Interesting. Increase blood pressure to deliver more blood to the brain.
I'd suggest other methods that aren't as likely to cause a hemorrhage. But I'm not medically trained so don't suggest these to your doctor.
If your doctor is doing nothing about oxygen delivery to the brain s/he is letting more neurons die than should. ARE YOU OK WITH THAT? Mine let 5.4 billion neurons die that first week.
No protocol, you need to fire the complete stroke department, starting with the board of directors. I would suggest one of these:
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?
Or
maybe this newest one I found about on Shark Tank, what is the
downside? You can't listen to anything I have to say, I'm not medically
trained, is your doctor?
Boost Oxygen on Shark Tank highlights
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.
AimTo test if patients with large vessel occlusion stroke treated with endovascular thrombectomy will benefit from induced hypertension.
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.
AimTo 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.
ProceduresPatients 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 outcomesThe 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.
AnalysisThe 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.
ProceduresPatients 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 outcomesThe 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.
AnalysisThe 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.
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.
Secondary safety outcomes
1.
Symptomatic intracranial hemorrhage is defined by the Safe Implementation of Thrombolysis in Stroke-Monitoring Study (SITS-MOST) definition as a Type 2 parenchymal hemorrhage with deterioration in National Institutes of Health Stroke Scale score of 4 points or death within 36 h.
2.
A composite outcome of intra-procedural complications including target vessel dissection or perforation, intracranial hemorrhage and groin hematoma.
Sample size
Simulations were run using relevant national mRS data to determine the sample size required for the comparison of the primary outcome of 90-day mRS between the two treatment groups. A minimum favorable shift in the 90-day mRS would equate to approximately one third of participants within each of the seven response categories improving their mRS score. Simulations using this scenario and comparing groups using the Mann-Whitney U test, demonstrated that 550 participants (225 per group) will provide 90% power to detect this difference in mRS outcome scores as statistically significant (two-tailed α = 0.05). This equates to an improvement in the percentage of participants with an independent outcome (mRS 0–2) from approximately 58% to 68%, a clinically important absolute effect size of 10%.
Interim analysis
An interim analysis for safety will be performed after 200 participants have completed 90-day follow-up. This analysis will be reviewed by the independent Data Safety Monitoring Committee.
Statistical analysis
The primary analysis will be an intention-to-treat analysis with no imputation of missing data. Baseline characteristics will be summarized by group using means and standard deviations (SD), medians and interquartile ranges (IQR), or counts and percentages as appropriate. Two-sided results will be reported with a p value < 0.05 indicating statistical significance. The primary analysis will use the Mann-Whitney U test to analyze the shift in the distribution of the seven-category mRS outcome. All binary outcomes will be compared between randomized groups using odds ratios with 95% confidence intervals (CI), generated from logistic regression analyses. The 90-day mortality, which will be estimated using the Kaplan-Meier method and compared using a log-rank test. A secondary per protocol analysis will be performed. A comprehensive statistical plan will be developed prior to database lock.
Subgroup analyses
A-priori subgroups have been identified for analyses. The subgroup analyses focus on the consistency of the treatment effect across the pre-defined sub-groups as indicated by the interaction term, sub-group × randomized treatment. The following subgroups will be explored.
1.
Age
2.
Sex
3.
Hypertension
4.
Time from stroke onset
5.
Baseline BP
6.
Admission NIHSS
7.
Use of thrombolytic agent
8.
Target vessel occlusion
9.
GA maintenance drug
Feasibility and safety
The MASTERSTROKE pilot trial5 was conducted to assess recruitment, adherence to SBP targets, data completeness, and safety. All feasibility targets were achieved. Recruitment was 3.5 patients per week and data completeness was over 99%. Adherence to the interventions was excellent with median (IQR [range]) of mean systolic blood pressure separation between groups of 139 (135–143 [115–154]) vs. 167 (150–175 [113–188]) mmHg, p < 0.001. The incidence of sICH was 2.0% compared to 4.4% in the HERMES collaboration meta-analysis of five RCTs,6 attesting to the safety of this trial protocol.
An independent Endpoint Adjudication Committee (EAC) adjudicates safety outcomes. Serious adverse events (SAEs) will be reported to and adjudicated by the EAC. The independent DSMC will review unblinded data for safety purposes.
Discussion
There is evidence that relative hypotension is harmful in acute ischemic stroke7 and may be especially harmful during GA8 due to impairment of cerebral autoregulation.1,2 The corollary is that induced hypertension may increase regional and penumbral blood flow, reducing final infarct size and improving clinical outcomes. Induced hypertension is known to increase regional blood flow and improve oxygen metabolism in stroke.9 Most patients with ischemic stroke have diagnosed or untreated hypertension.10 IH may be particularly beneficial in this group as CBF may fall if BP is lower than the lower limit of autoregulation.1,2 This will be the first clinical trial to test the effectiveness of induced hypertension (IH) in patients having GA for EVT.
IH is potentially therapeutic during ischemia but potentially harmful thereafter due to reperfusion injury and hemorrhagic change. The different effects of IH during ischemia and reperfusion means that overall effectiveness is unlikely in trials of stroke patients where reperfusion status is unknown. Previous trials assessing IH in ischemic stroke were not in patients undergoing EVT.11-13 Restricting IH to the ischemic phase prior to reperfusion may maximize collateral perfusion during the ischemic period while minimizing the risk of harm. The high procedural success rates of EVT5,6 will mean there will be a high proportion of patients who may benefit from IH.
Participants will be restricted to those having GA from the start of the procedure. Drugs used to maintain GA will likely further exacerbate the impaired cerebral autoregulation and IH will possibly make the intervention more effective. Furthermore, GA with tightly controlled physiology confers superior procedural conditions for EVT.14
In designing this trial, two fixed SBP targets have been chosen ensuring the SBP range will be within current guidelines.15 Choosing relative SBP targets based on prior diagnosis of hypertension or baseline SBP is more complicated and in the hyperacute setting prior health information may be unreliable or missing. The result will allow analysis by randomized group as well as stratifying by prior diagnosis of hypertension and baseline SBP. Exploratory analyses may help determine if there is an alternative ‘Goldilocks’ range of SBP different to the range assigned by randomization in this trial. The MASTERTROKE trial will provide level 1 evidence to guide BP management during GA for EVT where current guidance is limited.15,16 The interaction of abnormal cerebral physiology, BP, and GA drug effects has the potential for benefit and harm. A large RCT is warranted to provide robust guidance. MASTERSTROKE is the first trial of IH in EVT. It aims to provide further support for a targeted physiological and pharmacological approach in these patients. The MASTERSTROKE multicenter trial has recruited 190 patients to date and expects to be reporting the final result late in 2023.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: The MASTERSTROKE trial is funded by the Auckland District Health Board Research Trust, Auckland Medical Research Foundation, and the Neurological Foundation of New Zealand.
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.
Secondary safety outcomes
1.
Symptomatic intracranial hemorrhage is defined by the Safe Implementation of Thrombolysis in Stroke-Monitoring Study (SITS-MOST) definition as a Type 2 parenchymal hemorrhage with deterioration in National Institutes of Health Stroke Scale score of 4 points or death within 36 h.
2.
A composite outcome of intra-procedural complications including target vessel dissection or perforation, intracranial hemorrhage and groin hematoma.
Sample size
Simulations were run using relevant national mRS data to determine the sample size required for the comparison of the primary outcome of 90-day mRS between the two treatment groups. A minimum favorable shift in the 90-day mRS would equate to approximately one third of participants within each of the seven response categories improving their mRS score. Simulations using this scenario and comparing groups using the Mann-Whitney U test, demonstrated that 550 participants (225 per group) will provide 90% power to detect this difference in mRS outcome scores as statistically significant (two-tailed α = 0.05). This equates to an improvement in the percentage of participants with an independent outcome (mRS 0–2) from approximately 58% to 68%, a clinically important absolute effect size of 10%.
Interim analysis
An interim analysis for safety will be performed after 200 participants have completed 90-day follow-up. This analysis will be reviewed by the independent Data Safety Monitoring Committee.
Statistical analysis
The primary analysis will be an intention-to-treat analysis with no imputation of missing data. Baseline characteristics will be summarized by group using means and standard deviations (SD), medians and interquartile ranges (IQR), or counts and percentages as appropriate. Two-sided results will be reported with a p value < 0.05 indicating statistical significance. The primary analysis will use the Mann-Whitney U test to analyze the shift in the distribution of the seven-category mRS outcome. All binary outcomes will be compared between randomized groups using odds ratios with 95% confidence intervals (CI), generated from logistic regression analyses. The 90-day mortality, which will be estimated using the Kaplan-Meier method and compared using a log-rank test. A secondary per protocol analysis will be performed. A comprehensive statistical plan will be developed prior to database lock.
Subgroup analyses
A-priori subgroups have been identified for analyses. The subgroup analyses focus on the consistency of the treatment effect across the pre-defined sub-groups as indicated by the interaction term, sub-group × randomized treatment. The following subgroups will be explored.
1.
Age
2.
Sex
3.
Hypertension
4.
Time from stroke onset
5.
Baseline BP
6.
Admission NIHSS
7.
Use of thrombolytic agent
8.
Target vessel occlusion
9.
GA maintenance drug
Feasibility and safety
The MASTERSTROKE pilot trial5 was conducted to assess recruitment, adherence to SBP targets, data completeness, and safety. All feasibility targets were achieved. Recruitment was 3.5 patients per week and data completeness was over 99%. Adherence to the interventions was excellent with median (IQR [range]) of mean systolic blood pressure separation between groups of 139 (135–143 [115–154]) vs. 167 (150–175 [113–188]) mmHg, p < 0.001. The incidence of sICH was 2.0% compared to 4.4% in the HERMES collaboration meta-analysis of five RCTs,6 attesting to the safety of this trial protocol.
An independent Endpoint Adjudication Committee (EAC) adjudicates safety outcomes. Serious adverse events (SAEs) will be reported to and adjudicated by the EAC. The independent DSMC will review unblinded data for safety purposes.
Discussion
There is evidence that relative hypotension is harmful in acute ischemic stroke7 and may be especially harmful during GA8 due to impairment of cerebral autoregulation.1,2 The corollary is that induced hypertension may increase regional and penumbral blood flow, reducing final infarct size and improving clinical outcomes. Induced hypertension is known to increase regional blood flow and improve oxygen metabolism in stroke.9 Most patients with ischemic stroke have diagnosed or untreated hypertension.10 IH may be particularly beneficial in this group as CBF may fall if BP is lower than the lower limit of autoregulation.1,2 This will be the first clinical trial to test the effectiveness of induced hypertension (IH) in patients having GA for EVT.
IH is potentially therapeutic during ischemia but potentially harmful thereafter due to reperfusion injury and hemorrhagic change. The different effects of IH during ischemia and reperfusion means that overall effectiveness is unlikely in trials of stroke patients where reperfusion status is unknown. Previous trials assessing IH in ischemic stroke were not in patients undergoing EVT.11-13 Restricting IH to the ischemic phase prior to reperfusion may maximize collateral perfusion during the ischemic period while minimizing the risk of harm. The high procedural success rates of EVT5,6 will mean there will be a high proportion of patients who may benefit from IH.
Participants will be restricted to those having GA from the start of the procedure. Drugs used to maintain GA will likely further exacerbate the impaired cerebral autoregulation and IH will possibly make the intervention more effective. Furthermore, GA with tightly controlled physiology confers superior procedural conditions for EVT.14
In designing this trial, two fixed SBP targets have been chosen ensuring the SBP range will be within current guidelines.15 Choosing relative SBP targets based on prior diagnosis of hypertension or baseline SBP is more complicated and in the hyperacute setting prior health information may be unreliable or missing. The result will allow analysis by randomized group as well as stratifying by prior diagnosis of hypertension and baseline SBP. Exploratory analyses may help determine if there is an alternative ‘Goldilocks’ range of SBP different to the range assigned by randomization in this trial. The MASTERTROKE trial will provide level 1 evidence to guide BP management during GA for EVT where current guidance is limited.15,16 The interaction of abnormal cerebral physiology, BP, and GA drug effects has the potential for benefit and harm. A large RCT is warranted to provide robust guidance. MASTERSTROKE is the first trial of IH in EVT. It aims to provide further support for a targeted physiological and pharmacological approach in these patients. The MASTERSTROKE multicenter trial has recruited 190 patients to date and expects to be reporting the final result late in 2023.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: The MASTERSTROKE trial is funded by the Auckland District Health Board Research Trust, Auckland Medical Research Foundation, and the Neurological Foundation of New Zealand.
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