Anticoagulants and Antiplatelet Agents in Acute Ischemic Stroke: Report of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the American Stroke Association (a Division of the American Heart Association)
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"Aspirin remains the cornerstone of primary and secondary stroke prevention. It reduces the risk of early recurrent ischemic stroke when given within 48 h after stroke onset (absolute risk reduction , 0.7%) . Aspirin use in early stroke treatment confers a small but statistically significant risk reduction of recurrence from 3.9% to 2.8% (p = 0.03) . "
[Show abstract][Hide abstract]ABSTRACT: Background and aim:
Stroke recurrence is an important public health concern. One half of survivors remain disabled, and one seventh requires institutional care. Aspirin remains the cornerstone of primary and secondary stroke prevention; meanwhile, aspirin resistance is one of the possible causes of stroke recurrence. We aimed to evaluate the clinical and biochemical aspirin resistance in patients with recurrent ischemic stroke.
Patients and methods:
We studied demographic characteristics, vascular risk factors, stroke subtypes, radiologic findings and biochemical aspirin resistance tests using both arachidonic acid (AA) and adenosine diphosphate (ADP)-induced light transmittance aggregometry (LTA) on admission and 24 h after observed aspirin ingestion.
Of the 82 patients with recurrent cerebral ischemia included in this study, 37 (45%) patients were poor compliant with aspirin. There were no statistically significant differences between the two groups regarding the demographic characteristics, stroke severity, laboratory tests, radiological findings or vascular risk factors. On admission, 19.6% and 4.8% of patients showed aspirin resistance, while 24 h after supervised 300 mg single aspirin dose ingestion, it was 9.8% and 2.4% using ADP and AA-induced LTA respectively. Of the eight aspirin resistant patients, two only showed resistance using both AA and ADP. Aspirin resistance was statistically significantly higher in the male gender, older age, hyperlipidemia, smokers and in all lacunar strokes using AA.
Biochemical aspirin resistance in one's series was rather rare (2.4%) and was more prevalent in patients with lacunar strokes. Clinical aspirin failure may often be contributed to poor compliance with aspirin intake.
Full-text · Article · Oct 2012 · Clinical neurology and neurosurgery
"There are several therapies for patients with ischemic stroke that have been proven in clinical trials and are recommended widely in consensus guidelines [1-3]. These include prophylaxis for deep venous thrombosis (DVT) , antithrombotic therapy within 48 hours , and antithrombotic therapy at discharge . "
[Show abstract][Hide abstract]ABSTRACT: There are several proven therapies for patients with ischemic stroke or transient ischemic attack (TIA), including prophylaxis of deep venous thrombosis (DVT) and initiation of antithrombotic medications within 48 h and at discharge. Stroke registries have been promoted as a means of increasing use of such interventions, which are currently underutilized.
From 1999 through 2003, 86 U.S. hospitals participated in Ethos, a voluntary web-based acute stroke treatment registry. Detailed data were collected on all patients admitted with a diagnosis of TIA or ischemic stroke. Rates of optimal treatment (defined as either receipt or a valid contraindication) were examined within each hospital as a function of its length of time in registry. Generalized estimating equations were used to adjust for patient and hospital characteristics.
A total of 16,301 patients were discharged with a diagnosis of stroke or TIA from 50 hospitals that participated for more than 1 year. Rates of optimal treatment during the first 3 months of participation were as follows: 92.5% for antithrombotic medication within 48 h, 84.6% for antithrombotic medications at discharge, and 77.1% for DVT prophylaxis. Rates for all treatments improved with duration of participation in the registry (p < 0.05), with the most dramatic improvements in the first year.
In a large cohort of patients with stroke or TIA, three targeted quality-improvement measures improved among hospitals participating in a disease-specific registry. Although the changes could be attributed to interventions other than the registry, these findings demonstrate the potential for hospital-level interventions to improve care for patients with stroke and TIA.
"On theoretical grounds, unfractionated heparin (UH) is given to patients with acute ischemic stroke to improve neurological outcome, prevent thrombus progression , facilitate collateral circulation, hinder the development of early stroke recurrence, and prevent deep venous thrombosis or pulmonary embolism (Sherman et al., 1995). Although some experts have warned against the use of heparin in acute stroke (Gubitz et al., 2000; Coull et al., 2002), the available information is confined to the value of unadjusted doses (from low to moderate) of subcutaneous UH (International Stroke Trial Collaborative Group, 1997). Contrarily, the value of adjusted high-dose i.v. "
[Show abstract][Hide abstract]ABSTRACT: Unfractionated heparin (UH) decreases the extent of infarction after transient focal brain ischemia in the rat and abridges neuroinflammatory damage in patients with acute stroke. This study was aimed at assessing whether controlled and steady heparinemia in plasma can reduce infarct volume and exert neuroprotective effects after ischemia. Infarct volume was measured at 24 and 7 days following a 1-hr intraluminal middle cerebral artery (MCA) occlusion in rats treated with UH or with vehicle. After testing several UH administration protocols, we choose to give a bolus of 200 U/kg, which was started 3 hr after the occlusion, followed by a 24-hr intraperitoneal perfusion of 70 U/kg/hr, which maintained a 24-hr steady plasma heparinemia (0.3-0.6 U/ml) and caused no CNS or systemic bleeding. In addition, plasma IL-10 concentration was measured by ELISA, endothelial VCAM-1 expression was evaluated by i.v. injection of a (125)I-labeled monoclonal antibody against VCAM-1, and brain hemeoxygenase-1 (HO-1) expression was determined by Western blot. UH-treated rats showed smaller infarctions than rats treated with vehicle, as well as higher IL-10 plasma levels and HO-1 brain expression and lower endothelial VCAM-1 induction. The study shows that a stable plasma concentration of UH given at nonhemorrhagic doses reduces infarct volume after ischemia-reperfusion in the rat. It also shows that UH prevented the induction of cell adhesion molecules in the cerebral vasculature and increased the expression of molecules with antiinflammatory and prosurvival properties. These findings support further testing of the clinical value of parenteral, adjusted, high-dose UH in patients with acute stroke.
Full-text · Article · Sep 2004 · Journal of Neuroscience Research