Abstract
Managing hypertension after acute stroke has been a longstanding, and still ongoing, controversy. On the one hand, clinical studies are near consistent in showing positive relations between increasing blood pressure (BP) and adverse outcomes in both acute ischemic stroke (AIS) and intracerebral hemorrhage (ICH), which supports pathophysiological mechanisms of hypertension-induced endothelial stress and blood-brain barrier disruption.1 Conversely, randomized controlled trials of BP lowering have shown variable results in mixed and pathologically distinct stroke subtypes,2-4 which has fuelled debate over the potential for adverse effects of such treatment when cerebral autoregulation and collateral blood flow are disrupted by ischemia.
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