Cerebroprotection by hypertension in ischemic stroke: the crumbling of a hypothesis.

May not the elevation of systemic blood pressure be a natural response to guarantee a more normal circulation to the heart, brain and kidneys?”1 These words, taken from a renowned textbook of medicine, clearly illustrate that in the 1940s the teaching doctrine was to consider elevated blood pressure a compensatory mechanism serving to force blood through sclerotic arteries to the ischemic target organs. Hypertension was regarded as “essential” and therefore “should not be tampered with, even were it certain that we could control it.”2 We have since learned that hypertension is a powerful risk factor for stroke, heart attacks, and renal failure and that lowering blood pressure dramatically reduces the risk of these events. The only clinical situation in which blood pressure elevation often still is considered protective is in the sequence of an acute ischemic stroke. Indeed, authoritative voices such as that of Adams and Victor3 have warned and continue to warn against lowering blood pressure in this setting with statements such as, “We agree with Britton and colleagues that it is prudent to avoid antihypertensive drugs in the first few days unless. . .the blood pressure is high enough to pose a risk to other organs.”3 This statement can be found in the 1989 edition of this venerable neurology textbook and is repeated verbatim in every single subsequent edition until 2005. It thus has taught numerous neurologists that elevated blood pressure in the sequence of an ischemic stroke was a “noli me tangere” and that lowering blood pressure should be avoided. Because Adams and Victor obviously considered the referenced study to be definitive enough to be taught for many years, I took the liberty to look at it carefully. In their article, Britton et al4 reported on a series of 6 patients presenting with acute onset of neurological symptoms and extremely high blood pressure who had either a hypertensive crisis or a stroke. Five of 6 patients were comatose before admission, and in 4 of the 6 patients, a hemorrhagic (not an ischemic) stroke was documented. With prompt institution of antihypertensive therapy, systolic pressure was lowered precipitously to 100 mm Hg. Not unexpectedly, of the 6, only 1 patient survived. On the basis of their few cases, the authors concluded that convincing evidence of a beneficial effect of blood pressure reduction in the setting of an acute stroke was lacking but also considered that “the deterioration might have been the natural terminal cause in these patients with severe brain lesions.”4 Clearly, from this meager study, no conclusion can be drawn on the management of blood pressure in patients with ischemic stroke.