Abstract

In acute ischemic stroke, the most intuitive therapeutic approach is to restore perfusion to the ischemic territory, typically downstream from an occluded artery. Hemodynamic variables such as systemic blood pressure are seemingly obvious factors that may influence the evolution of ischemic injury and neurologic outcome. The impact of systemic blood pressure and subsidiary maintenance of cerebral perfusion pressure are basic elements of stroke pathophysiology, yet colossal research efforts have been diverted toward the more elusive goal of identifying critical molecular targets in the ischemic cascade. Augmentation of blood pressure in acute stroke may theoretically diminish cerebral ischemia, yet hypertension may also aggravate cerebral edema or precipitate hemorrhagic transformation. Such influential effects may play a pivotal role in acute stroke, yet the clinician has scant data to guide management of such patients. In a clinical scenario where every second lost may be equated with increasing brain damage, measurement of systemic blood pressure is a basic and universal step yet clinicians are paradoxically paralyzed with regard to management of this critical variable. A litany of reports has documented the typical pattern of elevated blood pressure during incipient stages of ischemic stroke and many have addressed the prognostic role of blood pressure in acute stroke, yielding only conflicting conclusions. We still do not know the answer to this obvious, and perhaps complex, question that has been addressed in simple analyses of stroke data sets. Few studies have endeavored to ask why blood pressure is elevated.