title: Acute post-stroke blood pressure relative to premorbid levels in intracerebral haemorrhage versus major ischaemic stroke: a population-based study.
abstract: BACKGROUND
  It is often assumed that blood pressure increases acutely after major stroke, resulting in so-called post-stroke hypertension. In view of evidence that the risks and benefits of blood pressure-lowering treatment in acute stroke might differ between patients with major ischaemic stroke and those with primary intracerebral haemorrhage, we compared acute-phase and premorbid blood pressure levels in these two disorders.
  
  
  METHODS
  In a population-based study in Oxfordshire, UK, we recruited all patients presenting with stroke between April 1, 2002, and March 31, 2012. We compared all acute-phase post-event blood pressure readings with premorbid readings from 10-year primary care records in all patients with acute major ischaemic stroke (National Institutes of Health Stroke Scale >3) versus those with acute intracerebral haemorrhage.
  
  
  RESULTS
  Of 653 consecutive eligible patients, premorbid and acute-phase blood pressure readings were available for 636 (97%) individuals. Premorbid blood pressure (total readings 13,244) had been measured on a median of 17 separate occasions per patient (IQR 8-31). In patients with ischaemic stroke, the first acute-phase systolic blood pressure was much lower than after intracerebral haemorrhage (158·5 mm Hg [SD 30·1] vs 189·8 mm Hg [38·5], p<0·0001; for patients not on antihypertensive treatment 159·2 mm Hg [27·8] vs 193·4 mm Hg [37·4], p<0·0001), was little higher than premorbid levels (increase of 10·6 mm Hg vs 10-year mean premorbid level), and decreased only slightly during the first 24 h (mean decrease from <90 min to 24 h 13·6 mm Hg). By contrast with findings in ischaemic stroke, the mean first systolic blood pressure after intracerebral haemorrhage was substantially higher than premorbid levels (mean increase of 40·7 mm Hg, p<0·0001) and fell substantially in the first 24 h (mean decrease of 41·1 mm Hg; p=0·0007 for difference from decrease in ischaemic stroke). Mean systolic blood pressure also increased steeply in the days and weeks before intracerebral haemorrhage (regression p<0·0001) but not before ischaemic stroke. Consequently, the first acute-phase blood pressure reading after primary intracerebral haemorrhage was more likely than after ischaemic stroke to be the highest ever recorded (OR 3·4, 95% CI 2·3-5·2, p<0·0001). In patients with intracerebral haemorrhage seen within 90 min, the highest systolic blood pressure within 3 h of onset was 50 mm Hg higher, on average, than the maximum premorbid level whereas that after ischaemic stroke was 5·2 mm Hg lower (p<0·0001).
  
  
  CONCLUSIONS
  Our findings suggest that systolic blood pressure is substantially raised compared with usual premorbid levels after intracerebral haemorrhage, whereas acute-phase systolic blood pressure after major ischaemic stroke is much closer to the accustomed long-term premorbid level, providing a potential explanation for why the risks and benefits of lowering blood pressure acutely after stroke might be expected to differ.
  
  
  BACKGROUND
  Wellcome Trust, Wolfson Foundation, UK Medical Research Council, Stroke Association, British Heart Foundation, National Institute for Health Research.
authors.affiliation: Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
authors.forename: Urs
authors.initials: U
authors.lastname: Fischer
authors.affiliation: Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
authors.forename: Marie Therese
authors.initials: MT
authors.lastname: Cooney
authors.affiliation: Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
authors.forename: Linda M
authors.initials: LM
authors.lastname: Bull
authors.affiliation: Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
authors.forename: Louise E
authors.initials: LE
authors.lastname: Silver
authors.affiliation: The George Institute for Global Health, University of Sydney, Australia.
authors.forename: John
authors.initials: J
authors.lastname: Chalmers
authors.affiliation: The George Institute for Global Health, University of Sydney, Australia.
authors.forename: Craig S
authors.initials: CS
authors.lastname: Anderson
authors.affiliation: Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
authors.forename: Ziyah
authors.initials: Z
authors.lastname: Mehta
authors.affiliation: Stroke Prevention Research Unit, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. Electronic address: peter.rothwell@clneuro.ox.ac.uk.
authors.forename: Peter M
authors.initials: PM
authors.lastname: Rothwell
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D002543:Cerebral Hemorrhage / Q000150:complications / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D008297:Male; D020521:Stroke / Q000150:complications / Q000503:physiopathology*