Impact of Alcohol Consumption on the Outcome of Ischemic Stroke and Thrombolysis

Abstract

Background and Purpose-Tissue-type plasminogen activator (tPA) is the only acute treatment for ischemic stroke.Unfortunately, the benefit of tPA-driven thrombolysis is not systematic, and understanding the reasons for this is mandatory. The balance between beneficial and detrimental effects of tPA might explain the limited overall efficiency of thrombolysis. Here, we investigated whether this balance could be influenced by excessive alcohol intake. Methods-We used a murine model of thromboembolic stroke, coupled to an array of biochemical assays, near-infrared or magnetic resonance imaging scans, 2-photon microscopy, hydrodynamic transfections, and immunohistological techniques. Results-We found that 6 weeks of alcohol consumption (10% in drinking water) worsens ischemic lesions and cancels the beneficial effects of tPA-induced thrombolysis. We accumulate in vivo and in vitro evidence showing that this aggravation is correlated with a decrease in lipoprotein receptor-related protein 1-mediated hepatic clearance of tPA in alcoholexposed mice. Conclusions-An efficient liver-driven clearance of tPA might influence the safety of thrombolysis after stroke.

Alcohol exposure–induced neurovascular inflammatory priming impacts ischemic stroke and is linked with brain perivascular macrophages

“…Alcohol-exposed mice showed significantly larger ischemic lesions than control mice (drinking only water) 24 hours after stroke onset ( Figure 5, A-C; n = 8 mice/group; P < 0.05 vs. control) (8). These data on lesion volume are part of a previously published figure (8). No hemorrhagic transformation was detected in any mice (data not shown).…”

“…Alcohol exposure aggravates stroke lesions and exacerbates neurovascular inflammatory responses after ischemic stroke in mice. Alcohol-exposed mice showed significantly larger ischemic lesions than control mice (drinking only water) 24 hours after stroke onset ( Figure 5, A-C; n = 8 mice/group; P < 0.05 vs. control) (8). These data on lesion volume are part of a previously published figure (8).…”

“…Current clinical studies are controversial and have described either an aggravating effect (4) or no effect of HD (5) on stroke severity. Preclinical reports have also described either a protective effect of low alcohol consumption on ischemic stroke (6,7) or larger infarcts in rodents exposed to higher alcohol dose (6,8). However, the mechanisms mediating this aggravation are not well understood.…”

“…This study opens potentially new therapeutic avenues aiming at blocking alcohol-induced exacerbation of the neurovascular inflammatory responses triggered after ischemic stroke. parameters (clot formation, stability, or sensitivity to fibrinolysis) (8). On the other hand, clinical and preclinical data have shown that alcohol consumption may have an impact on inflammation (11)(12)(13).…”

The experience of using thrombolysis in patients with acute disturbances of cerebral circulation: efficacy, safety, predictors of outcome and hemorrhagic transformation

“…Основными факторами, связанными с эффективностью ТЛТ, явились возраст, курение, исходный результат шкалы Рэнкина, наличие или отсутствие острого инфаркта на первичной КТ, кардиоэмболический вариант инсульта, концентрация общего билирубина, гипертрофия миокарда, атеросклероз сонных артерий и размер очага по МРТ. В целом полученные ассоциации соответствуют данным других авторов [18][19][20][21]. Примечательно, что у пациентов с перфузионными нарушениями факторов, влияющих на исход, не обнаружено.…”