High blood pressure (BP) is present in 80% of patients with acute ischaemic stroke and is independently associated with poor outcome. Although this epidemiology suggests that BP should be lowered acutely, concerns about dysfunctional cerebral autoregulation suggest otherwise. Several small randomised trials have assessed cerebral blood flow with various antihypertensive classes and agents in acute ischaemic stroke. Overall, these studies showed no change in cerebral perfusion, although the numbers of studies and patients are limited and there are methodological problems with some trials. There are no large published randomised trials assessing outcome with BP lowering in acute stroke. Calcium channel blockers did not alter outcome after ischaemic stroke (29 trials, 7,665 patients). However, some trials, especially those testing intravenous calcium channel blockers (INWEST) or oral beta-receptor antagonists (BEST) reported real or potential hazard. In contrast, oral candesartan reduced combined vascular events in 339 patients with ischaemic stroke (ACCESS) although it had no effect on disability. The CHHIPS trial found that death was reduced in patients randomised to active treatment (labetalol, lisinopril) as compared with placebo. Two larger trials reported that glucose-potassium-insulin therapy (GIST) or magnesium (IMAGES) lowered BP but had no effect on functional outcome. The INTERACT pilot trial studied patients with intracerebral haemorrhage and found that an intensive BP-lowering regime non-significantly reduced haematoma expansion. There are four large ongoing trials examining whether to continue or stop pre-stroke antihypertensive therapy (COSSACS, ENOS) or lower BP in acute stroke (ENOS, SCAST) or haemorrhage (INTERACT 2).
(c) 2009 S. Karger AG, Basel.