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Stroke Alert: A Review of Current Clinical Stroke Literature
By Matthew E. Fink, MD, Interim Chair and Neurologist-in-Chief, Director, Division of Stroke & Critical Care Neurology, Weill Cornell Medical College and New York Presbyterian Hospital
Stopping Aspirin May Increase Stroke Risk
Source: Rodriguez LAG, Soriano LC, Hill C, et al. Increased risk of stroke after discontinuation of acetylsalicylic acid. A UK primary care study. Neurology 2011;76:740-746.
The Health Improvement Network UK Primary Care Database was queried for all patients aged 50-84 who were prescribed low-dose aspirin (75-300 mg/day) for the secondary prevention of cardiovascular disease in 2000-2007. The study followed 39,512 individuals for a mean of 3.4 years to identify cases of ischemic stroke (IS) or transient ischemic attack (TIA), and a nested case-control analysis was used to assess the effects of aspirin discontinuation.
The overall incidence of IS or TIA was 5 per 1000 person-years, and was more common in patients with a previous history of cerebrovascular disease or atrial fibrillation. Compared with current users of low-dose aspirin, those who stopped treatment 31-180 days before the index date had a significantly increased risk of IS or TIA (relative risk = 1.40; 95% confidence interval [CI] 1.03-1.92). In conclusion, in patients prescribed low-dose aspirin for secondary prevention of cardiovascular events, discontinuation of aspirin was associated with a 40% increase in the risk of IS or TIA.
Warfarin Withdrawal Before Thrombolytic Therapy May Worsen Neurological Outcome
Source: Kim YD, Lee JH, Jung YH, et al. Effect of warfarin withdrawal on thrombolytic treatment in patients with ischemic stroke. European J Neurol 2011;doi:10.1111/j.1468-1331.2011.03363.x.
Sudden withdrawal of warfarin therapy is associated with a rebound prothrombotic state. In addition, thrombolytic drugs may paradoxically induce a prothrombotic condition, including platelet activation and thrombin generation. There is a theoretical risk of recurrent thrombosis after Continued on page 61 thrombolytic therapy in the setting of warfarin withdrawal, and these investigators from Seoul, Korea, sought evidence for this hypothesis. They compared the results of intravenous thrombolysis on 148 consecutive ischemic stroke patients with atrial fibrillation to a group of 14 patients who had warfarin withdrawn about 10 days before stroke occurred, because of a scheduled interventional procedure or due to patient choice.
There were no differences between groups in baseline NIH Stroke Scale (NIHSS) scores, recanalization rates, and hemorrhage frequencies, but the warfarin withdrawal group showed poorer outcomes. Increased NIHSS scores during the first 7 days were more frequent in the warfarin withdrawal group, and the median percent improvement in scores at 24 hours after thrombolysis was lower in the warfarin withdrawal group. Warfarin withdrawal was a strong predictor of poor functional outcome at 3 months (OR = 17, 95% CI 2.7-107.7).
Hyperglycemia Is Associated with Cerebral Hematoma Expansion
Source: Liu J, Gao BB, Clermont AC, et al. Hyperglycemia-induced cerebral hematoma expansion is mediated by plasma kallikrein. Nature Medicine 2011;17:206-210.
Intracerebral hemorrhage (ICH) accounts for about 10% of all strokes and has a high case fatality rate (40%-50%). Both diabetes and admission hyperglycemia are independently associated with early and long-term mortality. In addition, hyperglycemia is associated with symptomatic ICH in patients treated with intravenous tissue plasminigen activator (TPA). The investigators studied the possible mechanisms by which hyperglycemia might cause hematoma expansion in an experimental ICH animal model with hyperglycemic rats and diabetic mice.
Hematoma expansion after intracerebral injection of autologous blood, was greater in hyperglycemic animals than in normoglycemic animals, and this expansion was ameliorated by inhibition of plasma kallikrein. The investigators showed that plasma kallikrein inhibits collagen-induced platelet aggregation by binding collagen, and this response is enhanced by elevated glucose concentrations. This effect could be mimicked by infusing mannitol, further suggesting that the effect is due to a plasma kallikrein-mediated osmotic-sensitive inhibition of hemostatis. These experimental observations should be tested with clinical treatment trials of hyperglycemia in patients with ICH.