Published online: 2021-01-20

46

Blood Pressure Management Before, During,

and After Endovascular Thrombectomy for
Acute Ischemic Stroke
Adam de Havenon, MD1 Nils Petersen, MD, PhD2 Ali Sultan-Qurraie, MD3 Matthew Alexander, MD4
Shadi Yaghi, MD5 Min Park, MD6 Ramesh Grandhi, MD7 Eva Mistry, MBBS8

1 Department of Neurology, University of Utah, Salt Lake City, Utah Address for correspondence Adam de Havenon, MD, Department of
2 Department of Neurology, Yale University, New Haven, Connecticut Neurology, University of Utah, 175 N. Medical Dr, Salt Lake City, UT
3 Department of Neurology, University of Washington, Valley Medical 84132 (e-mail: adam.dehavenon@hsc.utah.edu).
Center, Seattle, Washington
4 Department of Radiology, University of Utah, Salt Lake City, Utah
5 Department of Neurology, New York University, New York, New York
6 Department of Neurosurgery, University of Virginia, Charlottesville,
Virginia
7 Department of Neurosurgery, University of Utah, Salt Lake City, Utah
8 Department of Neurology, Vanderbilt University Medical Center,

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Nashville, Tennessee

Semin Neurol 2021;41:46–53.

Abstract There is an absence of specific evidence or guideline recommendations on blood

Keywords
► blood pressure
► acute ischemic stroke
► large vessel occlusion
pressure management for large vessel occlusion stroke patients. Until randomized data
are available, the periprocedural blood pressure management of patients undergoing
endovascular thrombectomy can be viewed in two phases relative to the achievement
of recanalization. In the hyperacute phase, prior to recanalization, hypotension should
be avoided to maintain adequate penumbral perfusion. The American Heart Associa-
tion guidelines should be followed for the upper end of prethrombectomy blood
pressure:
185/110 mm Hg, unless post–tissue plasminogen activator administration
when the goal is <180/105 mm Hg. After successful recanalization (thrombolysis in
cerebral infarction [TICI]: 2b–3), we recommend a target of a maximum systolic blood
pressure of < 160 mm Hg, while the persistently occluded patients (TICI < 2b) may
require more permissive goals up to <180/105 mm Hg. Future research should focus
on generating randomized data on optimal blood pressure management both before
and after endovascular thrombectomy, to optimize patient outcomes for these
divergent clinical scenarios.

Historically, the effect of blood pressure (BP) on stroke out-
come has been shown to have a U-shaped curve, with extremes
in BP associated with worse outcomes.1 Provision of adequate
cerebral perfusion in acute ischemic stroke (AIS) patients with
large vessel occlusion (LVO) represents a critical aspect of
patient care in both the peri- and intraprocedural settings as
it relates to endovascular thrombectomy (EVT). Intuitively,
reductions in systemic BP before revascularization may result
in a cerebral perfusion decrement, compromised collateral
flow, and consequent infarct progression.2 This could be
particularly important in penumbral territory where a pres-
sure-passive system exists in which arteries and arterioles
maximally dilate in response to tissue ischemia and no longer
exhibit the capacity for pressure autoregulation. In this
manner, cerebral blood flow could be directly dependent on
systemic BP.3 However, hypertension could be damaging to the
stroke and penumbra by promoting edema, cytotoxic media-
tors, and hemorrhagic conversion.4–6

published online Issue Theme Acute Stroke; Guest © 2021. Thieme. All rights reserved. DOI https://doi.org/
January 20, 2021 Editors: Navdeep Sangha, MD, and Koto Thieme Medical Publishers, Inc., 10.1055/s-0040-1722721.
Ishida, MD 333 Seventh Avenue, 18th Floor, ISSN 0271-8235.
New York, NY 10001, USA
 Blood Pressure Management for Acute Ischemic Stroke Havenon et al. 47

Table 1 American Heart Association guidelines for bral collateral failure.6,11–13 Interventional trials to alter BP
perithrombectomy blood pressure8 prior to EVT or IV tPA are few, but there are ample data on BP
reduction in the hours and days after stroke onset using a
Clinical Blood Class of Level of variety of antihypertensive medications. The Prehospital
scenario pressure recommendation evidence
Transdermal Glyceryl Trinitrate in Patients with Ultra-acute
goal
presumed stroke (RIGHT-2) failed to show benefit in the
Pre-EVT,
185/110 IIa B-NR
hyperacute window.14 The Controlling Hypertension and
no tPA
Hypotension Immediately Post Stroke (CHHIPS) and Evalua-
Pre-EVT, <180/105 I B-R
tion of Acute Candesartan Cilexetil Therapy in Stroke Survi-
post-tPA
administration vors (ACCESS) reported a mortality benefit, but no functional
benefit of BP lowering during the acute phase of stroke.4,15
Peri-EVT,
180/105 IIa B-NR
no tPA BEST, a trial evaluating β-blockers in AIS, showed increased
mortality in patients randomized to early β-blocker use.16
Pre-EVT, <180/105 I B-R
post-tPA SCAST, a randomized study lowering BP in AIS patients using
administration candesartan, suggested a higher risk of poor outcome in the
Post-EVT,
180/105 IIa B-NR treatment group.17 Accordingly, a Cochrane review of 26 trials
no tPA concluded that there is “insufficient evidence that lowering BP
and TICI 0–2a during the acute phase of stroke improves functional out-
Post-EVT, <180/105 IIb B-NR come.”18 Recently, the ENCHANTED (Enhanced Control of
post-tPA

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or TICI 2b–3
Abbreviations: EVT, endovascular thrombectomy; TICI, thrombolysis in
cerebral infarction; tPA, tissue plasminogen activator.
Note: Class of recommendation: I ¼ strong, IIa ¼ moderate, IIb ¼ weak;
level of evidence: B-R ¼ randomized, B-NR ¼ nonrandomized.
Despite the inherent complexity to BP management in the
peri-EVT period, the current guideline treatment paradigm
of these patients is identical to the management of non-
occlusive AIS. The American Heart Association/American
Stroke Association (AHA/ASA) guidelines suggest permissive
hypertension, specifically recommending that “hypotension
and hypovolemia be corrected.”7 Unless intravenous tissue
plasminogen activator (IV tPA) is administered, hypertension
up to a BP of
185/110 mm Hg can be tolerated.8 The 2019
AHA guideline (►Table 1) is a revision of the prior 2018
guideline that allowed BP up to 220/120 mm Hg.7 Following
tPA administration, the goal is <180/105 mm Hg (►Table 1).
These guidelines do not distinguish between stroke etiology,
subtype, or severity. Ultimately, BP management surround-
ing EVT is deferred to the treating physician, and there is
considerable variability in practice.9 The intent of this review
article is to help guide BP management in the peri-EVT
period. Ultimately, further research will need to better define
specific BP goals in this patient population, taking into
account the stage of treatment, patient-level variables, and
recanalization status.
Preprocedural Blood Pressure
A recent multicenter study showed that, for patients under-
going EVT, a 15% decrease or increase in their mean arterial
pressure from pre-EVT baseline to postprocedural mean led
to the worst outcome in an adjusted analysis.10 These find-
ings suggest that lowering BP pre-EVT may lead to infarct
expansion and worsening ischemia, while, at the same time,
an increase in BP may be directly harmful to the brain or a
sign of worsening compensatory mechanisms such as cere-
Hypertension and Thrombolysis Stroke Study) trial applied
intensive BP lowering (target systolic BP [SBP]: 130–140 mm
Hg within 1 hour) versus guideline-recommended BP lowering
(target SBP < 180 mm Hg) to IV tPA eligible AIS patients.
Functional status at 90 days did not differ between the
groups.19 The cumulative impact of these studies is that
there is no tangible benefit to reducing BP immediately after
stroke onset.
This is further complicated by the fact that BP tends to be
spontaneously elevated in patients presenting with AIS for
adaptive physiologic perfusion, and typically declines over
time without intervention.20,21 The initial hypertensive
response presumably occurs in an effort to increase the collat-
eral flow to salvage the penumbral region.6 Despite the neutral
findings of the Head Positioning in Acute Stroke Trial (Head-
PoST), which compared lying flat or being allowed to sit up in
the days following stroke, some patients do improve with head-
of-bed flattening or elevating BP, the so-called induced hyper-
tension.22 This suggests that the ischemic penumbra’s viability
can be dependent on BP.23 It follows that elevating the BP in the
hyperacute phase could be beneficial to an ischemic brain
dependent on collaterals. Not surprisingly, animal models
have suggested the safety and efficacy of short-term induced
hypertension, even if there is an increased risk of vasogenic
edema with long-term use.24 Drummond et al showed that
phenylephrine-induced hypertension can acutely improve
local cerebral blood flow and reduce areas of critical hypoper-
fusion (<15 mL/100 g/min) in rats with brief middle cerebral
artery occlusion.25 In a primate model of stroke, this improve-
ment in local cerebral blood flow with induced hypertension
resulted in restitution of neuronal function, as assessed by
evoked potentials and improvement of focal neurologic
deficits.26,27
Because LVO patients have a relatively larger amount of
penumbral tissue compared with other stroke etiologies, they
may particularly benefit from BP elevation prior to recanaliza-
tion. However, the concept of induced hypertension has yet to
be substantiated by adequate prospective randomized studies.
In a small prospective study using phenylephrine to induce

Seminars in Neurology Vol. 41 No. 1/2021 © 2021. Thieme.

48 Blood Pressure Management for Acute Ischemic Stroke
higher BP, Rordorf et al concluded that patients with “large
extracranial or intracerebral vessel stenosis or occlusion” seem
to have the most benefit from induced BP.28 Hillis et al induced
higher BP in a small number of patients with perfusion–
diffusion mismatch and reported a “strong, statistically signif-
icant association between improved function and improved
perfusion.”29 In Hillis et al’s study, intravenous phenylephrine
was titrated to achieve a 10 to 20% increase in mean arterial
pressure over 1 to 8 hours, and this target was maintained for
at least 24 hours. Each patient in the intervention group
showed some degree of improvement on the NIHSS and a
cognitive battery after the treatment target was reached. On
day 3, the NIHSS score had improved by 4.2  1.0 in the
intervention group and by 1.2  3.0 in the control group. Based
on these and other studies,30–32 induced hypertension may be
a reasonable approach to the prethrombectomy LVO patient,
especially if there is a prolonged period between medical care
access and endovascular recanalization, such as in “hub and
spoke” stroke systems of care.33
That said, the studies cited earlier have sample sizes less
than 50 patients and methodological weaknesses. The
current AHA/ASA guidelines do not offer specific guidance
on the practice of induced hypertension, noting instead that
its “usefulness in patients with AIS is not well established.”8
Ultimately, in the absence of compelling data, the AHA
recommends permissive hypertension (
185/110 mm Hg),
or <180/105 mm Hg if IV tPA has been administered, prior to
EVT.8 The goal of
185/110 mm Hg is new in the 2019
guideline. The authors base this goal off criteria for the
recent randomized clinical trials of EVT, which had an
exclusion for BP >185/110 mm Hg.8 While this is a reason-
able suggestion, it is not an evidence in itself for improved
outcome with this goal. Future research may allow for more
patient-specific BP interventions aimed at improving the
survival of the ischemic penumbra.
Intraprocedural Blood Pressure
Although anesthetic considerations in patients undergoing EVT
for LVO are widely studied, there is a relative dearth in the
literature or guidelines regarding intraprocedural BP manage-
ment. A 2014 guideline by the Society of Neuroscience in
Anesthesiology and Critical Care recommended that SBP be
maintained between 140 and 180 mm Hg during EVT.34 The
AHA recommends a BP target of
180/105 mm Hg during EVT
(►Table 1).8 These guidelines, although motivated by presumed
mitigation of deleterious effects of extremes of intraprocedural
BP, lack strong supporting evidence. Given the absence of
research specific to intraprocedural BP, we can look at the
literature addressing anesthesia in this context. Jumaa et al
were the first to note improved clinical outcomes and smaller
final infarct volumes among patients who underwent EVT with
conscious sedation compared with general anesthesia.35
Subsequently, observational studies have highlighted better
outcomes in stroke patients undergoing conscious sedation
during EVT.36–39 Several explanations have been postulated
to account for the difference in outcomes, including (1) time
associated with intubation, (2) hypotension associated with
Seminars in Neurology Vol. 41 No. 1/2021 © 2021. Thieme.
Havenon et al.
anesthesia induction, and (3) vasodilation caused by use of
anesthetic gases resulting in a steal phenomenon, whereby
cerebral blood flow is shunted to healthy brain tissue from the
penumbra. However, randomized trials have failed to show a
difference in outcomes of patients treated with general anes-
thetics versus conscious sedation.40,41 One key factor that
putatively explains the better outcomes with general anesthesia
in observational studies versus in clinical trials may be the
prompt treatment of hypotensive episodes for anesthetized
patients in clinical trials.42
Recent publications have studied the impact of hypotension
on patient outcomes after EVT, independent of anesthetic
choice. By strictly analyzing their experience with patients
who underwent EVT under general anesthesia, Löwhagen
Hendén et al were able to control for the confounding effect
of anesthesia type, and noted that intraprocedural mean BP
reductions of >40% from baseline were predictive of poor
outcome.43 Similarly, Whalin et al studied patients who were
treated via conscious sedation and showed that for every
Downloaded by: University of Cambridge. Copyrighted material.
10 mm Hg decrease in intraprocedural mean arterial BP below
100 mm Hg, there was a 28% higher likelihood of poor out-
come.44 Most recently, Petersen et al demonstrated that before
vessel recanalization, larger intraprocedural BP reductions and
sustained relative hypotension were both independently
associated with worsened functional outcome, regardless of
reperfusion grade.2 For every 10 mm Hg reduction in the mean
BP during EVT compared with admission pressure, there was a
22% greater likelihood of unfavorable modified Rankin’s scale
score (3–6) at 90 days. In addition, larger intraprocedural BP
reductions were also predictive of infarct growth and final
infarct volume: every relative 10 mm Hg reduction in the mean
BP during EVT demonstrated a 4.1-mL increase in infarct
volume. Conversely, a post hoc analysis of the SIESTA trial
did not find any association between drops in BP from baseline
with functional outcomes, likely due to strictly protocolized BP
management interprocedurally.42
Thus, intraprocedural BP management during EVT may
represent a critical factor in the care of AIS patients with LVO.
Regardless of the manner of anesthesia provided during the
case, careful monitoring of BP, avoidance of hypotension, and,
potentially, treatment of hypotensive episodes appear to
be associated with better patient outcomes. In an era of
improved LVO patient throughput, as well as increasingly
effective and rapid recanalization techniques, focus on this
key aspect of patient care may represent an important step
forward in further improving outcomes.
Postprocedural Blood Pressure
Support for BP control following EVT comes from retrospective
series.45–47 Mistry et al identified a significant correlation
between maximum SBP and worse outcomes on 90-day modi-
fied Rankin’s score and hemorrhagic complications following
EVT in a three-center study of over 200 patients undergoing
EVT.45 This correlation between maximum SBP and 90-day
functional outcomes held when the authors performed a
subgroup analysis of patients undergoing successful (throm-
bolysis in cerebral infarction [TICI] 2b/3) versus unsuccessful
 Blood Pressure Management for Acute Ischemic Stroke
recanalization (TICI 0–2a). Similarly, Goyal et al examined
patients with LVOs following successful EVT.46 Patients who
died at 3 months from onset had higher maximum SBP levels
compared with those who did not (184  24 mm Hg vs.
167  21 mm Hg; p < 0.001), whereas patients who were func-
tionally independent at 3 months had a lower maximum SBP
level (163  20 mm Hg vs. 179  23 mm Hg; p < 0.001). Inter-
estingly, BP management was not associated with the develop-
ment of symptomatic intracerebral hemorrhages (sICH),
although the overall rates of sICH were relatively low (6.5%).
Anadani et al also identified BP following EVT as a determinant
of outcomes at 3 months.47 In their analysis of patients under-
going EVT for LVO, a lower average SBP was associated with
improved functional outcomes (modified Rankin’s scale: 0–2)
at 3 months. Interestingly, maximum SBP following EVT was
not associated with improved outcomes.
Conversely, the SIESTA investigators did not identify
changes in postprocedural BP to be associated with neuro-
logical improvement or long-term functional outcome in a
post hoc analysis.42 However, there were some distinct
differences between SIESTA and the previously discussed
retrospective series. The SIESTA trial had a target SBP range
of 140 to 160 mm Hg for EVT patients, which essentially
targeted both hyper- and hypotension. Given the conflicting
results of the existing data, BP management following EVT
continues to be an area of considerable practice variation.
A recent survey of StrokeNet sites identified significant
heterogeneity of postthrombectomy BP management.9 The
majority (52%) of the 58 responding centers did not use a
standard protocol, preferring to set individualized targets.
The recently published guidelines from the AHA recommend
BP
180/105 mm Hg for 24 hours following EVT (►Table 1),
unless the patient is post-tPA or has successful recanalization
(TICI: 2b–3), in which case the goal is <180/105.8 Based on
the retrospective data, some authors have advocated for goal
SBP < 180/105 mm Hg in patients with unsuccessful recana-
lization, and SBP < 140 or <160 mm Hg in patients with
successful recanalization following EVT, which appears rea-
sonable until more data are available.48
Blood Pressure Variability Postthrombectomy
In patients with AIS, increased BP variability (BPV), measured
by coefficient of variation, successive variation, standard devi-
ation, or more sophisticated methods, is associated with worse
neurologic outcome.49,50 The increase in BPV may be due to the
impaired autoregulation that can accompany stroke,51 which
could in turn harm the ischemic penumbra. Despite the
growing number of articles on BPV after stroke, there are little
data on the effect of BPV on outcome in patients receiving EVT.
One study included patients with AIS receiving EVT and
found there was an association between increased BPV and
worsening functional outcome, and that this association was
strongest in patients without successful recanalization as
opposed to those who achieved successful reperfusion.52
Another study showed that BPV was associated with early
neurological deterioration and worse outcome, which again
was particularly the case in patients with incomplete recan-
Havenon et al. 49
alization.53 Similar results were seen in a secondary analysis
of Mistry et al’s cohort of patients receiving EVT, where
elevated postprocedural BPV was associated with worse
90-day functional outcome. It remains unclear whether
increased BPV in the post-EVT period is the direct cause of
poor outcome or whether increased BPV is an epiphenome-
non of infarct growth or other physiologic stressors.
Discussion
Randomized controlled trial data are lacking to guide man-
agement of peri-EVT BP, but it has been common practice to
allow permissive hypertension to recruit collaterals in the
setting of vessel occlusion and then reduce BP following
recanalization.54–57 Eventually, guidelines were released
advocating for SBP
180/105 mm Hg for the first 24 hours
after treatment in patients undergoing EVT.7 Concurrently,
evidence emerged that lowering BP, at least post-EVT, could
provide some benefit.46,58,59 With the conceptual progress
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offered by these studies, it further became clear that not all
postthrombectomy patients should be treated equally, and
survey data indicate that most practitioners decide treat-
ment on a per-patient basis.3 The most important factor
affecting postthrombectomy BP management is recanaliza-
tion status. In patients with successful recanalization (TICI:
2b–3), more favorable outcomes have been found among
those with lower SBP.45,56 In successfully recanalized
patients, consensus is moving toward SBP goals such as
<160 mm Hg; others advocate for even more aggressive
measures, particularly for patients with potentially larger
infarct cores, as seen with the <140 mm Hg SBP goal in the
protocol for the DAWN trial.46,54,60 Care should be taken to
avoid hypotension, which can lead to stroke expansion,
increased risk of acute kidney injury, cardiac decompensa-
tion, and death in critically ill patients.24,61,62
For patients in whom satisfactory recanalization cannot
be obtained (TICI: 2a or lower), less evidence is available to
guide practice, but it seems reasonable to continue permis-
sive hypertension.3 Many advocate for an SBP goal of

180/105 mm Hg in such patients.45,46,63 Additionally, BPV
appears particularly detrimental in patients with no or
incomplete recanalization.52,64–66 Special consideration
should also be given to patients in whom IV tPA has been
administered. Guidelines for patients receiving IV tPA sug-
gest BP goals of <180/105 mm Hg, regardless of thrombec-
tomy status.7,67 In the NINDS trial that led to FDA approval of
IV tPA, hemorrhage rates nearly doubled (12.4 vs. 6.4%) in
patients with SBPs >180 mm Hg.68 Application of tPA-spe-
cific data to patients with LVO seems viable in the context of
them having received tPA.
In light of the absence of consensus of BP management
following EVT, the need for nuance persists and each patient
should be considered individually. For instance, it is important
to account for a patient’s baseline BP; overzealous reduction of
SBP in a chronically hypertensive patient could expand core
infarct.69,70 Most practitioners favor nicardipine as the optimal
choice for intravenous antihypertensive in these patients.45,56
Labetalol may be preferable if a patient is tachycardic, but it
Seminars in Neurology Vol. 41 No. 1/2021 © 2021. Thieme.
50 Blood Pressure Management for Acute Ischemic Stroke Havenon et al.

otherwise proves less easily titratable and often causes brady-
cardia.71 Nearly all high-quality data guiding management of
LVO patients involve only anterior circulation occlusions. Fur-
ther data are needed for posterior circulation patients, which,
for instance, accounted for 18% of thrombectomy cases in the
cohort of Goyal et al.46 Finally, patients with tandem disease or
underlying stenosis are now more commonly undergoing
angioplasty and stent placement of both extra- and intracranial
disease in conjunction with EVT. These patients merit addi-
tional consideration for reperfusion syndrome in addition to BP
control guidelines driven by EVT data.72
Future Research Directions
Future research should focus on optimizing not only biomarker
outcomes such as infarct volume but also functional outcomes
of EVT-treated patients. Data-driven and actionable BP targets
need to be generated in the pre-, peri-, and post-EVT period.
Large observational studies with sophisticated data-science
For the pre-EVT period, one research topic that has partic-
ular appeal is induced hypertension. Under normal circum-
stances, the cerebral vasculature has the intrinsic ability to
maintain relatively constant cerebral blood flow despite
changes in systemic BP, a mechanism known as cerebral
autoregulation.73 This mechanism ensures that the cerebral
blood flow matches the brain’s metabolic demands and
protects it from hypo- or hyperperfusion. After large-vessel
intracranial occlusion, the downstream perfusion pressure in
that vessel will be reduced below the lower autoregulatory
limit. Exhaustion of compensatory vasodilatory capacity and
the loss of intrinsic autoregulatory function in the ischemic
tissue leads to pressure passivity.74,75 This means that changes
in systemic BP are directly transmitted to the brain, and by
increasing BP, a corresponding increase in cerebral blood flow
to the ischemic tissue occurs.
Animal experiments have shown that even a short interval of
induced hypertension effectively augments cerebral blood flow
in LVO via an abrupt opening of collapsed collateral vessels.76

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methodologies need to be deployed in search of these targets,
and need to address how patient-specific variables such as core
size, quality of collaterals, site of occlusion, and recanalization
status affect the target BP. These targets need to be tested in
randomized trials with rigorous adjudication of safety and
efficacy. Lastly, the peri-EVT BP management needs to be
viewed as a continuum that follows the pathophysiology of
cerebral autoregulation relative to the recanalization status of
an LVO.
Worsening of cerebral edema and intracerebral hemorrhage
were not seen in these experiments, and have only been
described with prolonged ischemia and extreme hyperten-
sion.77 In humans, the direct relationship between BP and
cerebral blood flow can be observed in vivo using monitoring
of high-frequency physiological data or neuroimaging.78 BP
augmentation with induced hypertension may prolong
the viability of the ischemic penumbra via enhancement of
collateral flow (►Fig. 1). The induction of severe hypertension

Fig. 1 A patient with a left middle cerebral artery occlusion stroke (seen on diffusion weighted imaging [DWI]). The top row shows magnetic resonance
imaging perfusion with a mean arterial pressure (MAP) of 83 mm Hg and the bottom row shows the same patient 10 minutes later after an intravenous
phenylephrine infusion was started, raising MAP to 112 mm Hg. After blood pressure augmentation, there is noticeable improvement in the MRI perfusion
characteristics, with reduction in hypoperfused tissue (mean transit time, MTT) and improvement in cerebral blood flow (CBF).

Seminars in Neurology Vol. 41 No. 1/2021 © 2021. Thieme.

 Blood Pressure Management for Acute Ischemic Stroke
to the level of a hypertensive emergency should be avoided
because it can induce end-organ dysfunction including myo-
cardial infarction, renal impairment, and hemorrhagic stroke,79
but the induction of mild hypertension for a short duration
appears relatively safe based on preliminary data. Four nonran-
domized studies using IV vasopressors with treatment duration
between 3 and 7 days had only one major adverse event, a sICH
in a patient who was concurrently therapeutically anticoagu-
lated with IV heparin.28,31,80,81 However, despite compelling
conceptual reasons and pilot data, we will need rigorous clinical
trial evidence to support BP augmentation as a potential neuro-
protective strategy after acute stroke. Likewise, we will need
clinical trial data to support BP treatment strategies post-EVT,
when BP reduction could be beneficial. The existing data
support studies that would use calcium channel blockers or
nitric oxide donors as opposed to β-blockers or angiotensin-
converting enzyme inhibitors, given the potentially negative
effects of those medications in the acute stroke period.14,16–18
Conclusions
In conclusion, there is an absence of solid evidence on BP
management specific to LVO patients and further research is
urgently needed. Until compelling data are available, the
periprocedural BP management of an LVO patient undergoing
EVT can be viewed in two phases relative to the achievement of
recanalization (►Table 1). In the hyperacute phase prior to
recanalization, both in the pre-EVT and intraprocedural
periods, hypotension should be avoided to maintain adequate
penumbral perfusion, although the utility of this to maintain
collateral blood flow is not yet well established. Likewise, more
research is needed on the potentially deleterious impact of
increased BPV in AIS patients. Although the majority of prior
observational studies have noted an association between
higher postrecanalization BP and worse functional outcomes,
no randomized data are available regarding the safety and
efficacy of antihypertensive treatment following recanaliza-
tion. Prior to EVT, current AHA guidelines should be followed
(►Table 1):
185/110 mm Hg, unless post-tPA administration
when the goal is <180/105 mm Hg. After successful recanali-
zation (TICI: 2b–3), we believe that, in addition to the AHA goal
of
185/105, a target of a maximum SBP of < 160 mm Hg
appears reasonable, while the persistently occluded
patients (TICI: <2b) may require a more permissive goal of

180/105 mm Hg. Future research should focus on generating
randomized data on optimal BP management before, during,
and after EVT, to improve patient outcomes for these divergent
clinical scenarios.
Conflict of Interest
None.
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