High blood pressure (BP) is common in acute stroke and is independently associated with a poor outcome. Lowering BP might improve outcome if cerebral blood flow (CBF) is unaffected in the presence of dysfunctional autoregulation. We investigated the effect of telmisartan on systemic and cerebral haemodynamics in patients with recent stroke. Patients with ischaemic stroke (<5 days) were randomised to 90 days of telmisartan (80？mg) or placebo. CBF (primary outcome) was measured using xenon CT at baseline and 4 hours. BP and transcranial doppler (TCD) were performed at baseline, 4 hours after-treatment, and on days 4, 7, and 90. Cerebral perfusion pressure and zero filling pressure (ZFP) were calculated. Of a planned 24 patients, 17 were recruited. Telmisartan significantly accentuated the fall in systolic and diastolic BP over 90 days (treatment-time interaction , resp.) but did not alter BP at 4 hours after treatment (171/99 versus 167/87？mmHg), CBF, or CBF velocity. ZFP was significantly lower in the treatment group . Impairment at 7 days and dependency at 90 days did not differ between the groups. In this underpowered study, telmisartan did not significantly alter BP or CBF after the first dose. Telmisartan reduced BP over the subsequent 90 days and significantly lowered ZFP. This trial is registered with ISRCTN 41456162. 1. Introduction High blood pressure (BP) is common and associated independently with a poor outcome in patients with acute stroke [1–3]. However, there are no definitive data guiding the management of high BP. Individual small studies of BP modifying agents in acute stroke have indicated potential efficacy [4–6] or harm [7, 8]. A metaregression analysis of these and other trials suggested that systolic BP reductions in the order of 10–15？mmHg reduction were associated with a trend to reduced death at the end of trial, although the confidence intervals were wide and compatible with benefit or harm [9]; more extreme BP lowering or any form of BP elevation was associated with harm [3, 9]. The recently published large SCAST trial showed that candesartan only modestly lowered BP and had no beneficial effect on dependency or further vascular events [10]. Further large trials of BP lowering in acute stroke are underway including ENOS and INTERACT-2 [11]. However, since antihypertensive agents vary in their mode of action and their potential effects on cerebral blood flow, trials of individual agents may not be generalisable across all antihypertensive agents. Cerebral autoregulation is dysfunctional in acute stroke [12] and BP lowering could
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