Controlling BP in the acute stroke phase

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The theory that elevated systemic BP may compensate for the decreased cerebral blood flow in the ischemic region led to attempts to elevate blood pressure as a treatment for acute ischemic stroke. The hemody-namic and metabolic impact of pharmacologically increased systemic blood pressure on the ischemic core and penumbra was evaluated in rats. The mild induced hypertension was found to increase collateral flow and oxygenation and to improve cerebral metabolic rate of oxygen in the core and penumbra [12]. Several small studies in humans have addressed this question and administered vasopressors, including phenylephrine and norepinephrine, to patients with acute stroke [13-15]. Despite a documented improvement in CBF [16], the concept was abandoned because of the increased risk of hemorrhage and brain edema. In a systemic review of 12 relevant publications including 319 subjects, the small size of the trials and the inconclusive results limit conclusion as to the effects on outcomes, both benefits and harms. A randomized controlled trial is needed to determine the role of pressors in acute ischemic stroke [17].

Elevated systemic BP may compensate for the decrease of cerebral blood flow in the ischemic region, but raises the risks of hemorrhagic transformation, cerebral edema, recurrence of stroke and hypertensive encephalopathy.

According to a systematic review of the literature [3] no conclusive evidence to support the lowering of blood pressure in the acute phase of ischemic stroke was found and more research is needed to identify the effective strategies for blood pressure management in that phase [3]. Despite the controversy over the management of BP in the acute phase, the benefit of blood pressure reduction as a secondary prevention of stroke is well established and has been demonstrated in many studies. However, in most of these studies antihypertensive agents were administrated several weeks after stroke onset. Only a few trials were performed in the acute stage. The ACCESS trial [18] was a prospective, double-blind, placebo-controlled, randomized study evaluating the angiotensin receptor blocker candesartan vs. placebo for 342 hypertensive patients in the first week following stroke. Treatment was started with 4 mg candesartan or placebo on day 1 and dosage was increased to 8 or 16 mg candesartan or placebo on day 2, depending the blood pressure values. Treatment was aimed at a 10-15% blood pressure reduction within 24 hours. Although no difference was found in stroke outcome at 3 months, a significantly lower recurrent cardiovascular event rate and lower mortality after 1 year were documented in the treatment group. The authors concluded that when there is need for or no contraindication against early antihypertensive therapy, candesartan is a safe therapeutic option.

In the UK's Control of Hypertension and Hypotension Immediately Post-Stroke (CHHIPS) pilot trial [19], researchers randomized 179 patients who had suffered ischemic or hemorrhagic strokes within the previous 36 hours and who also had hypertension defined as systolic blood pressure greater than 160 mmHg. Patients received doses of either the anti-hypertensive drugs lisinopril at a dosage of 5 mg or labetalol at a dosage of 50 mg or a placebo at increasing doses for 14 days. Three months after treatment began, the active treatment group had a significantly lower mortality compared to the placebo group.

Despite the somewhat confusing and unclear data the current European Stroke Organisation (ESO) 2008 Guidelines [20] recommend that blood pressure up to 220 mmHg systolic or 120 diastolic may be tolerated in the acute phase without intervention unless there are cardiac complications. According to the American guidelines [21] it is generally agreed that patients with markedly elevated blood pressure may have their blood pressure lowered by not more than 15% during the first 24 hours after the onset of stroke. There is an indication to treat blood pressure only if it is above 220 mmHg systolic or if the mean blood pressure is higher than 120 mmHg. No data are available to guide selection of medication for the lowering of blood pressure in the setting of acute ischemic stroke. The recommended medication and doses are based on general consensus. More studies are needed to identify the optimal strategy for BP management. Several ongoing clinical trials such as the Efficacy of Nitric Oxide in Stroke (ENOS) trial may help answer the remaining questions.

Guidelines recommend blood pressure lowering therapy above 220 mmHg (European Stroke Organisation (ESO) 2008 Guidelines and American Guidelines) systolic blood pressure.

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