Protocol for the MAnagement of Systolic blood pressure during Thrombectomy by Endovascular Route for acute ischemic STROKE randomized clinical trial: The MASTERSTROKE trial

If this works then it is your responsibility to get this out to all stroke doctors and hospitals. Since we have fucking failures of stroke associations they don't have the ability to do easy stuff like that. Interesting that they want to maintain a high blood pressure instead of increasing the oxygen content of the red blood cells.

Possible solutions: Obviously not vetted coming from me. Don't do them.

You can look at the years these were reported on and tell how long your hospital has been incompetent.

• Normobaric oxygen (10 posts to January 2020)

• oxygen delivery (4 posts to January 2020)

• brain blood flow (3 posts to April 2019) 

 

How to Improve Your Brain Function with An Oxygen Concentrator April 2018 

Or is it more important to increase the loading ability of red blood cells to carry more oxygen? 

Like this?

University of Glasgow Study Demonstrates the Ability of Oxycyte® to Supply Oxygen to Critical Penumbral Tissue in Acute Ischemic Stroke  August 2012

Or like this?

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers. August 2017   

Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study May 2015 

Or this? having red blood cells release more oxygen.

Methylene blue shows promise for improving short-term memory

HOW FUCKING LONG WILL YOU LET YOUR INCOMPETENT STROKE HOSPITAL STILL TREAT PATIENTS LIKE NOTHING NEW HAS OCCURRED IN THE PAST 50 YEARS?

The latest here:

Protocol for the MAnagement of Systolic blood pressure during Thrombectomy by Endovascular Route for acute ischemic STROKE randomized clinical trial: The MASTERSTROKE trial

Doug Campbellhttps://orcid.org/0000-0002-4685-76111, Carolyn Deng1, Fiona McBryde2, Robyn Billing1, William K Diprose3, Timothy G Short1,4, Christopher Frampton5, Stefan Brew6, P Alan Barberhttps://orcid.org/0000-0003-2469-90233,7, and on behalf of the MASTERSTROKE Study Group
RegistrationAustralian New Zealand Clinical Trials Registry: ACTRN12619001274167p
RationaleCerebral blood flow is blood pressure-dependent when cerebral autoregulation is impaired. Cerebral ischemia and anesthetic drugs impair cerebral autoregulation. In ischemic stroke patients treated with endovascular thrombectomy, induced hypertension is a plausible intervention to increase blood flow in the ischemic penumbra until reperfusion is achieved. This could potentially reduce final infarct size and improve functional recovery.
Aim

To test if patients with large vessel occlusion stroke treated with endovascular thrombectomy will benefit from induced hypertension.
Design

Prospective, randomized, parallel group, open label, multicenter clinical trial with blinded assessment of outcomes.
Procedures

Patients with anterior circulation stroke treated with endovascular thrombectomy with general anesthesia within 6 h of symptom onset, and patients with ‘wake up’ stroke or presenting within 6 to 24 h with potentially salvageable tissue on computed tomography perfusion scanning, are included. Participants are randomized to a systolic blood pressure target of 140 mmHg or 170 mmHg from procedure initiation until recanalization. Methods to maintain the blood pressure are at the discretion of the procedural anesthesiologist.
Study outcomes 

The primary efficacy outcome is improvement in disability measured by modified Rankin Scale score at 90 days. The primary safety outcome is all-cause mortality at 90 days.
Analysis

The Mann-Whitney U test will be used to test the ordinal shift in the seven-category modified Rankin Scale score. All-cause mortality will be estimated using the Kaplan-Meier method and compared using a log-rank test.
Keywords
Clinical trial, acute stroke therapy, ischemic stroke, protocol, induced hypertension, reperfusion
1Department of Anaesthesia and Perioperative Medicine, Auckland City Hospital, Auckland, New Zealand
2Department of Physiology, University of Auckland, Auckland, New Zealand
3Department of Neurology, Auckland City Hospital, Auckland, New Zealand
4Department of Anaesthesiology, University of Auckland, Auckland, New Zealand
5Department of Statistics, University of Otago, Christchurch, New Zealand
6Department of Radiology, Auckland City Hospital, Auckland, New Zealand
7Department of Neurology, University of Auckland, Auckland, New Zealand
Corresponding author(s):
Doug Campbell, Department of Anaesthesia and Perioperative Medicine, Auckland City Hospital, Auckland 1023, New Zealand. Email: dcampbell@adhb.govt.nz
Introduction
Cerebral autoregulation, a protective mechanism preserving cerebral blood flow (CBF), is impaired after ischemic stroke1 and also by general anesthesia (GA).2 Consequently, global and regional CBF in ischemic territories of the brain become blood pressure-dependent during GA, and collateral blood flow to the ischemic penumbra may be decreased by relative hypotension and increased by induced hypertension.3 Induced hypertension has the potential to increase collateral blood flow to the ischemic penumbra, but also procedural complications such as groin hematoma, symptomatic intracranial hemorrhage, and cerebral reperfusion injury and edema. These harms can be mitigated by stopping induced hypertension when recanalization is achieved. Therefore, we aim to test the overall effectiveness of induced hypertension (systolic blood pressure [SBP] 170 mmHg) in comparison to current standard practice (SBP 140 mmHg) during GA for endovascular thrombectomy (EVT), by assessing functional recovery as measured by modified Rankin Score (mRS) score at 90 days.
Methods
The trial will be reported according to the CONSORT guidelines.4
Objective
To test whether an SBP target of 170 mmHg during GA for EVT leads to superior functional recovery at three months compared to an SBP target of 140 mmHg in patients with acute anterior circulation LVO stroke.
Design
Prospective, randomized, parallel group, open label, multicenter clinical trial with blinded assessment of outcomes. See Figure 1 for trial flow chart.
Figure 1. MASTERSTROKE trial flow chart.

Study setting
The trial is currently being conducted at academic hospitals with comprehensive stroke units.
Participant inclusion and exclusion criteria
Patients with anterior circulation stroke treated with EVT within 6 h of symptom onset, and patients with ‘wake up’ stroke or presenting within 6 to 24 h with potentially salvageable tissue on computed tomography (CT) perfusion scanning are included. Exclusion criteria include pre-stroke mRS >2, terminal illness with less than one year expected survival, cardiovascular disease where BP targeting is contraindicated, pregnancy, inability to participate in three-month follow-up, or EVT performed as a ‘rescue’ with stroke following medical or surgical procedures.
Written informed consent, waiver of consent, or two physician best interest agreement is sought prior to enrolment after approval of the regional ethics committee. Patients are screened for eligibility before randomization and enrolment.
Randomization and blinding
Group allocation is by web-based central randomization service undertaken with permuted blocks in a 1:1 ratio stratified by study center. The allocation sequence was computer-generated by an independent statistician. Blinding of the attending anesthesiologist is not possible. Participants, neuroradiologists, neurologists, and outcome assessors are blinded. One unblinded researcher collects BP adherence data. Site specific protocols were developed to maintain blinding.
Interventions
The anesthesiologist discloses anesthesia agent prior to randomization to avoid bias prior to randomization. Following randomization, one of two hemodynamic strategies from induction of GA until reperfusion is allocated, or the end of procedure if recanalization is not achieved.
1.
Target SBP of 140 ± 10 mm Hg
2.
Target SBP of 170 ± 10 mmHg
Techniques used to target SBP will be at the discretion of the anesthesiologist and may include vasoactive drugs, dosing of anesthetic maintenance drugs or intravenous fluids. In the pilot study,5 the predominant method to target SBP was titration of the vasopressor metaraminol, rather than anesthetic drug or intravenous fluid titration. Neuromuscular blocking agents will be used to facilitate endotracheal intubation, with control of hemodynamic physiology as described, but also intermittent positive pressure ventilation to normocarbia (end tidal CO2 [ETCO2] 4.5–6.0 kPa or PaCO2 4.5–6.0 kPa) to mitigate effects of abnormal PaCO2 on CBF. Normothermia and normoglycemia will be maintained. Doses and timing of drugs will be recorded in the electronic case record form. Other care during GA will be by routine institutional practice. The study intervention stops at recanalization (or time when thrombectomy attempts stop if the procedure is unsuccessful). Post-procedure blood pressure management is by usual institutional practice. Imaging will be routine 24-h non-contrast CT scanning.
Primary efficacy outcome
Disability measured by the mRS measured at 90 days.
Secondary efficacy outcomes
1.
Functional independence (mRS of 0, 1, or 2 at 90 days)
2.
Excellent functional outcome (mRS of 0 or 1 at 90 days)
3.
Home days, which are the number of days a participant resides at their pre-stroke domicile in the first 90 days post-stroke.
Primary safety outcomes
Incidence of all-cause mortality at 90 days.