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(Stroke. 2001;32:1697-a.)
© 2001 American Heart Association, Inc.

Letters to the Editor

Hypertension in Acute Stroke: What to Do?

Philip Bath, FRCP

Division of Stroke Medicine, University of Nottingham, Nottingham, UK

Gudren Boysen, MD

Department of Neurology, Bispebjerg Hospital, Copenhagen, Denmark

Geoff Donnan, MD

National Stroke Research Institute, Heidelberg, Australia

Markku Kaste, MD

Department of Neurology, University of Helsinki, Helsinki, Finland

Kennedy R Lees, FRCP

Acute Stroke Unit, Western Infirmary, Glasgow, UK

Tom Olsen, MD

Department of Neurology, Gentofte University Hospital, Hellerup, Denmark

Karsten Overgaard, MD

The Copenhagen Stroke Unit, Frederiksberg Hospital, Copenhagen, Denmark

Peter Sandercock, FRCP

Department of Clinical Neurosciences, Western General Hospitals, Edinburgh, UK

Nils-Gunnar Wahlgren, MD

Department of Neurology, Karolinska Hospital, Stockholm, Sweden

To the Editor:

Hypertension is common during the acute phase of stroke, and its management remains controversial. To explore this issue further, we held an ad hoc workshop at the World Stroke Conference, Melbourne, November 2000, and report here its discussion and conclusions.

Hypertension is common (>50%) in both ischemic and hemorrhagic stroke, although its incidence depends on definitions and when and how blood pressure (BP) measurements are made. Hypertension is associated with a poor outcome,¹ a relationship which is probably independent of stroke severity or clinical subtype. The cause of the negative relationship between BP and outcome is unclear but may relate to the development of reinfarction, cerebral edema, or hemorrhagic transformation.

Our workshop agreed that trials are needed to test whether BP should be lowered in subjects with acute primary intracerebral hemorrhage. In contrast, significant differences of opinion existed on whether BP should be elevated or reduced in acute ischemic stroke. Existing data do not provide an answer: trials of beta receptor antagonists (ß-RA) and some calcium channel blockers (CCB)—in which BP lowering occurred—and diaspirin cross-linked hemoglobin (which increases BP) were all complicated by worsened outcome in the treatment group.^{2 3 4 5 6 7} It is unlikely that a single mechanism explains these findings, but CCB can reduce cerebral perfusion.^{8 9} We did not feel that the BP management strategy utilized in the NINDS and ECASS II thrombolysis trials^{10 11} helped in deciding how to manage BP in general, because patients not treated with thrombolytics are a different population with a different natural history.

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