Abstract

Persistence of the controversy over whether hypertension should be treated in acute ischemic stroke is a testament to the power of tradition and authority in medicine. It also probably reflects the tendency of physicians to be unduly influenced by the most recent adverse events that they remember in their own patients.1 Concern about worsening of stroke with excessive lowering of blood pressure has been based to a large extent on inappropriate historical hypotensive therapies that cannot be controlled, such as “sublingual” nifedipine or intramuscular hydralazine.2 As I pointed out with Del Maestro in 1985,3 there are some circumstances in which severe hypertension must be treated in acute ischemic stroke. Two examples I have seen are aortic dissection picking off a renal and a carotid origin, with sudden severe renovascular hypertension, hypertensive encephalopathy in the territory of the patent carotid artery, and ischemia in the territory of the occluded internal carotid, and severe hypertension with acute pulmonary edema in the setting of myocardial ischemia, with acute embolic stroke from the myocardial infarction. The question, therefore, is not whether hypertension should be treated in the setting of acute cerebral ischemia but when and how. Since the publication of the National Institutes of Health trial of recombinant tissue plasminogen activator for acute stroke,4 treating hypertension in acute stroke has …

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