It has traditionally been taught that it is inadvisable to lower blood pressure (BP) acutely in both acute ischemic and hemorrhagic stroke.1,2 The acute lowering of BP following acute stroke can reduce cerebral perfusion and may result in worsening of neurologic status. Consensus guidelines recommend that BP not be decreased acutely in ischemic stroke unless BP is very high (systolic BP >220 mm Hg or diastolic BP >120 mm Hg) or the patient has active coronary artery disease, congestive heart failure, or aortic dissection; when indicated, BP should be lowered cautiously by about 15% during the first 24 hours.2–4 The American Heart Association/American Stroke Association published guidelines in 2007 that recommend that antihypertensive medications may be restarted relatively safely 24 hours after cerebrovascular accident onset in patients with preexisting hypertension and patients who are neurologically stable, unless a specific contraindication to treatment is identified.4 Candidates for lytic therapy with acute ischemic stroke should have their BP maintained at <180/105 mm Hg for at least 24 hours after intravenous tissue plasminogen activator therapy.4 Three observational studies have shown that lowering BP acutely after acute ischemic stroke onset can have adverse outcomes.1,5,6 Odds ratios of poor outcome were similar in the first 2 studies, 1.9 per 10% decrease in systolic BP (95% confidence interval, 1.02–3.52) in a Brazilian study1 and 3.8 for a >25% reduction in diastolic BP (95% confidence interval, 1.2–12.1) in an Austrian study.5 A third study, from Spain, showed that a decrease in systolic BP of >20 mm Hg in the first day was the most important variable associated with neurologic deterioration and poor outcomes.6 Intracerebral hemorrhage (ICH) guidelines differ slightly. Here it is recommended that decreases in BP may be beneficial by minimizing further bleeding and continued vascular damage and that systolic BP should be maintained between 140 and 160 mm Hg; patients should be monitored for signs of cerebral hypoperfusion.7,8 Two recent studies presented at the 2008 International Stroke Conference in abstract form challenge these BP-lowering premises after acute stroke. Physicians from the United Kingdom presented the Control of Hypertension and Hypotension Immediately Post-Stroke (CHHIPS) pilot study.9 In the CHHIPS study, 179 patients with acute ischemic or hemorrhagic stroke within the prior 36 hours and a systolic BP >160 mm Hg were randomized to receive lisinopril, labetalol, or placebo. Doses of the drugs were increased over 14 days. Participants in the 3 groups were similar with regard to age, baseline BP level, stroke type, time to treatment, and prevalence of dysphagia. Patients who received one of the active treatment regimens had a greater decline in systolic BP during the first 24 hours compared with those who received placebo. After 2 weeks, BP declines were significantly greater in participants receiving active treatment than in the placebo group (31 mm Hg compared with 24 mm Hg). Three months after treatment began, the active treatment group had a lower mortality compared with the placebo group. The patients in the placebo group were 2.2 times more likely to die than those in the treatment group.10 Obviously, larger, more definitive studies are needed to confirm this information. Another study looked at acute lowering of BP in acute hemorrhagic stroke. Researchers in the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT) enrolled 44 patients from 44 hospitals in China, Korea, and Australia.11 Adult patients with acute hemorrhagic stroke on computed tomography (CT) with elevated systolic BP values of 150 to 220 mm Hg were studied. Each patient was in a monitored setting within 6 hours of the acute ICH. Patients were randomly assigned to receive either intensive antihypertensive treatment based on available intravenous agents or less intensive treatment, based on American Heart Association guidelines. The BP goal in the first group was a decrease in systolic BP to 140 mm Hg; the target in the second group was 180 mm Hg. After the first hour, systolic BP was an average of 13.3 mm Hg lower in the intensive group. Average hematoma growth was 22.6% lower in the intensive group than in the group in which guidelines were followed, after adjusting for initial hematoma volume and time from onset of ICH to CT. This was equated to 2.5 mL less blood in the brain. Frequency of substantial hematoma growth, defined as ongoing bleeding of more than one-third of the initial volume, was 36% lower in the intensive treatment group than in the guideline group. There was no evidence that early intensive BP lowering increased the risks of serious adverse events or resulted in a poor outcome at 90 days. The results of INTERACT suggest that drug therapy to lower BP can be given quickly and safely to patients with ICH. Both of these studies represent small pilot studies presented at meetings and are not yet peer-reviewed. They do, however pique one's interest in seeing well-done studies applied to the acute stroke situation. We look forward to seeing the full data in printed form.