Blood Pressure in Intracerebral Hemorrhage — How Low Should We Go?

Abstract

Intracerebral hemorrhage is one of the most devastating forms of stroke. The median 1-month case fatality rate is 40%, and only 12 to 39% of patients achieve functional independence.1 Although previous trials of therapies for patients with this condition have not shown a benefit with respect to outcome,2,3 targeted blood-pressure management after an intracerebral hemorrhage has been both a promising and a contentious area of recent study. Early elevations of blood pressure are common after an intracerebral hemorrhage, and many have debated whether this response is adaptive (to maintain perfusion to an ischemic penumbra surrounding the hematoma) or potentially deleterious (resulting in rebleeding, perihematoma edema expansion, or both). Current American Heart Association guidelines suggest a target mean arterial pressure of less than 110 mm Hg or a blood pressure of less than 160/90 mm Hg, with some consideration given to maintaining a reasonable cerebral perfusion pressure in patients with suspected elevations of intracranial pressure.4 These guidelines, however, acknowledge that this blood-pressure target is arbitrary and not evidence-based. A lower-level recommendation was given for reducing blood pressure to a systolic target of 140 mm Hg. This recommendation was based, in part, on the promising pilot results of the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT), which showed a small, but significant, attenuation in hematoma growth over the course of 72 hours with aggressive lowering of blood pressure (systolic pressure of <140 mm Hg), without an increased risk of adverse events.5,6 Anderson et al. now report in the Journal the eagerly anticipated results of the international phase 3 INTERACT2 trial.7 This trial provides the best data, to date, on acute, targeted blood-pressure control after spontaneous intracerebral hemorrhage. The reasons behind the trend toward improved outcomes remain a mystery, however. There were no significant absolute or relative changes in hematoma growth in the intensive-treatment group as compared with the standard-treatment group. Indeed, the volume differences between the groups was minute (adjusted mean volume, 1.4 ml). It remains a possibility that elevated blood pressure could have other systemic effects that affect the outcome. In addition, in patients with disturbed autoregulation, elevated blood pressure could lead to increased cerebral blood volume and consequently elevated intracranial pressure. If the results of this study with respect to the primary outcome were not as robust as some may have hoped, practitioners should be reassured by the safety data presented in the trial. The authors found no significant differences between patients receiving intensive blood-pressure–lowering treatment and those receiving the standard treatment with respect to neurologic deterioration, expansion of the intracerebral hemorrhage, ischemic stroke, cardiovascular events, or severe symptomatic hypotension — findings that were consistent with the results of previous positron-emission tomographic neuroimaging studies, which failed to show an ischemic penumbra surrounding an intracerebral hematoma.