Higher Blood Glucose Is Associated with the Severity of Hemorrhagic Transformation After Endovascular Therapy for Stroke

 If you're not going to tell how to prevent this problem, YOU DID ABSOLUTELY FUCKING USELESS RESEARCH!

Higher Blood Glucose Is Associated with the Severity of Hemorrhagic Transformation After Endovascular Therapy for Stroke

• Yasmin N Aziz, MD
• Vaibhav Vagal, BS
• Tapan Vijaykumar Mehta, MD, MPH
• 
  
• Shadi Yaghi, MD
• Pooja Khatri, MD, MSc
• Eva A Mistry, MBBS, MSCI
• Show all authors

Published:June 14, 2024DOI:https://doi.org/10.1016/j.jstrokecerebrovasdis.2024.107823

Highlights

• •
  Large vessel occlusion stroke may be particularly vulnerable to the effects of hyperglycemia.
• •
  We analyzed intracerebral hemorrhage severity as a result of hyperglycemia-induced toxicity.
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  Increasing blood glucose was associated with increasing severity of intracerebral hemorrhage.
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  Future study is needed to determine if glycemic control improves outcomes in this population.

ABSTRACT

Objectives

Hyperglycemia is associated with poor outcome in large vessel occlusion (LVO) stroke, with mechanism for this effect unknown.

Materials and Methods

We used our prospective, multicenter, observational study, Blood Pressure After Endovascular Stroke Therapy (BEST), of anterior circulation LVO stroke undergoing endovascular therapy (EVT) from 11/2017-7/2018 to determine association between increasing blood glucose (BG) and intracerebral hemorrhage (ICH). Our primary outcome was degree of ICH, classified as none, asymptomatic ICH, or symptomatic ICH (≥4-point increase in National Institutes of Health Stroke Scale [NIHSS] at 24 hours with any hemorrhage on imaging). Secondary outcomes included 24-hour NIHSS, early neurologic recovery (ENR, NIHSS 0-1 or NIHSS reduction by ≥8 within 24 hours), and 90-day modified Rankin Scale (mRS) using univariate and multivariable regression.

Results

Of 485 enrolled patients, increasing BG was associated with increasing severity of ICH (adjusted OR, aOR 1.06, 95% CI 1.02-1.1, p<0.001), higher 24-hour NIHSS (aOR 1.22, 95% CI 1.11-1.34, p<0.001), ENR (aOR 0.90, 95% CI 0.82-1.00, p<0.002), and 90-day mRS (aOR 1.06, 95% CI 1.03-1.09, p<0.001) when adjusted for age, presenting NIHSS, ASPECTS, 24-hour peak systolic blood pressure, time from last known well, and successful recanalization.

Conclusions

In the BEST study, increasing BG was associated with greater odds of increasing ICH severity. Further study is warranted to determine whether treatment of will decrease ICH severity following EVT.

Safety and Efficacy of Tight Versus Loose Glycemic Control in Acute Stroke Patients: A Meta-Analysis of Randomized Controlled Trials

Will your competent? doctor and hospital ensure further research occurs? Or WILL THEY INCOMPETENTLY DO NOTHING?

Weren't they already aware of this  and knew further research was needed?

• glycaemic control (2 posts to May 2023)

Do you prefer your  doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

 

Safety and Efficacy of Tight Versus Loose Glycemic Control in Acute Stroke Patients: A Meta-Analysis of Randomized Controlled Trials

Shuangzhe Wu, Yuke Mao, […], and Donghua Mi https://orcid.org/0000-0001-8845-8769 midonghua131@163.com+5View all authors and affiliations

Accepted Manuscripts

https://doi.org/10.1177/17474930241241994

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Abstract

Background:

Hyperglycemia is associated with worse stroke outcomes but it is uncertain whether tight glycaemic control during the acute stroke period is associated with a better outcome. We conducted a meta-analysis to compare the effect of tight glycemic control versus loose glycemic control in the acute phase of stroke patients.

Methods:

A literature search was performed to identify randomized controlled trials (RCTs) comparing the safety and efficacy of tight glycemic control with a relatively loose control of blood glucose of acute stroke (ischemic or hemorrhagic) patients within 24 hours after stroke onset. We required that the blood glucose level of the patients should not be lower than 6.11mmol/L at the time of enrollment, and for the intensive blood glucose control range, we defined the blood glucose level as lower than that of the control group.Tight glycaemic control was defined as blood glucose ≥ 6.11 mmol/L. The primary efficacy outcome measure was deaths from any cause at 90 days. Secondary efficacy outcomes comprised the number of participants with modified Rankin score (mRS), We define mRS scores 0-2 as favorable scores, recurrent stroke, and the National Institute of Health stroke scale (NIHSS) or the European Stroke Scale (ESS) scores. We defined the number of participants with hypoglycemia as our primary safety outcome. Subgroup analysis was performed according to age, the variety of interventions, maintained glucose level, and status of hypoglycemia on NIHSS scores or ESS scores.

Results:

Fifteen RCTs with 2957 participants meeting the including criteria were identified and included in this meta-analysis, although not all included data on every outcome measure. Data on the primary efficacy endpoint, mortality at 90 days, was available in 11 RCTs a total of 2575 participants. There was no significant difference between the intervention and control groups (OR: 1.00; 95%CI: 0.81 to 1.23; P=0.99). For secondary endpoints, there was no difference between intervention and control groups for a mRS < from 0-2 (OR: 0.96; 95%CI: 0.80 to 1.15; P=0.69; data from 9 RCTs available), or recurrent stroke (OR: 1.34; 95%CI: 0.92 to 1.96; P=0.13; data from 3 RCTs available). For NIHSS scores or ESS scores, there was a small difference in favor of intensive controls (SMD: -0.29; 95%CI: -0.54 to -0.04; P=0.02) There was a marked increase in hypoglycemia with tight control: (OR of 9.46 (95%CI: 4.59 to 19.50; P<0.00001; data from 9 RCTs available)

Conclusions:

There was no difference between tight and loose glycemic control on mortality, independence, or recurrent stroke outcome in acute stroke, but an increase in hypoglycaemia. There was a small effect improvement on neurological scales but the relevance of this needs confirming in future adequately powered studies.

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Management of Poststroke Hyperglycemia: Results of the TEXAIS Randomized Clinical Trial

FYI

Management of Poststroke Hyperglycemia: Results of the TEXAIS Randomized Clinical Trial

Christopher F. Bladin,

Ngai Wah Cheung,

Helen M. Dewey,

Leonid Churilov,

Sandy Middleton,

Vincent Thijs,

Elif Ekinci,

Christopher R. Levi,

Richard Lindley,

… See all authors

Originally published27 Nov 2023https://doi.org/10.1161/STROKEAHA.123.044568Stroke. 2023;54:2962–2971

Abstract

BACKGROUND:

Hyperglycemia in acute ischemic stroke reduces the efficacy of stroke thrombolysis and thrombectomy, with worse clinical outcomes. Insulin-based therapies are difficult to implement and may cause hypoglycemia. We investigated whether exenatide, a GLP-1 (glucagon-like peptide-1) receptor agonist, would improve stroke outcomes, and control poststroke hyperglycemia with minimal hypoglycemia.

METHODS:

The TEXAIS trial (Treatment With Exenatide in Acute Ischemic Stroke) was an international, multicenter, phase 2 prospective randomized clinical trial (PROBE [Prospective Randomized Open Blinded End-Point] design) enrolling adult patients with acute ischemic stroke ≤9 hours of stroke onset to receive exenatide (5 µg BID subcutaneous injection) or standard care for 5 days, or until hospital discharge (whichever sooner). The primary outcome (intention to treat) was the proportion of patients with ≥8-point improvement in National Institutes of Health Stroke Scale score (or National Institutes of Health Stroke Scale scores 0–1) at 7 days poststroke. Safety outcomes included death, episodes of hyperglycemia, hypoglycemia, and adverse event.

RESULTS:

From April 2016 to June 2021, 350 patients were randomized (exenatide, n=177, standard care, n=173). Median age, 71 years (interquartile range, 62–79), median National Institutes of Health Stroke Scale score, 4 (interquartile range, 2–8). Planned recruitment (n=528) was stopped early due to COVID-19 disruptions and funding constraints. The primary outcome was achieved in 97 of 171 (56.7%) in the standard care group versus 104 of 170 (61.2%) in the exenatide group (adjusted odds ratio, 1.22 [95% CI, 0.79–1.88]; P=0.38). No differences in secondary outcomes were observed. The per-patient mean daily frequency of hyperglycemia was significantly less in the exenatide group across all quartiles. No episodes of hypoglycemia were recorded over the treatment period. Adverse events of mild nausea and vomiting occurred in 6 (3.5%) exenatide patients versus 0 (0%) standard care with no withdrawal.

CONCLUSIONS:

Treatment with exenatide did not reduce neurological impairment at 7 days in patients with acute ischemic stroke. Exenatide did significantly reduce the frequency of hyperglycemic events, without hypoglycemia, and was safe to use. Larger acute stroke trials using GLP-1 agonists such as exenatide should be considered.

REGISTRATION:

URL: www.australianclinicaltrials.gov.au; Unique identifier: ACTRN12617000409370. URL: https://www.clinicaltrials.gov; Unique identifier: NCT03287076.

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Effect of Moderate and Severe Persistent Hyperglycemia on Outcomes in Patients With Intracerebral Hemorrhage

So you described a problem, but did nothing to solve it. USELESS!

I'd have everyone involved in this fired.

 

Effect of Moderate and Severe Persistent Hyperglycemia on Outcomes in Patients With Intracerebral Hemorrhage

Adnan I. Qureshi

,

Wei Huang

,

Iryna Lobanova

,

Premkumar N. Chandrasekaran

,

Daniel F. Hanley

,

Chung Y. Hsu

,

Renee H. Martin

,

Thorsten Steiner

,

Jose I. Suarez

,

Haruko Yamamoto

and

Kazunori Toyoda

Originally published30 Nov 2021https://doi.org/10.1161/STROKEAHA.121.034928Stroke. 2022;53:1226–1234

Abstract

Background:

We evaluated the effect of persistent hyperglycemia on outcomes in 1000 patients with intracerebral hemorrhage enrolled within 4.5 hours of symptom onset.

Methods:

We defined moderate and severe hyperglycemia based on serum glucose levels ≥140 mg/dL—<180 and ≥180 mg/dL, respectively, measured at baseline, 24, 48, and 72 hours. Persistent hyperglycemia was defined by 2 consecutive (24 hours apart) serum glucose levels. We evaluated the relationship between moderate and severe hyperglycemia and death or disability (defined by modified Rankin Scale score of 4–6) at 90 days in the overall cohort and in groups defined by preexisting diabetes.

Results:

In the multivariate analysis, both moderate (odds ratio, 1.8 [95% CI, 1.1–2.8]) and severe (odds ratio, 1.8 [95% CI, 1.2–2.7]) hyperglycemia were associated with higher 90-day death or disability after adjusting for Glasgow Coma Scale score, hematoma volume, presence or absence of intraventricular hemorrhage, hyperlipidemia, cigarette smoking, and hypertension (no interaction between hyperglycemia and preexisting diabetes, P=0.996). Among the patients without preexisting diabetes, both moderate (odds ratio, 1.8 [95% CI, 1.0–3.2]) and severe (odds ratio, 2.0 [95% CI, 1.1–3.7]) hyperglycemia were associated with 90-day death or disability after adjusting for above mentioned potential confounders. Among the patients with preexisting diabetes, moderate and severe hyperglycemia were not associated with 90-day death or disability.

Conclusions:

Persistent hyperglycemia, either moderate or severe, increased the risk of death or disability in nondiabetic patients with intracerebral hemorrhage.

Registration:

URL: https://www.clinicaltrials.gov; Unique identifier: NCT01176565.

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Serum glucose may help identify those admitted for stroke at greatest risk for recurrence

 What is the name of the test we need to be asking our doctors to perform? And the readout that is a concern? Since doctors and hospitals don't read and implement research findings it is up to stroke survivors to fill in the gaps.

Serum glucose may help identify those admitted for stroke at greatest risk for recurrence

By Scott Buzby

Source/Disclosures

ADD TOPIC TO EMAIL ALERTS

Presence of hyperglycemia at hospital admission for stroke was linked with elevated risk for subsequent stroke by 90 days, an increase that dual antiplatelet therapy seemingly failed to curtail, researchers reported.

According to research published in the Journal of the American Heart Association, serum glucose measurement may represent a quick and easy assay to identify patients hospitalized for transient ischemic attack or minor ischemic stroke who are at particularly high risk for subsequent stroke.

Source: Adobe Stock

“The risk of subsequent stroke is as high as 17% in the 90 days following the index event, but this risk is front-loaded within the first 7 days. For this reason, there is a need to incorporate dynamic physiological metrics into risk stratification schemes, and not simply long-term risk factors,” Brian Mac Grory, MB BCh BAO, MRCP, assistant professor of neurology at Duke University School of Medicine, and colleagues wrote. “Serum glucose is an intriguing potential predictor of recurrent stroke risk, because it is already assessed in the majority of patients with acute stroke using widely available, low-cost assays.”

Researchers conducted a secondary analysis of the POINT trial to assess the relationship between hyperglycemia ( 180 mg/dL) compared with normoglycemia (< 180 mg/dL) and 90-day outcomes following stroke hospitalization. Researchers also evaluated the effects of DAPT in this population. The primary endpoint was subsequent ischemic stroke.

POINT was a randomized controlled trial that assessed the effects of aspirin plus clopidogrel compared with aspirin alone for prevention of recurrent stroke among patients with TIA or minor ischemic stroke.

As Healio previously reported, although DAPT may lower risk for recurrent stroke compared with aspirin alone, it may increase risk for major hemorrhagic bleeding.

Impact of hyperglycemia on secondary stroke risk

Among the 4,878 participants in the POINT study, by 90 days, 267 experienced recurrent stroke, with a cumulative incidence of 9.7% in patients with hyperglycemia and 5.2% in those normoglycemic (log-rank P < .001).

After adjusting for age, sex, race, ethnicity, treatment assignment, index event classification and vascular risk factors as covariates, researchers observed significant association between hyperglycemia at hospital admission for TIA or minor ischemic stroke and risk for subsequent stroke compared with normoglycemia (HR = 1.5; 95% CI, 1.05-2.14; P = .01).

According to the study, hyperglycemia at stroke admission was also tied to a composite of ischemic stroke, MI or vascular death compared with normoglycemia (HR = 1.55; 95% CI, 1.1-2.2; P = .01).

In a similarly adjusted model, researchers found no association between hyperglycemia and major hemorrhage compared with normoglycemia (HR = 0.47; 95% CI, 0.11-1.99; P = .31).

DAPT in hyperglycemia following stroke

Researchers reported no risk reduction for subsequent stroke with DAPT initiation in patients with hyperglycemia (HR = 1.18; 95% CI, 0.69-2.03), but found there was lower risk in patients with normoglycemia (HR = 0.63; 95% CI, 0.48-0.83; P for interaction = .04).

“The benefits of clopidogrel/aspirin were not apparent in the small subgroup of patients with hyperglycemia, with an interaction observed between clopidogrel and serum glucose on subsequent stroke,” the researchers wrote.

In a sensitivity analysis that incorporated serum glucose as a continuous variable, researchers saw evidence of a nonlinear relationship between serum glucose and risk for subsequent stroke (P < .001).

 

Influence of glucose levels on clinical outcome after mechanical thrombectomy for large-vessel occlusion: a systematic review and meta-analysis

 So follow up research needed to actually get beyond just knowledge. Your doctor and hospital are responsible for getting such research initiated. If they don't that means the board of directors has completely failed at setting the correct goals for the stroke hospital.

Influence of glucose levels on clinical outcome after mechanical thrombectomy for large-vessel occlusion: a systematic review and meta-analysis

1. http://orcid.org/0000-0003-4241-7368Carlos Perez-Vega1,
2. http://orcid.org/0000-0002-8950-1762Ricardo A Domingo1,
3. Shashwat Tripathi1,2,
4. Andres Ramos-Fresnedo1,
5. http://orcid.org/0000-0003-0777-3172Samir Kashyap3,
6. Alfredo Quinones-Hinojosa1,
7. Michelle P Lin4,
8. http://orcid.org/0000-0002-7762-9902W Christopher Fox1,
9. Rabih G Tawk1

1. Correspondence to Dr Rabih G Tawk, Department of Neurosurgery, Mayo Clinic, Jacksonville, Florida FL 32224, USA; tawk.rabih@mayo.edu

Abstract

Mechanical thrombectomy (MT) represents the mainstay of treatment for patients with acute ischemic stroke due to large-vessel occlusion (LVO). Intravenous thrombolysis has been associated with worse clinical outcome in patients presenting with high blood glucose levels at admission; to date the true effect of hyperglycemia in the setting of MT has not been fully elucidated. In this meta-analysis, we analyzed the influence of high blood glucose levels at admission on clinical outcome after MT. Ovid EMBASE, PubMed, Scopus, and Cochrane Library databases were searched from their dates of inception up to March 2021. An initial search identified 2118 articles representing 1235 unique studies. After applying selection criteria, three prospective and five retrospective studies were analyzed, yielding a pooled cohort of 5861 patients (2041 who presented with hyperglycemia, and 3820 who presented with normal blood glucose levels). Patients in the hyperglycemia group were less likely to have a modified Ranking Scale (mRS) score <3 (risk ratio (RR): 0.65; 95% CI 0.59 to 0.72; p<0.0001; I²=13%), and had an increased risk of symptomatic intracranial hemorrhage (sICH) (RR: 2.07; 95% CI 1.65 to 2.60; p<0.0001; I²=0%) and mortality (RR: 1.73; 95% CI 1.57 to 1.91; p<0.0001; I²=0%). Patients who present with hyperglycemia and undergo MT for treatment of LVO have an increased risk of unfavorable clinical outcome, sICH, and mortality. Glucose levels at admission appear to be a prognostic factor in this subset of patients. Further studies should focus on evaluating control of the glucose level at admission as a modifiable risk factor in patients undergoing MT for LVO.

http://dx.doi.org/10.1136/neurintsurg-2021-017771

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Footnotes

• Twitter @carlosperezv, @wchrisfox

• Contributors RGT had the idea for the article. CP-V, RAD, ST, and AR-F performed the literature review, data collection, data analysis, and writing of the article. RGT, WCF, MPL, AQ-H, and SK performed critical evaluation, writing of the article evaluation, and revised the final version.

• Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

• Competing interests None declared.

• Provenance and peer review Not commissioned; externally peer reviewed.

• Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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Chronic hyperglycemia before acute ischemic stroke impairs the bilateral cerebrovascular response to exercise during the subacute recovery period

 So what? What is your solution to that problem? NO SOLUTION, YOU DID USELESS RESEARCH. 

I can see no purpose for including the term bilateral in the title.

Chronic hyperglycemia before acute ischemic stroke impairs the bilateral cerebrovascular response to exercise during the subacute recovery period

Carolyn S. Kaufman

Stephen X. Bai

Sarah M. Eickmeyer

Sandra A. Billinger

First published: 08 December 2020

https://doi.org/10.1002/brb3.1990

Abstract

Background and Purpose

Chronic hyperglycemia contributes to cerebrovascular dysfunction by damaging blood vessels. Poor glucose control has been tied to impairments in cerebral blood flow, which may be particularly detrimental for people recovering from major cerebrovascular events such as acute ischemic stroke. In this secondary analysis, we explore for the first time the connection between chronic hyperglycemia before acute stroke and the cerebrovascular response (CVR) to exercise 3 and 6 month into the subacute recovery period.

Methods

We recorded middle cerebral artery velocity (MCAv) using transcranial Doppler ultrasound bilaterally at rest and during moderate‐intensity exercise in stroke patients at 3 (n = 19) and 6 (n = 12) months post‐stroke. We calculated CVR as the difference between MCAv during steady‐state exercise and resting MCAv. We obtained hemoglobin A1c levels (HbA1c; a measure of blood glucose over the prior 3 months) from the electronic medical record (EMR) and divided participants by HbA1c greater or less than 7%.

Results

Participants with high HbA1c (>7%) at the time of acute stroke had significantly lower CVR to exercise for both the stroke‐affected (p = .009) and non‐affected (p = .007) hemispheres at 3 months post‐stroke. These differences remained significant at 6 months post‐stroke (stroke‐affected, p = .008; non‐affected, p = .016).

Conclusions

Patients with chronic hyperglycemia before acute ischemic stroke demonstrated impaired cerebrovascular function during exercise months into the subacute recovery period. These findings highlight the importance of maintaining tight glucose control to reduce morbidity and improve recovery post‐stroke and could have implications for understanding cerebrovascular pathophysiology.

1 INTRODUCTION

Chronic hyperglycemia causes systemic vascular damage. (Duckworth et al., 2009; Hemmingsen et al., 2011; Patel et al., 2008) Therefore, the American College of Physicians (ACP) and American Diabetes Association (ADA) recommend long‐term glucose control—specifically, a hemoglobin A1c (HbA1c) level below 7%—in order to minimize severity and frequency of vascular complications in diabetes mellitus (DM) (Qaseem et al., 2018; Targets, 2019). Without adequate control, chronic hyperglycemia increases the risk of stroke and negatively affects cerebrovascular function in other neurological disorders such as Alzheimer's disease and vascular cognitive impairment. (Ergul et al., 2012) Elevated blood glucose causes damage to both large and small vessels with increasing evidence that stroke and vascular cognitive impairment are the result of a combination of pathology in both types of cerebral vessels. (Huber, 2008) Reduced middle cerebral artery velocity (MCAv), a surrogate measure of cerebral blood flow (CBF), has been reported in those with DM at rest and in response to stimuli (e.g., hypercapnia) when compared to control groups. (Cui et al., 2017; Jansen et al., 2016; Kadoi et al.,; Novak et al., 2006) Additionally, we previously reported that cognitively normal older adults with higher cardiovascular risk level, including those with DM, have lower MCAv at rest and in response to moderate‐intensity exercise. (Perdomo et al.,)

In people with stroke, DM is often a comorbid condition along with other traditional cardiovascular risk factors. (Kernan et al., 2014) Two recent reports have shown that people with stroke may have altered cerebrovascular function when compared to their peers. (Kempf & A., Lui, Y., 2019; Robertson et al., 2019) However, specific contributing factors to this cerebrovascular dysfunction, such as chronic hyperglycemia (HbA1c > 7%), have yet to be explored. Thus, it is unknown whether chronic hyperglycemia in the months prior to acute ischemic stroke affects resting and exercising MCAv during the subacute stage of stroke recovery.

To address this gap in the literature, the objective of this secondary analysis was to explore whether elevated HbA1C at the time of acute stroke was associated with impaired MCAv measures during rest and exercise at 3 and 6 months post‐stroke. Specifically, we divided participants into those with chronically uncontrolled blood glucose (defined according to ADA and ACP guidelines as HbA1c > 7%) or controlled blood glucose (HbA1c < 7%) at the time of acute stroke. We hypothesized that the group with elevated HbA1c would have: 1) lower resting MCAv, 2) reduced cerebrovascular response to exercise (CVR, defined as exercising MCAv – resting MCAv), and 3) smaller percent change in MCAv (%ΔMCAv, calculated to control for resting baseline values) from rest to exercise at 3 and 6 months post‐stroke. As an exploratory aim, we evaluated the CVR in participants stratified by Type 2 DM diagnosis with the hypothesis that the CVR would be significantly negatively correlated with HbA1c level for individuals with Type 2 DM.

 

Treatment with exenatide in acute ischemic stroke trial protocol: A prospective, randomized, open label, blinded end-point study of exenatide vs. standard care in post stroke hyperglycemia

So all we need done is get this written up into a stroke protocol and distributed to every stroke hospital in the world. Hospitals not implementing this within a month need to be shut down. Damn it all, we need some action in stroke and that probably requires a lot of hospitals to be closed and stroke professionals fired.  Cleaning house will not be done by the stroke medical world, they are the cause of the problems. We need survivors to take charge.
http://journals.sagepub.com/doi/full/10.1177/1747493018784436?

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Claire Muller, N Wah Cheung, Helen Dewey, ...

First Published July 18, 2018 Product Review

https://doi.org/10.1177/1747493018784436

Article information

Abstract

Rationale

Post-stroke hyperglycemia occurs in up to 50% of patients presenting with acute ischemic stroke. It reduces the efficacy of thrombolysis, increases infarct size, and worsens clinical outcomes. Insulin-based therapies have generally not been beneficial in treating post-stroke hyperglycemia as they are difficult to implement, may cause hypoglycaemia, possibly increase mortality and worsen clinical outcomes. Exenatide may be a safer, simpler, and more effective alternative to insulin in acute ischemic stroke.

Design

TEXAIS is a three year, Phase 2, multi-center, prospective, randomized, open label, blinded end-point trial comparing exenatide to standard of care. It aims to recruit 528 patients with a primary end point of major neurological improvement at 7 days defined as a ≥8-point improvement in NIHSS score, or NIHSS 0–1. Secondary outcomes of hyper- and hypoglycaemia at 5 days and NIHSS and mRS at 90 days will be measured. The treatment arm will receive exenatide 5 µg subcutaneously twice daily. The control arm will receive standard stroke unit care. Continuous glucose monitors will track the dynamic variability of glucose.

Conclusion

TEXAIS aims to show that exenatide is safe and effective in the treatment of post-stroke hyperglycemia. It has been designed to be highly generalizable with an ability to enroll a large percentage of patients with acute ischemic stroke, regardless of admission blood glucose level, diabetes status, or stroke severity, with very low risk of hypoglycemia.
Trial registration: ClinicalTrials.gov/ANZCTR NTA1127

Keywords Acute stroke therapy, incretin, glucagon-like peptide-1 analog, exenatide, hyperglycemia, ischemic stroke, neuroprotection

Background

The prevalence of post-stroke hyperglycemia (PSH) varies between 20 and 60% at admission, particularly in stroke patients with pre-existing diabetes.^1–4 In patients without a previous diagnosis of diabetes, PSH is associated with an up to five-fold increased risk of death.^2,5 Subsequent glucose normalization is associated with improved survival.^2,5,6 Persistent hyperglycemia on serial glucose monitoring is an independent determinant of infarct expansion and is associated with increased short-term and long-term mortality and morbidity.⁷ Despite this, PSH is often poorly recorded, and uncertainty remains regarding appropriate management.⁸ Insulin protocols are difficult to implement, can cause hypoglycemia, and most studies have failed to show that insulin therapy reduces mortality or improves clinical outcomes.^9–12 An Australian multi-centre, stroke care implementation study (n = 1086) using a clearly defined insulin regimen reported that protocol adherence was poor with only 40% of intervention group PSH patients being treated with insulin.⁸
The concept of hyperglycemic “neurotoxicity” has been suggested by both animal models of stroke and clinical trials that report accelerated penumbra-into-infarction conversion, and poor vessel recanalization.^2,5,13,14 Hyperglycemia promotes intracellular lactic acidosis, directly damaging ischemic tissue and increasing blood–brain barrier disruption which in turn augments further inflammation^6,15,16 and predisposes to symptomatic intracerebral hemorrhage.^17,18 PSH is an independent risk factor for reduced tPA recanalization,⁵ reduces fibrinolytic activity,^6,16 and increases oxidative stress and inflammation, all of which culminate in a state of relative hypercoagulation. These deleterious effects of PSH are more pronounced in patients who have early reperfusion,^5,19 highlighting the need for a prompt and early PSH intervention.
Exenatide is a short acting, synthetic, incretin hormone mimetic, i.e. a glucagon-like peptide-1 receptor (GLP-1R) agonist. Following subcutaneous injection, exenatide has a median peak plasma concentration of 2.1 h. It increases insulin secretion in a glucose-dependent manner such that the risk of hypoglycemia is very low.
In acute ischaemic stroke (AIS) animal models, exenatide attenuates oxidative-induced apoptosis, promotes anti-apoptotic proteins, and reduces infarct volume by more than 50%.^20,21 Small clinical trials in ST elevation myocardial infarction patients receiving percutaneous coronary intervention indicate periprocedural exenatide lowered glucose levels and increased myocardial salvage by 30%.²² Following a successful safety and feasibility pilot study,²³ our group undertook a larger randomized study of 17 consecutive patients with AIS comparing subcutaneous exenatide 5 µg twice daily for 5 days with routine standard of care. Exenatide was safe and simple to use, and well tolerated by all patients. The aim of TEXAIS is to confirm these findings, and test efficacy, in a larger Phase 2 study.
More at link. 

Correlation of hyperglycemia with mortality after acute ischemic stroke

So your doctor will need a treatment protocol to address this, hopefully you don't need to remember this or you might die.
http://journals.sagepub.com/doi/abs/10.1177/1756285617731686

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Donghua Mi, Pingli Wang, Bo Yang, ...

First Published October 11, 2017 Research Article

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Abstract

Background:

Hyperglycemia has been considered a predictor of stroke outcomes. In this article we study the correlation between blood glucose levels within the first 24 h after stroke onset and patients’ outcomes in mortality and hemorrhagic transformations.

Methods:

Ninety-one non-diabetic patients with acute ischemic stroke admitted to a neurological intensive unit were recruited. Their blood glucose was measured twice within 6 h (baseline) and at every hour after stroke onset. Patients were collected into four groups as follows: those in which normoglycemia and no hyperglycemia were observed at either baseline or 24 h; those with baseline hyperglycemia and hyperglycemia only at baseline; those with 24 h hyperglycemia and hyperglycemia only at 24 h after stroke; and those with persistent hyperglycemia and hyperglycemia at both baseline and at 24 h. Endpoints were designated as the patient’s death within 30 days and/or hemorrhagic transformation under computerized tomography within the first 7 days after stroke onset.

Results:

Persistent hyperglycemia was correlated with an increased risk of mortality within 30 days (OR = 24.0; 95% CI = 2.8–199.3) and it was also correlated with hemorrhagic transformation (OR = 13.3; 95% CI = 2.7–66.1). Baseline or delayed hyperglycemia were not correlated with any outcome.

Conclusions:

Persistent hyperglycemia was correlated with mortality after acute ischemic stroke.