This document summarizes several studies on the relationship between blood pressure (BP) and outcomes in patients with intracerebral hemorrhage (ICH). The studies found that: 1) Higher systolic BP variability during the initial 24 hours of ICH was associated with worse neurological outcomes and mortality. Stable BP control may improve prognosis. 2) Higher systolic BP loads (proportion of readings above 180 mmHg) within 24 hours independently predicted hematoma expansion and neurological deterioration. 3) Lower achieved systolic BP levels (median of 135 mmHg) within 24 hours through intensive BP reduction were associated with less hematoma growth compared to higher BP levels.

2. Introduction
Elevated blood pressure (BP)
Associated with hematoma expansion
Neurological deterioration
Unfavorable outcomes
Associations B/W early blood pressure (BP) variability and
clinical outcomes with ICH after antihypertensive therapy
clarified by a post hoc analysis of Intensive Blood Pressure
Reduction in Acute Cerebral Hemorrhage Trial 2 (INTERACT2)
Confirmed in Stroke Acute Management with Urgent
Risk-factor Assessment and Improvement
(SAMURAI)-intracerebral hemorrhage study cohort

3. AIM
To confirm associations between early BP variability, clinical and
functional outcome at 3 months

4. The SAMURAI-ICH study was a prospective, multicenter,
observational study
Criteria for inclusion are as follows:
≥20 years of age
Glasgow Coma Scale score ≥5
Initial SBP >180 mm Hg
Computed tomography <2.5 hours of onset demonstrating a
supratentorial intraparenchymal hematoma with manual
volume measurement <60 mL
Absence of extensive intraventricular hemorrhage.

5. Kothari et al
The ABC/2 volume estimation is based on simplification
of the ellipsoid volume equation
A=maximum length (in cm), B=width perpendicular to A
on the same head CT slice, and C=the number of slices
multiplied by the slice thickness

6. The predefined standardized protocol of AHT was used to
lower and maintain the SBP level below 160 mm Hg and
above 120 mm Hg.
Titrating of intravenous nicardipine was initiated at a rate of
5 mg/h within 3 hours of symptom onset and continued for 24
hours.
Levels of BP and pulse rate were measured every 15 minutes
during the first 2 hours after initiation of AHT and every 60
minutes during the next 22 hours, as well as at 48 and 72
hours.
Oral antihypertensive agents were started after the first 24
hours

7. Clinical outcomes include hematoma expansion (>33% in
volume from baseline to 24 hours)
Neurological deterioration (a decrease of ≥2 in Glasgow Coma
Scale or an increase of ≥4 in the National Institutes of Health
Stroke Scale score from baseline to 72 hours)
Unfavorable outcome (modified Rankin Scale score, 4–6 at 3
months)
Hematoma expansion evaluated by an absolute volume
difference and a relative volume change

8. Of the 211 patients in the registry, 205 (81 women,
median age 65 [interquartile range, 59–75] years median
initial National Institutes of Health Stroke Scale score
13
[8–17]) whose BP data were available throughout the 24
hour observation period were studied

10. Correlations between rates of clinical outcomes and systolic
blood pressure variability quartiles

11. Correlations between rates of clinical outcomes and diastolic
blood pressure variability quartiles
Neither SD nor SV of diastolic BP demonstrated associations with
any clinical outcome

12. Correlations between rates of clinical outcomes and systolic
blood pressure variability quartiles.
Tanaka E et al. Stroke. 2014;45:2275-2279

13. Correlations between rates of clinical outcomes and diastolic
blood pressure variability quartiles.
Tanaka E et al. Stroke. 2014;45:2275-2279

14. The major findings that variability of SBP assessed
using both SD and SV during the initial 24 hours of
ICH
was independently associated with both early
neurological deterioration and unfavorable outcome
at 3 months
Positive association between SBP variability and
absolute and relative changes in hematoma volume

15. A difference between the INTERACT2 and the
present study was the timing of points of BP
measurement within the initial 24 hours (6
versus 24 points).
SV which reflects the serial BP variation in a time
sequence, was used as indicator of variability, as
well as SD

16. Increased BP variability is associated with female sex, advanced age,
and hypertension
Mechanisms to connect BP variability and clinical outcomes
Autonomic dysfunction, including sympathetic overactivity and
diminished baroreflex sensitivity
The impaired baroreflex sensitivity increased BP variability and
accordingly altered cerebral perfusion, leading to secondary brain
injury
Sympathetic overactivity affects the factors that boost the secondary
brain injury and enhance brain edema, such as leukocytosis,
proinflammatory cytokine production, hyperglycemia, hyperthermia,
and increased blood–brain barrier permeability

17. Blood pressure variability and outcome after acute intracerebral
haemorrhage: a post-hoc analysis of INTERACT2, a randomised
controlled trial
Background
High blood pressure is a prognostic factor for acute stroke, but blood pressure
variability might also independently predict outcome.
Methods
INTERACT2 enrolled 2839 adults with spontaneous intracerebral haemorrhage (ICH)
and high systolic blood pressure (150—220 mm Hg) without a definite indication or
contraindication to early intensive treatment to reduce blood pressure. Participants were
randomly assigned to intensive treatment (target systolic blood pressure <140 mm Hg
within 1 h using locally available intravenous drugs) or guideline-recommended
treatment (target systolic blood pressure <180 mm Hg) within 6 h of onset of ICH.
The primary outcome was death or major disability at 90 days (modified Rankin
Scale score ≥3) and the secondary outcome was an ordinal shift in modified Rankin
Scale scores at 90 days, assessed by investigators masked to treatment allocation. Blood
pressure variability was defined according to standard criteria: five measurements
were taken in the first 24 h (hyperacute phase) and 12 over days 2—7 (acute
phase). We estimated associations between blood pressure variability and
outcomes with logistic and proportional odds regression models

18. Result
We studied 2645 (93·2%) participants in the hyperacute phase and 2347 (82·7%)
in the acute phase. In both treatment cohorts combined, SD of systolic blood
pressure had a significant linear association with the primary outcome for both the
hyperacute phase (highest quintile adjusted OR 1·41, 95% CI 1·05—1·90;
ptrend=0·0167) and the acute phase (highest quintile adjusted OR 1·57, 95% CI
1·14—2·17; ptrend=0·0124). The strongest predictors of outcome were
maximum systolic blood pressure in the hyperacute phase and SD of systolic
blood pressure in the acute phase. Associations were similar for the secondary
outcome (for the hyperacute phase, highest quintile adjusted OR 1·43, 95% CI
1·14—1·80; ptrend=0·0014; for the acute phase OR 1·46, 95% CI 1·13—1·88;
ptrend=0·0044).
Interpretation
Systolic blood pressure variability seems to predict a poor outcome in patients
with acute intracerebral haemorrhage. The benefits of early treatment to reduce
systolic blood pressure to 140 mm Hg might be enhanced by smooth and sustained
control, and particularly by avoiding peaks in systolic blood pressure.

19. Conclusion
SBP variability during the initial 24 hours of hyperacute ICH was
independently associated with neurological deterioration and 3-
month unfavorable outcome. Stability with appropriate AHT may
ameliorate clinical outcomes in patients with hyperacute ICH. BP
variability seems to be an important therapeutic target in
acute ICH

20. Impact of blood pressure changes and course on hematoma growth in acute
intracerebral hemorrhage
European Journal of Neurology
Background and purpose
An association between high blood pressure (BP) in acute intracerebral hemorrhage
(ICH) and hematoma growth (HG) has not been clearly demonstrated.
Methods
In total, 117 consecutive patients with acute (<6 h) supratentorial ICH underwent
baseline and 24-h CT scans, CT angiography for the detection of the spot sign and non-invasive
BP monitoring at 15-min intervals over the first 24 h. Maximum and
minimum BP, maximum BP increase and drop from baseline, and BP variability values
from systolic BP (SBP), diastolic BP and mean arterial pressure (MAP) were calculated.
SBP and MAP loads were defined as the proportion of readings >180 and
>130 mmHg, respectively.
HG (>33% or >6 ml)
Early neurological deterioration (END) and 3-month mortality were recorded.

21. Results
Baseline BP variables were unrelated to either HG or clinical
outcome. Conversely, SBP 180-load independently predicted HG
(odds ratio 1.05, 95% CI 1.010–1.097, P = 0.016), whilst both SBP
180-load (odds ratio 1.04, 95% CI 1.001–1.076, P = 0.042) and SBP
variability (odds ratio 1.2, 95% CI 1.047–1.380, P = 0.009)
independently predicted END. Although none of the BP monitoring
variables was associated with HG in the spot-sign-positive group,
higher maximum BP increases from baseline and higher SBP and
MAP loads were significantly related to HG in the spot-sign-negative
group.
Conclusions
In patients with acute supratentorial ICH, SBP 180-load
independently predicts HG, whilst both SBP 180-load and SBP
variability predict Early neurological deterioration

22. Hypertension. 2010 Nov;56(5):852-8
Lower treatment blood pressure is associated with greatest reduction in hematoma
growth after acute intracerebral hemorrhage.
Abstract
The pilot phase of the Intensive Blood Pressure Reduction in Acute Cerebral
Haemorrhage Trial (INTERACT) showed that rapid blood pressure (BP) lowering can
attenuate hematoma growth in acute intracerebral hemorrhage. INTERACT included
404 patients with computed tomographic-confirmed intracerebral hemorrhage,
elevated systolic BP (150 to 220 mm Hg), and capacity to commence BP lowering
treatment within 6 hours of onset. CT was done at baseline and at 24 hours using
There was no significant association between baseline systolic BP levels and either the
absolute or proportional growth in hematoma volume (P trend=0.26 and 0.12,
respectively). By contrast, achieved on-treatment systolic BP levels in the first 24 hours
were clearly associated with both absolute and proportional hematoma growth (both P
trend=0.03). Maximum reduction in hematoma growth occurred in the one third of
participants with the lowest on-treatment systolic BP levels (median: 135 mm Hg).
Intensive BP reduction to systolic levels between 130 and 140 mm Hg is likely to
provide the maximum protection against hematoma growth after intracerebral
hemorrhage.

23. J Korean Med Sci. 2012 Sep;27(9):1085-90. doi: 10.3346/jkms
Antihypertensive treatment of acute intracerebral hemorrhage by intravenous
nicardipine hydrochloride: prospective multi-center study
Abstract
This study included 88 patients (mean age: 58.3 yr, range 26-87 yr) with ICH and acute
hypertension in 5 medical centers between August 2008 and November 2010, who were
treated using intravenous nicardipine. Administration of nicardipine resulted in a
decrease from mean systolic blood pressure (BP) (175.4 ± 33.7 mmHg) and diastolic
BP (100.8 ± 22 mmHg) at admission to mean systolic BP (127.4 ± 16.7 mmHg) and
diastolic BP (67.2 ± 12.9 mmHg) in 6 hr after infusion (P < 0.001, mixed-effect linear
models). Among patients who underwent follow-up by computed tomography,
hematoma expansion at 24 hr (more than 33% increase in hematoma size at 24 hr) was
observed in 3 (3.4%) of 88 patients. Neurological deterioration (defined as a decrease in
initial Glasgow coma scale ≥ 2) was observed in 2 (2.2%) of 88 patients during the
treatment. Aggressive nicardipine treatment of acute hypertension in patients with
ICH can be safe and effective with a low rate of neurological deterioration and
hematoma expansion.

24. Stroke. 2013 Mar;44(3):620-6. doi: 10.1161/STROKEAHA.111.000188
The Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial.
Abstract
BACKGROUND AND PURPOSE:
Acute blood pressure (BP) reduction aimed at attenuation of intracerebral hemorrhage
(ICH) expansion might also compromise cerebral blood flow (CBF). We tested the
hypothesis that CBF in acute ICH patients is unaffected by BP reduction
METHODS:
Patients with spontaneous ICH <24 hours after onset and systolic BP > 150 mm Hg
were randomly assigned to an intravenous antihypertensive treatment protocol
targeting a systolic BP of <150 mm Hg (n=39) or <180 mm Hg (n=36). Patients
underwent computed tomography perfusion imaging 2 hours postrandomization. The
primary end point was perihematoma relative (relative CBF).

25. RESULTS:
Treatment groups were balanced with respect to baseline systolic BP: 182±20 mm
Hg (<150 mm Hg target group) versus 184±25 mm Hg (<180 mm Hg target
group; P=0.60), and for hematoma volume: 25.6±30.8 versus 26.9±25.2 mL
(P=0.66). Mean systolic BP 2 hours after randomization was significantly lower in
the <150 mm Hg target group (140±19 vs 162±12 mm Hg; P<0.001).
Perihematoma CBF (38.7±11.9 mL/100 g per minute) was lower than in
contralateral homologous regions (44.1±11.1 mL/100 g per minute; P<0.001) in all
patients. The primary end point of perihematoma relative CBF in the <150 mm Hg
target group (0.86±0.12) was not significantly lower than that in the <180 mm Hg
group (0.89±0.09; P=0.19; absolute difference, 0.03; 95% confidence interval -
0.018 to 0.078). There was no relationship between the magnitude of BP change
and perihematoma relative CBF in the <150 mm Hg (R=0.00005; 95% confidence
interval, -0.001 to 0.001) or <180 mm Hg target groups (R=0.000; 95% confidence
interval, -0.001 to 0.001).
CONCLUSIONS:
Rapid BP lowering after a moderate volume of ICH does not reduce
perihematoma CBF. These physiological data indicate that acute BP reduction
does not precipitate cerebral ischemia in ICH patients

26. Stroke. 2013 Mar;44(3):816-8. doi: 10.1161/STROKEAHA.112.681007
Impact of early blood pressure variability on stroke outcomes after
thrombolysis: the SAMURAI rt-PA Registry.
METHODS:
In 527 stroke patients receiving intravenous alteplase (0.6 mg/kg), BP was
measured 8 times within the first 25 hours. BP variability was determined as ΔBP
(maximum-minimum), standard deviation (SD), coefficient of variation, and
successive variation.
RESULTS:
The systolic BP course was lower among patients with modified Rankin Scale
(mRS) 0 to 1 than those without (P<0.001). Most of systolic BP variability profiles
were significantly associated with outcomes. Adjusted odds ratios (95% confidence
interval) per 10 mm Hg (or 10% for coefficient of variation) on symptomatic
intracerebral hemorrhage were as follows: ΔBP, 1.33 (1.08-1.66); SD, 2.52 (1.26-
5.12); coefficient of variation, 3.15 (1.12-8.84); and successive variation, 1.82
(1.04-3.10). The respective values were 0.88 (0.77-0.99), 0.73 (0.48-1.09), 0.77
(0.43-1.34), and 0.76 (0.56-1.03) for 3-month mRS 0 to 1; and 1.40 (1.14-1.75),
2.85 (1.47-5.65), 4.67 (1.78-12.6), and 1.99 (1.20-3.25) for death.Initial BP
values before thrombolysis were not associated with any outcomes.
CONCLUSIONS:
Early systolic BP variability was positively associated with symptomatic
intracerebral hemorrhage and death after intravenous thrombolysis.

27. Stroke. 2009 Jul;40(7):2442-9. doi: 10.1161/STROKEAHA
Relationship of blood pressure, antihypertensive therapy, and
outcome in ischemic stroke treated with intravenous thrombolysis:
retrospective analysis from Safe Implementation of Thrombolysis in
Stroke-International Stroke Thrombolysis Register (SITS-ISTR)
BACKGROUND AND PURPOSE:
The optimal management of blood pressure (BP) in acute stroke remains
unclear. For ischemic stroke treated with intravenous thrombolysis,
current guidelines suggest pharmacological intervention if systolic BP
exceeds 180 mm Hg.We determined retrospectively the association of
BP and antihypertensive therapy with clinical outcomes after stroke
thrombolysis.

28. METHODS:
The SITS thrombolysis register prospectively recorded 11 080 treatments from 2002
to 2006. BP values were recorded at baseline, 2 hours, and 24 hours after
thrombolysis. Outcomes were symptomatic (National Institutes of Health Stroke
Scale score deterioration >or=4) intracerebral hemorrhage Type 2, mortality, and
independence at (modified Rankin Score 0 to 2) 3 months. Patients were
categorized by history of hypertension and antihypertensive therapy within 7 days
after thrombolysis: Group 1, hypertensive treated with antihypertensives
(n=5612); Group 2, hypertensive withholding antihypertensives (n=1573);
Group 3, without history of hypertension treated with antihypertensives
(n=995); and Group 4, without history of hypertension not treated with
antihypertensives (n=2632). For 268 (2.4%) patients, these data were missing.
Average systolic BP 2 to 24 hours after thrombolysis was categorized by 10-mm Hg
intervals with 100 to 140 used as a reference.

29. RESULTS:
In multivariable analysis, high systolic BP 2 to 24 hours after thrombolysis
as a continuous variable was associated with worse outcome (P<0.001) and
as a categorical variable had a linear association with symptomatic
hemorrhage and a U-shaped association with mortality and independence
with systolic BP 141 to 150 mm Hg associated with most favorable
outcomes. OR (95% CI) from multivariable analysis showed no difference
in symptomatic hemorrhage (1.09 [0.83 to 1.51]; P=0.58) and independence
(1.03 [0.93 to 1.10]; P=0.80) but lower mortality (0.82 [0.73 to 0.92];
P=0.0007) for Group 1 compared with Group 4. Group 2 had a higher
symptomatic hemorrhage (1.86 [1.34 to 2.68]; P=0.0004) and mortality
(1.62 [1.41 to 1.85]; P<0.0001) and lower independence (0.89 [0.80 to 0.99];
P=0.04) compared with Group 4. Group 3 had similar results as Group 1
CONCLUSIONS:
There is a strong association of high systolic BP after thrombolysis with
poor outcome. Withholding antihypertensive therapy up to 7 days in
patients with a history of hypertension was associated with worse
outcome, whereas initiation of antihypertensive therapy in newly recognized
moderate hypertension was associated with a favorable outcome

37. What Blood Pressure Level Is Considered to Be Too High and Requiring
Immediate Reduction?
Answer: Despite absence of definitive supportive evidence, some experts believe
that a SBP of >180 mm Hg or a mean arterial pressure (MAP) of >130 mm Hg
would warrant immediate lowering. In the presence of conditions such as acute
heart failure, hypertensive encephalopathy, active cardiac ischemia, and so on,
lower BP targets may be appropriate.
What Is the Appropriate Target Blood Pressure in Patients With ICH?
Answer: Immediately after an ICH, it is perhaps more appropriate to tailor the
target BP to each patient rather than using a “one size fits all” approach. The
possibility of increased ICP and a history of chronic untreated hypertension
should be considered while choosing the target. Recognizing the absence of
definitive data, the American Heart Association/American Stroke Association
(AHA/ASA) guidelines suggest maintaining a cerebral perfusion pressure of 60
to 80 mm Hg in patients with possible increased ICP and a BP of 160/90 or a
MAP of 110 mm Hg in other patients

38. What Blood Pressure Level Is Considered to Be Too High and Requiring
Immediate Reduction?
Answer: Despite absence of definitive supportive evidence, some experts believe
that a SBP of >180 mm Hg or a mean arterial pressure (MAP) of >130 mm Hg
would warrant immediate lowering. In the presence of conditions such as acute
heart failure, hypertensive encephalopathy, active cardiac ischemia, and so on,
lower BP targets may be appropriate.
What Is the Appropriate Target Blood Pressure in Patients With ICH?
Answer: Immediately after an ICH, it is perhaps more appropriate to tailor the
target BP to each patient rather than using a “one size fits all” approach. The
possibility of increased ICP and a history of chronic untreated hypertension
should be considered while choosing the target. Recognizing the absence of
definitive data, the American Heart Association/American Stroke Association
(AHA/ASA) guidelines suggest maintaining a cerebral perfusion pressure of 60
to 80 mm Hg in patients with possible increased ICP and a BP of 160/90 or a
MAP of 110 mm Hg in other patients

39. How Fast Should Blood Pressure Be Lowered?
Answer: results of small studies suggest that rapidly lowering MAP by
approximately 15% does not lower cerebral blood flow, whereas
reductions of >20% can do so. Therefore, if BP-lowering is considered,
current guidelines suggest cautious lowering of BP by no more that 20%
in the first 24 hours.
What Antihypertensive Agents Are Appropriate for Use in the Acute
Setting?
Answer: Short and rapidly acting intravenous antihypertensive agents
are preferred. In the United States, labetalol, hydralazine, esmolol,
nicardipine, enalapril, nitroglycerin, and nitroprusside have been
recommended.Intravenous urapidil is also used in. Sodium
nitroprusside and nitroglycerin should be used with caution because
these agents can potentially increase ICP.

42. Should Blood Pressure Be Lowered in Patients With Elevated BP After an
Ischemic Stroke?
Answer: As per the AHA/ASA guidelines, it is recommended that before
intravenous thrombolytic treatment, BP should be lowered if >185 mm Hg
systolic or >110 mm Hg diastolic. After thrombolytic treatment, SBP should
be kept <180 mm Hg and DBP <105 mm Hg. Intravenous labetalol,
nitropaste, nicardipine infusion, and, if BP remains elevated, sodium
nitroprusside are the recommended agents. Despite the absence of
supporting evidence, these recommendations are often applied to patients
receiving other forms of reperfusion therapy (eg, intra-arterial thrombolysis,
clot retrieval, and so on).Patients with other indications for BP-lowering such
as acute heart failure, aortic dissection, and so on should have the BP
lowered.

43. Should Blood Pressure Be Elevated to Improve Cerebral Perfusion in
Patients With Ischemic Stroke?
Answer: A few small case series have shown neurological
improvement with induced hypertensive therapy. Studies are
underway to assess the usefulness of this form of therapy in
patients with a diffusion–perfusion mismatch on MRI. In the
meantime, it is reasonable to try volume expansion and/or
vasopressors in patients with hypotensive stroke or in patients who
have had a worsening of the neurological deficit in association with
a drop in BP.

44. Should Patients on Antihypertensive Agents Have Their
Medications Held or Continued?
Answer: There are no substantial clinical data available to answer
this question and a clinical trial is underway to address this issue
(Continue or stop poststroke antihypertensives study).The
AHA/ASA guidelines recommend restarting antihypertensives at
24 hours in previously hypertensive neurologically stable
patients unless contraindicated

45. When Is It Safe to Lower BP After an Acute Ischemic Stroke for the Purpose of
Recurrent Stroke Prevention?
Answer: While awaiting the arrival of more definitive data, the available
evidence suggests that it might be reasonable to start oral antihypertensives
as soon as 24 to 72 hours after onset of symptoms provided there are no
contraindications such as a presumed hemodynamic mechanism of stroke
What Is the Target BP Goal?
Answer: The precise target goal is not definitively known. In the PROGRESS
trial, BP was lowered by approximately 10/5 mm Hg, and this BP target has
been suggested as a reasonable one for patients according to the AHA/ASA
guideline. However, there is variability of absolute BP level and response to
BP-lowering by the patient, especially when age is taken into account, and this
must be considered before attempting to lower BP. A reasonable goal, if it can
be safely achieved after ischemic stroke, is the Seventh Report of the Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure (JNC 7) target of <140/90 mm Hg for uncomplicated
hypertensive patients and <130/80 mm Hg for those with diabetes mellitus or
chronic kidney disease
5

46. Which BP-Lowering Agent Is Most Effective?
Answer: Some studies have suggested that angiotensin-converting enzyme
inhibitors and angiotensin receptor blockers may be more effective in
recurrent stroke prevention than other antihypertensive agents. The choice
of the antihypertensive agent should probably depend more on the
associated medical conditions rather than any specific cerebrovascular
protective effects of a specific class of antihypertensive agents. β-blockers
may have a reduced ability to protect against stroke (particularly atenelol),
may favor weight gain, and dyslipidemia and impaired glycemic control
Therefore, persons at risk for or with multiple metabolic factors may not be
good candidates for β-blocker administration unless they are vasodilator β-
blockers, which may not be associated with these latter side effects.
Thiazide diuretics also may have dyslipidemic and diabetogenic effects
when used at high doses, although this has been questioned by the findings
of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart
Attack trial that failed to support the preference for calcium channel
blockers, α-blockers, or angiotensin-converting enzyme inhibitors
compared with thiazide-type diuretics in patients with metabolic
syndrome.The AHA/ASA guideline recommends consideration of a diuretic
in combination with an angiotensin-converting enzyme inhibitor

47. Intracranial pressure treatment algorithm
Morgenstern L B et al. Stroke. 2010;41:2108-2129
Copyright © American Heart Association, Inc. All rights reserved.

48. Important randomised controlled trials of intervention versus control. SBP:
systolic blood pressure, MAP: mean arterial pressure, AH: antihypertensive
agents, p.o.: per os, i.v.: intravenous, n.p.: not published. (The phase II trial
ACCESS comparing candesartan versus placebo has not been included, as the
following phase III trial SCAST has been)
Name
Year of
publicatio
n
Initial
median
blood
pressure
(mmHg)
Time to
treatment
(hours)
Substance
Administr
ation
Stroke
subgroup
BEST 1988 302 n.p. 22–25.3
Atenolol,
Propanolol
p.o.
Ischemic
+
hemorrha
gic
INWEST 1994 295
SBP 159–
161
10.5–11.5
Nimodipin
e
i.v. Ischemic
Rashid et
al.
2003 90 SPB 151 51
Glyceryl
Trinitrate
transderm
al
Ischemic
+
hemorrha
gic
IMAGES 2004 2589 MAP 108 7
Magnesiu
m
i.v.
Ischemic
+
hemorrha
gic
CHHIPS 2009 179 SBP 181 17.4–20.5
Labetalol,
Lisinopril
p.o., i.v.,
sublingual
Ischemic
+
hemorrha