Interventions for Deliberately Altering Blood Pressure in Acute Stroke
It is unclear whether blood pressure (BP) should be altered actively during the acute phase of stroke. This is an update of a Cochrane review first published in 1997 and previously updated in 2001 and 2008.
To assess the clinical effectiveness of altering BP in patients with acute stroke. The primary outcome was combined death or dependency/disability at end of trial (≥1 month after stroke). Death or dependency was defined as modified Rankin Scale >2 (or >3 as available). Death or disability was defined using the Barthel index <60.
We searched the Cochrane Stroke Group Trials Register (last searched in February 2014), the Cochrane Database of Systematic Reviews and the Cochrane Central Register of Controlled Trials (The Cochrane Library 2014, Issue 2), as well as MEDLINE (1966 to May 2014), EMBASE (1974 to May 2014), Science Citation Index (1981 to May 2014) and the Stroke Trials Registry (http://www.strokecenter.org/trials/). We also searched reference lists, abstracts, conference proceedings and contacted authors, researchers, and pharmaceutical companies.
Published and unpublished randomized controlled trials evaluating single or multiple agents, regardless of drug dosage or route of treatment, aimed at altering BP within 1 week of acute ischemic or hemorrhagic stroke were eligible. We also included trials assessing effects of continuing or stopping preexisting antihypertensive treatment.
Data Collection and Analysis
Using an a priori protocol, 2 reviewers independently applied the inclusion criteria, assessed trial quality, and extracted data. Outcomes were assessed according to drug class, stroke type, stroke location, and by time to treatment. Results were reported as odds ratio with 95% confidence interval (CI) for dichotomous data and as mean difference for continuous data.
We included 26 trials involving 17 011 patients.1 Of these, 24 assessed BP lowering in 15 432 patients; 2 trials (involving 2860 patients) evaluated whether to continue or stop prestroke antihypertensive treatment. One trial (15 patients) studied the effects of BP elevation. BP lowering did not reduce death or dependency (odds ratio, 0.98; 95% CI, 0.92 to 1.05) and did not differ by drug class or stroke type. Treatment within 6 hours, but not beyond, was associated with reduced death or dependency (odds ratio, 0.86; 95% CI, 0.76 to 0.99; Figure). Although death or dependency did not differ between patients who continued prestroke antihypertensive treatment versus those who stopped it temporarily (worse outcome with continuing treatment, odds ratio, 1.06; 95% CI, 0.91 to 1.24), disability scores at end of trial were worse in patients randomized to continue treatment (Barthel Index, mean difference, −3.2; 95% CI, −5.8 to mean difference 0.6). Insufficient data were available to assess the effect of BP elevation.
BP lowering during the acute phase of stroke did not improve functional outcome. However, early initiation of treatment may be beneficial, and additional studies are required to test this question. Continuing prestroke antihypertensive drugs immediately after acute stroke may be harmful.
Implications for Practice
The lack of definitive results for BP lowering, and limited data for raising BP, mean that no firm recommendations can be made. There is no evidence to support the routine policy of continuing prestroke antihypertensive drugs immediately after acute stroke.
More randomized controlled trials are needed to assess whether BP lowering started early (prehospital/hyperacute) after stroke onset is of clinical benefit.
This article is based on a Cochrane Review published in The Cochrane Library 2014, Issue 10 (http://www.thecochranelibrary.com for information). Cochrane Reviews are regularly updated as new evidence emerges and in response to feedback, and The Cochrane Library should be consulted for the most recent version of the review.
Sources of Funding
Kailash Krishnan was funded, in part, by the Medical Research Council/National Institute of Health Research (NIHR) Efficacy and Mechanism Evaluation programme.
Dr Bath is Stroke Association Professor of Stroke Medicine. K. Krishnan reports no conflicts.
- Received November 11, 2014.
- Revision received November 11, 2014.
- Accepted November 12, 2014.
- © 2014 American Heart Association, Inc.