Hypertension in Acute Ischemic Stroke: A Compensatory Mechanism or an Additional Damaging Factor?

Andrea Semplicini, MD; Valentina Benetton, MD; Lorenzo Calò, MD; Anna Realdi, MD; Vania Mascagna, MD; Michelangelo Sartori, MD


Cardiovasc Rev Rep. 2004;25(2) 

In This Article


This review and the data we collected for a recent study[26] show that after an acute ischemic stroke, clinical outcome is dependent on the type and severity of stroke presentation and the level of blood pressure during the first 24 hours following the acute event. In our series,[26] patients with the highest blood pressure on admission, within the range of 140-220 mm Hg systolic and 70-110 mm Hg diastolic, had the best neurologic outcome. This applies in particular to patients with lacunar infarction, whereas patients with POCI, who presented with the lowest blood pressure, had the poorest prognosis. Collectively, from the analysis of the patients with LACI and those with LVA and cardioembolic stroke within the blood pressure range of 140-220 mm Hg for the systolic and 70-110 for the diastolic, the higher the blood pressure, the better the clinical outcome. This suggests that, in the acute phase of stroke, hypertension represents a compensatory mechanism to maintain cerebral perfusion, which is associated with poor outcome when it fails. It is therefore highly unlikely that the neurologic outcome of patients with ischemic stroke can be improved by blood pressure reduction with antihypertensive treatment within the above-mentioned range.

According to American Heart Association guidelines, in cases of blood pressure values repeatedly above 220/120 mm Hg, labetalol or other short-acting antihypertensive drugs should be given as IV infusion.[66] This suggestion is based on the clinical observations collected in this review. However, we also report evidence that low blood pressure correlates to poor outcome. This suggests that if there is no other clinical indication (such as myocardial infarction or heart failure) the blood pressure target shortly after acute ischemic stroke should not be a normal blood pressure but around 180 mm Hg systolic and 100 mm Hg diastolic in hypertensive patients and above 150 mm Hg systolic in previously normotensive patients. Therefore, in patients who are not already undergoing antihypertensive therapy and with systolic pressure 180-220 mm Hg and diastolic pressure lower than 120 mm Hg, antihypertensive therapy should not be given for the first 48 hours after an ischemic stroke unless thrombolytic therapy is indicated. If the patient is already receiving chronic oral antihypertensive therapy and has systolic pressure 180-220 mm Hg and diastolic pressure lower than 120 mm Hg, antihypertensive therapy should be continued to avoid rebound hypertension and with the aim of maintaining 180-220 mm Hg systolic and less than 120 mm Hg diastolic. Only if systolic pressure is higher than 220 mm Hg and diastolic pressure is higher than 120 mm Hg are IV antihypertensive drugs recommended to keep blood pressure around 180-220 mm Hg systolic and 100-120 mm Hg diastolic.

Due to the physiopathologic and clinical heterogeneity of acute stroke within a wide blood pressure range (i.e., 140-220 mm Hg systolic and 70-110 mm Hg diastolic), it is highly unlikely that reduction of blood pressure with antihypertensive therapy during the first 48 hours after ischemic stroke will improve clinical outcomes in unselected patients. In many patients the use of antihypertensive drugs is unnecessary and the transient blood pressure rise that is common in the acute phase and in previously normotensive patients tends to spontaneously fade away after the first 24 hours after onset.


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