Acute hypertensive response in patients with intracerebral hemorrhage pathophysiology and treatment

Abstract

Acute hypertensive response is a common systemic response to occurrence of intracerebral hemorrhage which has gained unique prominence due to high prevalence and association with hematoma expansion and increased mortality. Presumably, the higher systemic blood pressure predisposes to continued intraparenchymal hemorrhage by transmission of higher pressure to the damaged small arteries and may interact with hemostatic and inflammatory pathways. Therefore, intensive reduction of systolic blood pressure has been evaluated in several clinical trials as a strategy to reduce hematoma expansion and subsequent death and disability. These trials have demonstrated either a small magnitude benefit (second intensive blood pressure reduction in acute cerebral hemorrhage trial and efficacy of nitric oxide in stroke trial) or no benefit (antihypertensive treatment of acute cerebral hemorrhage 2 trial) with intensive systolic blood pressure reduction compared with modest or standard blood pressure reduction. The differences may be explained by the variation in intensity of systolic blood pressure reduction between trials. A treatment threshold of systolic blood pressure of ≥180 mm with the target goal of systolic blood pressure reduction to values between 130 and 150 mm Hg within 6 h of symptom onset may be best supported by current evidence.

Keywords: Hypertensive response; hematoma expansion; intracerebral hemorrhage; randomized clinical trials; systolic blood pressure.

Figure 1.

The distribution of modified Rankin scale scores according to treatment groups in large randomized clinical trials.

Figure 2.

The systolic blood pressure profiles in patients according to treatment group in INTERACT 2 and ATACH 2 trial. Note that the graph derived from INTERACT 2 is based on average systolic blood pressure and that derived from ATACH 2 is based on minimum systolic blood pressure.