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
May not the elevation of systemic blood pressure be anatural response to guarantee a more normal circulationto the heart, brain and kidneys?”1 These words,taken from a renowned textbook of medicine, clearly illustratethat in the 1940s the teaching doctrine was to consider elevatedblood pressure a compensatory mechanism serving to forceblood through sclerotic arteries to the ischemic target organs.Hypertension was regarded as “essential” and therefore “shouldnot be tampered with, even were it certain that we could controlit.”2 We have since learned that hypertension is a powerful riskfactor for stroke, heart attacks, and renal failure and thatlowering blood pressure dramatically reduces the risk of theseevents. The only clinical situation in which blood pressureelevation often still is considered protective is in the sequence ofan acute ischemic stroke. Indeed, authoritative voices such asthat of Adams and Victor3 have warned and continue to warnagainst lowering blood pressure in this setting with statementssuch as, “We agree with Britton and colleagues that it is prudentto avoid antihypertensive drugs in the first few days unless. . .theblood pressure is high enough to pose a risk to other organs.”3This statement can be found in the 1989 edition of this venerableneurology textbook and is repeated verbatim in every singlesubsequent edition until 2005. It thus has taught numerousneurologists that elevated blood pressure in the sequence of anischemic stroke was a “noli me tangere” and that lowering bloodpressure should be avoided. Because Adams and Victor obviouslyconsidered the referenced study to be definitive enough tobe 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 patientspresenting with acute onset of neurological symptoms andextremely high blood pressure who had either a hypertensivecrisis or a stroke. Five of 6 patients were comatose beforeadmission, and in 4 of the 6 patients, a hemorrhagic (not anischemic) stroke was documented. With prompt institution ofantihypertensive therapy, systolic pressure was lowered precipitouslyto 100 mm Hg. Not unexpectedly, of the 6, only 1patient survived. On the basis of their few cases, the authorsconcluded that convincing evidence of a beneficial effect ofblood pressure reduction in the setting of an acute stroke waslacking but also considered that “the deterioration might have
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