High Blood Pressure in Acute Stroke and Subsequent Outcome

A Systematic Review
Mark Willmot, Jo Leonardi-Bee, Philip M.W. Bath
AbstractHigh blood pressure (BP) is common in acute stroke and might be associated with a poor outcome, although
observational studies have given varying results. In a systematic review, articles were sought that reported both admission BP
and outcome (death, death or dependency, death or deterioration, stroke recurrence, and hematoma expansion) in acute stroke.
Data were analyzed by the Cochrane Review Manager software and are given as odds ratios (ORs) or weighted mean
differences (WMDs) with 95% confidence intervals (CIs). Altogether, 32 studies were identified involving 10 892 patients.
When all data were included, death was significantly associated with an elevated mean arterial BP ([MABP] OR, 1.61; 95%
CI, 1.12 to 2.31) and a high diastolic BP ([DBP] OR, 1.71; 95% CI, 1.33 to 2.48). Combined death or dependency was
associated with high systolic BP ([SBP] OR, 2.69; 95% CI, 1.13 to 6.40) and DBP (OR, 4.68; 95% CI, 1.87 to 11.70) in
primary intracerebral hemorrhage (PICH). Similarly, high SBP (11.73 mm Hg; 95% CI, 1.30 to 22.16), MABP
(9.00 mm Hg; 95% CI, 0.92 to 17.08), and DBP (6.00 mm Hg; 95% CI, 0.19 to 11.81) were associated with death or
dependency in ischemic stroke. Combined death or deterioration was associated with a high SBP (OR, 5.57; 95% CI, 1.42
to 21.86) in patients with PICH. In summary, high BP in acute ischemic stroke or PICH is associated with subsequent death,
death or dependency, and death or deterioration. Moderate lowering of BP might improve outcome. Acute BP lowering needs
to be tested in 1 or more large, randomized trials. (Hypertension. 2004;43:18-24.)
Key Words: stroke, thrombotic stroke, hemorrhagic blood pressure morbidity mortality
igh blood pressure (BP 140/90 mm Hg, as defined by
the World Health Organization) occurs in acute stroke in
up to 75% of cases.1,2 Subsequently, BP settles over a period
of about a week, although 40% of patients remain hypertensive. The causes of this pathophysiologic response are
multifactorial and are related to preexisting high BP, activation of the neuroendocrine systems (sympathetic nervous
system, renin-angiotensin axis, and glucocorticoid system),
increased cardiac output, and white coat hypertension.37
It has been suggested that high BP is associated with a poor
outcome after acute stroke, although the results of observational studies have given conflicting results. Some authors
have even demonstrated better outcomes in patients with high
initial BP.8,9 Data from the International Stroke Trial (IST)
confirmed that the risk of early death and late death or
dependency was independently associated with increasing
systolic BP (SBP) in 17 398 patients.10 We report here a
systematic review of observational studies of BP and outcome and assess the relation between the two.

Methods
Study Identification
Published observational studies that reported baseline BP and outcome (death, death or dependency, or death or deterioration) or
mechanisms for poor outcome (recurrent stroke, hemorrhagic trans-

formation, development of cerebral edema, or hematoma expansion)

in acute (7 days) stroke were sought. Systematic searches of
EMBASE and PUBMED were made by M.W. The search strategy
used 10 key words: blood pressure, hypertension, outcome, prognosis, death, mortality, recovery, stroke, cerebr*, and acute. Additional
studies were found from reference lists of identified articles and
reviews.1113 Disability or dependency was typically measured with
the Barthel Index or Rankin Scale; deterioration was defined as
worsening on a stroke neurologic impairment scale, eg, National
Institutes of Health stroke scale, or where an ordinal scale (eg,
improved, unchanged, or worse) was used. Publications were
excluded if they were a randomized trial (these tend not to enroll
consecutive patients and might therefore have a biased sample), gave
insufficient data, used other outcomes, or were duplicate articles.
Decisions on inclusion and exclusion of studies were made by M.W.
and P.M.W.B.

Data Extraction
Two authors (M.W. and J.L.-B.) independently extracted data;
discrepancies were resolved by P.M.W.B. Studies with dichotomous
data were analyzed separately from those with continuous data.
Within both types, the studies were subdivided by outcome measure
(death, death or dependency, death or deterioration, stroke recurrence, cerebral edema, or hematoma expansion) and by BP measurement (SBP, diastolic BP [DBP], or mean arterial BP [MABP]). The
articles were then arranged by stroke type (primary intracerebral
hemorrhage [PICH], ischemic stroke, or mixed). Figures 1A and 1B
show typical forest plots and illustrate the layout of studies.
In cases where articles quoted several BP measurements, the
earliest readings were used. Outcomes after the longest follow-up

Received August 26, 2003; first decision September 15, 2003; revision accepted October 24, 2003.
From the Institute of Neuroscience, University of Nottingham, Nottingham, UK.
Correspondence to Prof Philip Bath, Division of Stroke Medicine, University of Nottingham, City Hospital Campus, Nottingham, NG5 1PB UK. E-mail
philip.bath@nottingham.ac.uk
2003 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org

DOI: 10.1161/01.HYP.0000105052.65787.35

18
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Willmot et al

High Blood Pressure, Acute Stroke, and Outcome

19

Figure 1. A, Forest plot of OR for death

in high vs low/normal DBP. B, Forest
plot of WMD (mm Hg) for SBP in dead or
dependent patients compared with good
outcome.

period were used when present at multiple time points. Some articles
gave outcome data for several BP strata (eg, mortality with SBP
140 mm Hg, 141 to 180 mm Hg, and 180 mm Hg).14 In such
instances, the data were dichotomized into a high-BP and a combined normal/low-BP group by using a cut point nearest to
150 mm Hg because outcome might be best at this level.10 Likewise,
publications with DBP or MABP in several strata were dichotomized
as close as possible to 90 mm Hg and 110 mm Hg, respectively.
Additionally, some articles gave continuous BP data in 2 groups
(eg, SBP for patients with improved, unchanged, or worse
neurologic status). These studies were incorporated into the review
after the data were transformed into 2 groups (eg, combined
improved/unchanged and worse). This was achieved by generating pseudo-random BP data (assuming a normal distribution for
BP) and then merging this before recalculating an overall combined
mean BP and SD.

Analysis
Data were analyzed with the Cochrane Collaboration Review Manager (version 4.1) software. Dichotomous data are given as odds ratio
(OR) and 95% confidence interval (CI) and as weighted mean
difference (WMD) with 95% CI for continuous data. These were
calculated with a random-effects model, and statistical heterogeneity
was assessed with a 2 test. We explored the causes of heterogeneity

by using sensitivity analyses based on type of stroke. Publication

bias was assessed with the Egger asymmetry test15 (STATA function
Metabias) on dichotomous outcome data. Significance was set at
P0.05.

Results
A flow diagram illustrating the search process is given in
Figure 2. Altogether, 32 studies with a total of 10 892 patients
(median size, 184) were included (Table 1). Eleven of these
focused on PICH and 5 on ischemic stroke, and the rest
included patients with either type of stroke. Another 64
studies were excluded; 35 did not provide BP and/or outcome
data in a suitable form, 26 did not assess BP within 7 days of
onset, and 3 were duplicate publications.
BP was recorded at admission in 18 of the included
articles. The method used was given in only 9 studies; 5 used
clinic BP measurement, 3 used both clinic BP measurement and ambulatory BP monitoring, and 1 used ambulatory
BP monitoring alone. The criteria used to define high BP
varied considerably: SBP thresholds ranged from 150 to
200 mm Hg,16 18 MABP levels of 140 to 145 mm Hg,16,19 and

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20

Hypertension

January 2004

Figure 2. Search process.

DBP between 90 and 115 mm Hg.16,20 22 One article did not

specify the criteria used for defining high BP23; this study was
analyzed with the publications that dichotomized according
to MABP. In addition, 3 studies allocated subjects to the
TABLE 1.

high-BP group when SBP, DBP, or both exceeded certain

threshold values.24 26 These articles were also analyzed with
publications that dichotomized according to MABP.
Death was the most commonly reported outcome measure
(survival status present in 7242 patients, 66.5%). There were
fewer data for combined death or dependency (1290, 11.8%)
and combined death or deterioration (1196, 11.0%). These
outcomes were assessed with validated stroke scales in 7
articles (Rankin score,2731 Scandinavian Neurological Stroke
Scale,30,32 Canadian Neurological Score,33 or National Institutes of Health Scale29). The other studies used either nonvalidated scales9 or qualitative assessments, such as discharge
disposition.18,25 Patient follow-up varied considerably between 6 days and 6 years, although most articles chose to
measure outcome at discharge from hospital. Potential
mechanisms of poor outcome were reported in 4 articles.
Three looked at PICH (708, 6.5%) and assessed the
relation between BP and hematoma expansion; the other
study investigated early recurrence in ischemic stroke
(1273, 11.7%). No studies assessed cerebral edema or
hemorrhagic transformation.
There was no publication bias (Egger test P0.21) in
articles reporting SBP and mortality data. When stroke as a

Included Studies

Study

Stroke Type

BP Timing

BP Method

BP Data

Outcome Measure

Outcome Timing

497
148

Admission

Not given

Admission, 24 hours

Not given

Death

4.6 years (mean)

Death or dependency

Armario et al27

49

IS

Admission and daily

2 and 6 months

Not given

Death or dependency

Bhalla et al30

72

Discharge

1 day, 7 days

Manual, ABPM

Death or dependency

Britton et al25

388

1 week

Admission

Manual

Death; death or dependency

Discharge

Brott et al48

103

Carlberg et al14

916

PICH

3 hours

Not given

Hematoma growth

4 hours

Admission

Manual

Death

Dandapani et al16

87

30 days

PICH

Admission

Not given

Death; death or dependency

30 days

Dawson et al28

92

Dunne et al18

40

IS

3 days

Manual, ABPM

Death or dependency

30 days

Cerebellar PICH

Admission

Not given

Death or deterioration

Fogelholm et al49

141

6 days

IS (brainstem)

24 hours

Not given

Death

46.5 months (median)

Fogelholm et al50
Fuji et al39

282

PICH

24 hours

Manual

Death

28 days

419

PICH

24 hours

Not given

Hematoma growth

2 days

Fullerton et al51

206

1248 hours

Not given

Death; death or dependency

6 months

Harmsen et al26

97

Admission

Manual

Death

Discharge

Jorgensen et al32

868

Admission

Not given

Death or deterioration

Day 2, weekly; at discharge

Kazui et al40

186

PICH

24 hours

Not given

Hematoma growth

5 days

Latorre et al52

200

Admission

Not given

Death

Discharge

Acheson et al

22

Allen et al9

Longo-Mbenza et al34

1032

Admission

Not given

Death

Discharge

Marquarsden et al20

371

Admission, day 1, day 7

Not given

Death

5 years

Marshall et al21

251

Admission

Not given

Death

6 years

Mbala-Mukendi et al53

388

Admission

Not given

Death

Discharge

55

24 hours

ABPM

Death

2 years

Portenoy et al23

112

PICH

Admission

Not given

Death or dependency

At last recorded follow-up

Qureshi et al19

182

PICH

Admission

Manual

Death

Discharge

Rankin et al24

247

7 days

Not given

Death

Discharge

Robinson et al29

136

24 hours

Manual, ABPM

Death or dependency; death or deterioration

30 days

1273

IS

7 days

Not given

Recurrent stroke

30 days

107

PICH

Admission

Not given

Death

Discharge

1701

PICH

24 hours

Not given

Death

Discharge

152

IS

5 hours

Not given

Death or deterioration

Discharge

94

PICH

Admission

Not given

Death

30 days

Panayiotou et al54

Sacco et al55
Tennent et al56
Terayama et al57
Toni et al33
Tuhrim et al17

IS indicates ischemic stroke; M, mixed; C, continuous; D. dichotomous; and ABPM, ambulatory BP monitoring.

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Willmot et al
TABLE 2.

High Blood Pressure, Acute Stroke, and Outcome

21

BP in Acute Stroke by Outcome

Dichotomous BP

Outcome

Continuous BP

Studies/Subjects

OR (95% CI)

Heterogeneity

Studies/Subjects

WMD (95% CI)

Heterogeneity

SBP

6/1211

1.85 (1.17, 2.93)

0.01*

0.03*

5/1799

0.10

0.04*

MABP

6/1912

1.61 (1.12, 2.31)

0.01*

0.15

2/1983

11.40 (8.21, 14.58)

0.01*

0.27

DBP

6/1655

1.71 (1.33, 2.18)

0.01*

0.38

5/1799

0.05 (2.56, 2.47)

1.00

0.23

SBP

1/87

2.69 (1.13, 6.40)

0.03*

0.01*

MABP

3/587

1.92 (0.83, 4.44)

0.13

DBP

1/87

4.68 (1.87, 11.70)

0.01*

2/91

1.86 (0.28, 12.50)

0.50

Death
4.81 (0.98, 10.60)

Death/disability
0.05*

6/691

5.11 (3.00, 13.22)

0.20

1/92

9.00 (0.92, 17.08)

0.03*

6/691

2.55 (1.53, 6.62)

0.20

0.04*

Death/deterioration
SBP

0.01*

DBP

3/1155

1.04 (7.59, 5.50)

0.80

0.21

3/1155

0.59 (3.55, 4.73)

0.80

0.12

2/284

7.24 (2.63, 17.10)

0.15

0.31

2/284

0.81 (4.57, 6.19)

0.80

0.76

Recurrent stroke
SBP

1/1273

1.52 (0.80, 2.88)

0.20

DBP

1/1273

2.19 (1.16, 4.14)

0.02*

SBP

2/600

1.93 (1.22, 3.06)

0.01*

DBP

1/180

1.14 (0.47, 2.75)

0.80

PICH enlargement
0.43

*P0.05.

whole was assessed, patients with high SBP or DBP were at

a 1.5- to 5.0-fold increased risk of dying or combined death
or dependency/deterioration (Table 2). Similarly, high MABP
was associated with increased odds for combined death and
dependency. In patients with poor outcome, judged as death
and death or dependency/deterioration, there was a trend for
higher SBP/DBP levels of 5/3 mm Hg. Heterogeneity was
present in several of these analyses (Table 2), so the data were
further examined by stroke type.

Ischemic Stroke
Limited data were available for studies specifically including
patients with ischemic stroke. SBP/DBP were higher by 12/
6 mm Hg in patients who died or became dependent (Table 4).
Similarly, ischemic stroke patients had a 2-fold increase in the
risk of stroke recurrence when their DBP was elevated (Table 2).

Mixed Stroke Studies

Primary Intracerebral Hemorrhage

The odds of death were doubled in patients with high DBP.

SBP was higher by 6.39 mm Hg in patients who subsequently
died (Table 4).

Increased odds of death and death or disability/deterioration

were found in patients with high BP (Table 3). Additionally,
MABP was higher in patients who died after PICH (Table 4).
The odds of hematoma expansion were increased for patients
with high SBP (Table 2).

High SBP, MABP, and DBP in the acute phase of stroke are
associated with a poor outcome, assessed either as death or as
combined death or disability, and possibly as combined death

TABLE 3.

Discussion

Outcome by Type of Stroke for Dichotomous Data

PICH

Outcome

Infarct

Studies/Subjects

OR (95% CI)

SBP

3/244

3.55 (1.80, 7.00)

0.01*

MABP

3/354

2.26 (1.40, 3.66)

0.01*

DBP

2/162

1.74 (0.88, 3.46)

0.11

SBP

1/87

2.69 (1.13, 6.40)

0.03*

MABP

2/199

2.90 (1.57, 5.36)

0.01*

DBP

1/87

4.68 (1.87, 11.70)

0.01*

1/40

5.57 (1.42, 21.86)

0.01*

Mixed

Studies/Subjects

OR (95% CI)

1/831

0.96 (0.60, 1.54)

0.90

Studies/Subjects

OR (95% CI)

3/967

1.40 (0.85, 2.30)

0.18

3/727

1.56 (0.98, 2.48)

0.06

4/1493

1.71 (1.24, 2.36)

0.01*

1/388

0.87 (0.40, 1.91)

0.70

1/851

0.79 (0.59, 1.05)

0.11

Death

Death/disability

Death/deterioration
SBP
*P0.05.

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22

Hypertension

TABLE 4.

January 2004

Outcome by Type of Stroke for Continuous Data

PICH

Outcome

Studies/
Subjects

WMD (95% CI)

Infarct

Mixed

Studies/
Subjects

WMD (95% CI)

Studies/
Subjects

WMD
(95% CI)

1/131

2.04 (12.76, 8.68)

0.70

4/1668

6.39 (0.70, 12.09)

0.03*

1/131

2.22 (4.86, 9.30)

0.50

4/1668

0.18 (3.04, 2.68)

0.90

0.03*

4/550

2.95 (7.38, 13.28)

0.60

Death
SBP
MABP
DBP

2/1983

11.40 (8.21,14.58)

0.01*

Death/disability
SBP

2/141

11.73 (1.30, 22.16)

MABP

1/92

9.00 (0.92, 17.08)

0.03*

DBP

2/141

6.00 (0.19, 11.81)

0.04*

4/550

1.32 (3.91, 6.55)

0.60

SBP

1/152

3.00 (6.70, 12.70)

0.50

2/1003

1.99 (11.83, 7.85)

0.70

DBP

1/52

0.80

2/1003

4.44 (8.18, 17.07)

0.50

Death/deterioration
0.60 (5.20, 4.00)

*P0.05.

or early deterioration. This observation was present irrespective of stroke type. The result, based on 32 studies involving
10 892 patients, is similar to that found in IST, which found
that a high SBP (140 mm Hg) was independently related to
an increased risk of early death and combined death or
dependency in 17 398 patients with acute ischemic stroke.10
The individual studies that form the basis of this systematic
review were generally either positive or neutral for the
association between BP and outcome. The neutral findings in
some studies probably reflect their small size and therefore,
limited statistical power. Three articles found improved
outcomes for high SBP9,32 and DBP34; however, when analyzed with other studies, there was no evidence of a protective
effect for high BP.
This review has found evidence for mechanisms that might
link high BP to poor outcome. In ischemic stroke, high DBP
was associated with a 2-fold increase in risk of early
recurrence. SBP was an important determinant of recurrent
stroke in IST, wherein an initial SBP of 200 mm Hg or more
conferred a 50% higher risk of recurrence than did an SBP
of 130 mm Hg.10 No studies investigating the relation between BP and hemorrhagic transformation or cerebral edema
in ischemic stroke fulfilled our inclusion criteria. Nevertheless, evidence that was excluded from the review suggests
that an acutely elevated SBP is associated with increased fatal
cerebral edema.10,35 Also, several studies have observed that
high BP promotes hemorrhagic transformation in animal
models,36 38 although this was not found in the IST.10 As far
as PICH is concerned, patients with high SBP were almost
twice as likely to have hematoma expansion. This could
support the concept that high BP in the acute phase of
hemorrhagic stroke leads to a worse outcome, at least in part,
by promoting continued intracerebral bleeding. However, this
relation might be confounded by the timing of inclusion,
because patients with severe PICH tend to present earlier and
are at greater risk of rebleeding.
Although this review has demonstrated a positive association between high BP and subsequent events in acute stroke,
the findings are limited by several factors. First, there were

considerable differences in patient eligibility, case mix (including baseline BP), definition of high BP, measurement and
timing of BP, and type and timing of outcome among the
studies. This could be considered an advantage, because it
means that the relations observed are more likely to be
generalizable. However, it might also have led to statistical
heterogeneity. To assess whether stroke type was a potential
source of heterogeneity in the review, we analyzed ischemic
stroke and PICH separately. The relation between outcome
and BP tended to be stronger in patients with PICH (OR, 2.26
to 5.57) compared with those with ischemic stroke. Similarly,
patients who had a poor outcome had a higher BP if they had
PICH (MABP, 11 mm Hg) than ischemic stroke (SBP/DBP,
12/6 mm Hg, equivalent to an MABP of 8 mm Hg).
Nevertheless, these comparisons are indirect and not precise.
Other explanations for heterogeneity among the studies are
likely, but we were unable to explore these owing to the
paucity of data.
A second limiting factor is that we were unable to judge
whether the relations that we observed were independent of
other factors such as age, premorbid BP status, drug therapy,
stroke severity, or timing of BP measurement. A meta-analysis of the studies, based on individual patient data, would be
required to investigate this further. This issue is important,
because some of the relations might have been different if
potential confounding factors had been accounted for. For
example, the relation between BP and rebleeding in PICH is
probably mostly explained by an interaction between timing
of BP measurement and severity.39,40 Likewise, high premorbid BP contributes to elevated BP in acute stroke and could
contribute, in part, to poor outcome through previous cerebral
vascular damage. Third, the strategy of dichotomizing BP,
though clinically relevant, might create artificial strata for the
analysis. For example, several articles have reported a
U-shaped relation between BP and outcome, with the least
poor outcome at an SBP of 140 to 160 mm Hg in the IST
(judged by the nadir of the U).10,41,42 Hence, studies including
a significant proportion of patients with a BP below a cut
point of 160 mm Hg might be expected to miss a relation

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Willmot et al
between high BP and poor outcome. Unfortunately, because
only 1 article gave sufficient data on low BP in acute stroke,
it was not possible to examine how it influenced outcome.
Last, it is worth noting a consistent weakness in the observational studies themselves, namely, the lack of reporting on
how BP was measured. All studies assessing BP should give
information on equipment (manufacturer, model, technique,
validation), user (how trained, assessed, and reassessed), and
patient (number and site of readings, position).43

Perspectives
This article assesses data from all available observational
studies and shows that there is a positive association between
high BP and poor outcome in acute stroke. This relation
might be mediated, at least in part, by early recurrence in
patients with ischemic stroke and possibly, by early rebleeding in those with PICH. Although these relations suggest that
high admission BP is directly causal, we cannot rule out that
this relation was independent of other factors, such as stroke
severity or timing of measurements. Nevertheless, because
lowering a high BP prevents first and recurrent stroke, it can
be hypothesized that moderate lowering of a high BP in acute
stroke might similarly reduce early death and deterioration
and late death and dependency. Aggressive lowering of BP
will do harm through inducing cerebral hypoperfusion. Also,
some animal data and limited clinical data support the
alternative concept of induced hypertension as a treatment
strategy.44,45 Until the results of ongoing randomized, controlled trials are available,46 the management of high BP in
acute stroke will remain controversial.

Acknowledgments
M.W. has a clinical fellowship from the Hypertension Trust.
P.M.W.B. is Stroke Association Professor of Stroke Medicine. The
Division of Stroke Medicine receives core funding from the Stroke
Association (UK). This work was presented, in part, at the 11th
European Stroke Conference, Geneva, May 2002.47

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High Blood Pressure in Acute Stroke and Subsequent Outcome: A Systematic Review
Mark Willmot, Jo Leonardi-Bee and Philip M.W. Bath
Hypertension. 2004;43:18-24; originally published online December 8, 2003;
doi: 10.1161/01.HYP.0000105052.65787.35
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 2003 American Heart Association, Inc. All rights reserved.
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