke patients, the extent of the secondary inflammatory response that immediately follows ischemic brain injury, is suggested to be significantly accountable for the outcome in ischemic stroke [1,2,3,4,5]. (MCP-1) attracts leukocytes to ischemic tissue [6]. These activated leukocytes accumulate in the cerebral microvessels and trigger the inflammatory reaction by further release of cytokines, oxygen-free radicals and proteolytic enzymes like matrix-metalloproteinases [7]. Former preclinical and clinical studies have suggested anti-inflammatory properties of dipyridamole, such as scavenging of active oxygen metabolites, reduction of the TNF-alpha and IL-8 concentration and inhibition of the adhesion of neutrophils to vascular endothelium in acute ischemic stroke patients [8,9,10,11,12,13]. We hypothesized that early treatment with ASA + ER-DP (acetylsalicylic acid + extended-release dipyridamole) in patients with ischemic stroke or TIA will result in reduced levels of MCP-1
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