Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label diabetes. Show all posts
Showing posts with label diabetes. Show all posts

Thursday, August 6, 2026

Three Factors Tied to 13 Additional Dementia-Free Years

 Ask your competent? doctor how your stroke affects these possibilities! There better be an answer.

Three Factors Tied to 13 Additional Dementia-Free Years

Key Takeaways

  • Midlife vascular health was associated with nearly 13 more dementia-free years in a prospective U.S. cohort study.
  • At age 55, healthier study participants averaged 30.1 additional years without dementia.
  • Smoking, hypertension, and diabetes together sharply increased dementia risk and mortality.

Maintaining three key health factors during midlife -- normal blood pressure, no diabetes, and not smoking -- was associated with nearly 13 additional dementia-free years, a study of 12,000 people in the U.S. showed.

Individuals who met these criteria at age 55 lived an average 30.1 more years dementia-free, reported Josef Coresh, MD, PhD, of NYU Langone Health in New York City, and co-authors.

Conversely, those who smoked, had hypertension, and had diabetes at age 55 had dementia-free survival of only 17.5 years, Coresh and colleagues wrote in Neurology Open Access.

People with all three risk factors had a higher incidence of dementia (HR 2.69, 95% CI 1.94-3.73) and a higher incidence of dying before a dementia diagnosis (HR 5.61, 95% CI 4.67-6.74) compared with those who had no risk factors.

Overall, women lived longer without dementia than men at all risk levels. White participants had more years free of dementia than Black participants, and APOE4 carriers had shorter dementia-free survival than noncarriers.

"Our findings argue that people need to actively avert these factors in midlife as a strategy for preserving brain health for more than a decade," Coresh said in a statement. "Discovering new ways to delay dementia is crucial with 42% of Americans at risk for developing the condition at any time after age 55."

The findings were based on 12,409 participants in the prospective Atherosclerosis Risk in Communities (ARIC) study, which started in 1986 to evaluate midlife vascular risk factors and late-life dementia.

Previous research from the ARIC cohort suggested that 22% to 44% of dementia risk by age 80 could be attributed to three vascular risk factors measured in midlife and early late life, after accounting for risk factor concurrence and interactions.

Hypertension was defined as systolic blood pressure ≥130 mm Hg, diastolic blood pressure ≥80 mm Hg, or the use of blood pressure medication; diabetes as fasting glucose ≥126 mg/dL, non-fasting glucose ≥200 mg/dL, a physician's diagnosis, or the use of any diabetes medication; and current smoking was self-reported.

"Our study complements this important work by shifting focus from probability-based and attributable risk metrics to a time-based estimand -- dementia-free survival years, which quantifies the expected duration of life lived cognitively intact," Coresh and colleagues wrote.

"This outcome integrates two clinically relevant processes: incident dementia and death before dementia, therefore reflecting the competing risks that shape real-world aging trajectories," they pointed out. "In contrast to previous ARIC studies, this framework emphasizes how vascular health influences the balance between longevity and cognitive health over the life course."

In the current analysis, ARIC participants had a mean baseline age of 56 and 56% were women. Dementia was tracked through cognitive assessments, informant interviews, and continuous surveillance. Deaths without dementia were captured from multiple sources including the National Death Index.

Over a median follow-up of 26.3 years, 3,008 cases of dementia and 5,238 deaths without dementia were documented. Better vascular health was linked with longer dementia-free survival in a dose-response pattern.

"Several biologic pathways likely underlie our observed associations between vascular health and dementia-free survival, including chronic cerebrovascular injury, neuroinflammation triggered by vascular damages through hypertension and diabetes, and cumulative oxidative stress resulting from smoking," Coresh and colleagues wrote. "Together, these factors likely accelerate atherosclerosis, increase stroke risk, and may facilitate Alzheimer's disease pathology through promoting amyloid plaques and tau tangles."

The findings relied on one midlife assessment of risk factors, the researchers acknowledged. Dementia ascertainment may have differed between participants who attended recent visits and those who didn't. In addition, the study was observational and residual confounding may have influenced outcomes.

Wednesday, August 5, 2026

Midlife Vascular Health Adds Nearly 13 Dementia-Free Years

 My blood pressure didn't spike until age 60, now controlled, the rest I'm good at. But ask your competent? doctor if your stroke negates these factors! NO answer; PURE FUCKING INCOMPETENCE!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Midlife Vascular Health Adds Nearly 13 Dementia-Free Years

Summary: Maintaining healthy blood pressure, avoiding diabetes, and not smoking between ages 48 and 68 is associated with nearly 13 additional years of dementia-free life.

While the presence of all three vascular risk factors significantly accelerated dementia onset and reduced dementia-free survival across all groups, the researchers noted key demographic variations: women lived longer without dementia than men regardless of risk profile, and white participants experienced longer dementia-free lifespans than Black participants under similar risk conditions.

Key Facts

  • 13-Year Healthspan Gain: Individuals free of hypertension, diabetes, and smoking from ages 48 to 68 lived an average of nearly 13 additional years without developing dementia compared to those with all three risk factors (30 years vs. 17 years post-baseline).
  • Broad Cohort Scope: Analyzed 12,409 participants (average baseline age of 56) followed over a 26-year tracking period, during which 3,008 developed dementia and 5,238 died dementia-free.
  • Sex-Based Differences: Women consistently maintained longer dementia-free survival than men across equivalent risk categories (18.1 years for women with all three risk factors vs. 16.6 years for men).
  • Racial Disparities: White participants with all three risk factors lived an average of 19.6 dementia-free years compared to 16.0 years for Black participants, emphasizing the need for targeted midlife interventions in vulnerable populations.
  • Critical Prevention Window: Emphasizes age 48 to 68 as a crucial developmental window where aggressive vascular risk modification directly safeguards cognitive reserve in later life.

Source: NYU

Having normal blood pressure, no diabetes, and not smoking from age 48 to 68, are associated with nearly 13 additional years on average of dementia-free life, a new study shows.

Led by NYU Langone Health researchers, the new work also found that, no matter how many risk factors they had, women lived longer without dementia than men, and that white study participants had more dementia-free years than Black participants.

This shows a man and a brain.
Avoiding midlife vascular risk factors adds nearly 13 additional years of dementia-free life. Credit: Neuroscience News

Published online Aug. 5 in Neurology, the study results underscore the dual impact of the identified midlife risk factors, the presence of which was linked to both accelerated dementia onset and shortened overall dementia-free lifespans.

“Our findings argue that people need to actively avert these factors in midlife as a strategy for preserving brain health for more than a decade,” said study senior investigator Josef Coresh, MD, PhD, founding director, Optimal Aging Institute, NYU Langone.

“Discovering new ways to delay dementia is crucial with 42 percent of Americans at risk for developing the condition at any time after age 55.” Dr. Coresh is also the Terry and Mel Karmazin Professor, Department of Population Health, NYU Langone.

For the new study, the researchers analyzed data in the community-based Atherosclerosis Risk in Communities (ARIC) Study, which started in 1986 and followed participants over decades into late life, measuring midlife vascular risk factors and dementia.

The current study looked at 12,409 people with an average age of 56 who were free of dementia. Participants were assessed for three risk factors: high blood pressure, diabetes, and smoking. They were then followed for an average of 26 years. During that time, 3,008 developed dementia and 5,238 people died without developing dementia. Those who had no risk factors lived without developing dementia nearly 13 years longer than people with the three risk factors (30 years total after the study’s start versus 17 years).

The team also sought to determine how cardiovascular risk factors in midlife influenced dementia-free survival across demographics. Women with all three risk factors lived an average of 18.1 years from the start of tracking without developing dementia, compared to 16.6 years for male study participants. White participants with all three risk factors lived an average of 19.6 years without developing dementia, compared to 16 years for Black participants.

“These results suggest that vascular risk reduction may benefit all groups, but that certain populations, such as Black adults, may especially benefit from targeted prevention efforts,” Dr. Coresh added. “Hopefully, these results will encourage people to stop smoking and watch their vascular health closely from age 48 on.”

Importantly, the study was not designed to prove that avoiding these vascular risk factors caused the observed delay in dementia — only that they were associated with each other. Another limitation of the study was that the risk factor measurement was performed just once, so changes over time were not captured.

Funding: This study was supported by National Institutes of Health (NIH) grants K24HL152440 and K01DK138273, and the ARIC study was funded by grants NIH U01HL096812, U01HL096814, U01HL096899, U01HL096902 and U01HL096917.

Along with Dr. Coresh, study authors are Jiaqi Hu, Institute for Hospital Management, Tsinghua University in Beijing (lead author); Jason Smith, University of North Carolina School of Medicine; A. Richey Sharrett, Elizabeth Selvin and Michael Fang, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health; Rebecca F. Gottesman, Stroke Branch, National Institute of Neurological Disorders and Stroke; Pamela Lutsey, Division of Epidemiology and Community Health, School of Public Health, University of Minnesota; Thomas H. Mosley Jr., MIND Center, University of Mississippi Medical Center School of Medicine, Jackson; and Jordan Weiss, Department of Medicine (Division of Precision Medicine) and Optimal Aging Institute, NYU Grossman School of Medicine.

Key Questions Answered:

Q: Why are midlife vascular factors so influential on dementia risk decades later?

A: Midlife hypertension, diabetes, and smoking cause cumulative structural damage to the brain’s microvasculature. Chronic hypoperfusion, small vessel disease, inflammation, and blood-brain barrier breakdown reduce cognitive resilience and accelerate pathological protein accumulation, laying the groundwork for clinical dementia late in life.

Q: What did the study reveal regarding health disparities between demographic groups?

A: Even when carrying the same three vascular risk factors, Black participants experienced shorter dementia-free lifespans (16.0 years) than white participants (19.6 years). This highlights that systemic healthcare disparities, social determinants of health, and differences in baseline disease severity likely amplify the cognitive burden of vascular risk in Black communities.

Q: Did the study establish that treating these risk factors directly prevents dementia?

A: The study demonstrated a strong prospective association rather than direct causation. Because risk factors were measured at baseline, the observational design does not capture how midlife treatment changes over time impact dementia trajectories, though the robust 26-year tracking strongly supports midlife risk reduction as a primary preventative strategy.

Editorial Notes:

  • This article was edited by a Neuroscience News editor.
  • Journal paper reviewed in full.
  • Additional context added by our staff.

About this dementia and aging research news

Author: David March
Source: NYU
Contact: David March – NYU
Image: The image is credited to Neuroscience News

Original Research: The findings will appear in Neurology

Wednesday, June 25, 2025

Role of human urinary kallikrein in reducing progressive ischemic stroke among acute ischemic stroke patients with concurrent hypertension and diabetes: a hospital-based retrospective cohort study

Where is the protocol located so all stroke hospitals will find and implement it? Oh, you INCOMPENTLY DIDN'T DO THAT? You're fired!

 Role of human urinary kallikrein in reducing progressive ischemic stroke among acute ischemic stroke patients with concurrent hypertension and diabetes: a hospital-based retrospective cohort study


Zeyang Zheng&#x;Zeyang ZhengYuelong Li&#x;Yuelong LiShanshan YangShanshan YangYuanqi XuYuanqi XuLian YiLian YiYushuang LiuYushuang LiuLi ZhangLi ZhangZhongling Zhang
Zhongling Zhang*
  • Department of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin, China

Background: Progressive ischemic stroke (PIS) poses significant challenges in the management of acute ischemic stroke (AIS), with higher morbidity and mortality rates, especially among patients with vascular risk factors such as hypertension and diabetes. This study evaluates the efficacy of human urinary kallidinogenase (HUK) in reducing the incidence of PIS in patients with AIS, with a particular focus on subgroups based on vascular pathology and thrombolytic treatment.

Methods: This retrospective cohort study included 916 patients with AIS treated at a single tertiary care center between January 2022 and September 2023. The patients were divided into two groups based on whether they received HUK treatment in addition to standard care or standard care alone. The primary outcome was the incidence of PIS. Independent sample t-tests or chi-squared tests were used for univariate analysis between groups to identify potential predictors associated with the occurrence of PIS, with factors achieving a p-value < 0.1 considered for multivariate binary logistic regression analysis. Multivariate analysis adjusted for potential confounders to determine independent predictors significantly associated with PIS. The significance threshold was set at p < 0.05. In addition, subgroup analyses were conducted based on stroke subtype (TOAST classification), thrombolysis treatment, and infarction location.

Results: HUK treatment significantly reduced the incidence of PIS (p < 0.001), with the most notable effects observed in patients with large-artery atherosclerosis and small-artery occlusion, those not undergoing intravenous thrombolysis, and those with anterior circulation infarctions. Conversely, no significant reduction was noted in patients with cardioembolic stroke, other etiologies of infarction, intravenous thrombolysis, posterior circulation infarctions, or both anterior and posterior circulation infarctions. Factors such as low body mass index (BMI) and high activated partial thromboplastin time are associated with an increased risk of PIS.

Conclusion: HUK treatment appears to be an effective strategy for reducing the risk of PIS in patients with AIS, particularly in those at higher risk owing to specific vascular pathologies. These findings support the use of HUK in clinical practice to improve the outcomes of patients with stroke. Future prospective, multicenter, randomized controlled trials are warranted to validate these findings and further elucidate the underlying mechanisms.

1 Introduction

Stroke remains the second leading cause of death worldwide and the third most common cause of disability and mortality. Ischemic strokes, representing 62.4% of all new stroke cases, disproportionately affect populations in low to upper-middle-income countries, accounting for over 80% of stroke-related disability-adjusted life years (DALYs) (1). Notably, approximately 25 to 33% of stroke survivors develop PIS within days following the initial event, presenting with worsening neurological deficits and generally poorer prognostic outcomes (2).

HUK, a serine protease derived from urine, has garnered attention for its therapeutic potential in AIS, primarily through enhancing collateral circulation, stimulating angiogenesis, and improving cerebral perfusion (35). A longitudinal study involving 300 patients demonstrated that those receiving HUK exhibited notably lower scores on the modified Rankin Scale (mRS) at a 12-month follow-up compared to their counterparts in the control group (6). Moreover, a meta-analysis incorporating data from 24 studies quantified the neurologic improvement attributable to HUK, indicating a 0.56-fold increase in recovery rates (7). Focusing on patients with large artery atherosclerosis, another retrospective analysis revealed that HUK treatment was associated with significantly reduced National Institutes of Health Stroke Scale (NIHSS) scores (8).

Hypertension and diabetes are prevalent risk factors in the AIS patient demographic, with the National Inpatient Sample highlighting that 79% of these patients suffer from hypertension, and 34% are diabetic (911). Endothelial dysfunction, insulin resistance, and impaired vascular reactivity caused by hypertension and diabetes may increase the adverse risks in AIS patients. Previous studies have demonstrated that blood pressure levels in AIS patients are significantly associated with their neurological outcomes. Maintaining appropriate blood pressure levels can significantly improve the prognosis of AIS patients (1213). Given the high prevalence of these comorbidities and their significant impact on stroke outcomes, investigating the therapeutic potential in this high-risk subgroup is of great clinical significance. Despite these statistics, research into HUK’s effectiveness specifically for patients with AIS concurrently diagnosed with these conditions remains sparse. One study reported that patients with AIS with stage 3 hypertension undergoing HUK treatment showed substantial improvements in mRS scores and recovery rates 3 months post-treatment (14). Another study contrasting patients with AIS with abnormal glucose metabolism observed a significant reduction in NIHSS scores following HUK treatment, although mRS scores did not differ significantly between the treated and control groups (15).

Thus, the present study aimed to investigate the effects of HUK on the incidence of PIS post-admission in patients with AIS with both hypertension and with diabetes, with a subgroup analysis by site of lesions, TOAST subtypes, and the use of intravenous thrombolysis.


More at ink.

Friday, May 23, 2025

Type 1 or Type 2: Which Patients With Diabetes Face Greater Stroke Risk?

 Will your competent? doctor ENSURE you don't get a stroke with either type? That would be my definition of competence.

Type 1 or Type 2: Which Patients With Diabetes Face Greater Stroke Risk?

Ischemic stroke risk was associated with higher A1C levels among individuals with type 1 and type 2 diabetes.

Compared with the general population, individuals with type 1 diabetes (T1D) had a higher risk for both ischemic stroke and hemorrhagic stroke; however, those with type 2 diabetes (T2D) had a significantly higher risk for ischemic stroke vs hemorrhagic stroke. These are the findings of a study published in Neurology.

Diabetes is associated with increased risk for cardiovascular complications, including ischemic stroke, however, the relationship with hemorrhagic stroke risk remains unclear.

Researchers from the University of Gothenburg sourced data for this study from the National Diabetes Register (NDR) and Total Population Register (TPR), which are nationwide databases from Sweden. Patients with T1D (n=47,720) or T2D (n=686,158) in 2005 to 2019 were each matched with 3 individuals without diabetes (T1D: n=143,160; T2D: n=2,058,474) and evaluated for incident stroke through 2022.

Further research is needed to better understand the mechanisms behind the increased hemorrhagic stroke risk in type 1 diabetes and to refine stroke prevention strategies for both diabetes types.

Table 1 presents the demographic characteristics and anticoagulant and antiplatelet usage of participants with T1D, T2D, and their respective control groups.

Group% MenMean Age (years)% Using Anticoagulants% Using Antiplatelets
T1D55.2%34.42.4%14.9%
T1D Control Group55.2%34.45.8%17.4%
T2D56.7%65.312.0%37.7%
T2D Control Group56.7%65.36.7%18.3%

During follow-up, 0.6% of patients with T1D and 1.0% of patients with T2D had an incident hemorrhagic stroke compared with 0.3% and 1.0% among their respective control cohorts. Both patients with T1D (4.0% vs 1.5%) and T2D (9.0% vs 6.1%) had higher rates of incident ischemic stroke during follow-up than control individuals, respectively.

In the T1D analyses, T1D was associated with risk for both hemorrhagic (hazard ratio [HR], 1.88; 95% CI, 1.57-2.26; P <.001) and ischemic (HR, 2.54; 95% CI, 2.36-2.73; P <.001) stroke. Conversely, in the T2D analyses, T2D was not associated with hemorrhagic stroke risk (HR, 0.99; 95% CI, 0.96-1.02; P =.621) but was associated with ischemic stroke risk (HR, 1.37; 95% CI, 1.35-1.38; P <.001).

In both T1D and T2D analyses, additional predictors for hemorrhagic and ischemic stroke risk included increased age, male gender, hypertension, a history of stroke, lower income, and lower education. Ischemic stroke was additionally related with antiplatelet use, alcohol use, atrial fibrillation, myocardial infarction, and heart failure.

When glycated hemoglobin (HbA1c) levels were considered, in T1D hemorrhagic stroke risk was associated with HbA1c of 52 mmol/mol or greater (HR range, 1.58-2.56; all P ≤.022) and ischemic stroke with HbA1c of 42 mmol/mol or greater (HR range, 1.65-3.83; all P ≤.001). In T2D, hemorrhagic stroke risk was associated with HbA1c greater than 72 mmol/mol (HR, 1.21; P <.001) and ischemic stroke with any level of HbA1c (HR range, 1.13-1.82; all P ≤.001).

This study was limited by only including covariate data collected at baseline and did not account for longitudinal changes in sociodemographic or clinical characteristics.

“Further research is needed to better understand the mechanisms behind the increased hemorrhagic stroke risk in type 1 diabetes and to refine stroke prevention strategies for both diabetes types,” the researchers concluded.

References:

Sunday, March 30, 2025

GLP-1 may have potential to improve poststroke outcomes, prognosis

 You're living in la-la land if you think your doctors and hospital implement research without YOU insisting it get tried. 

GLP-1 may have potential to improve poststroke outcomes, prognosis

               ByScott Buzby

Fact checked byRichard Smith

Key takeaways:

  • Liraglutide may improve outcomes and prognosis after minor stroke/transient ischemic attack in patients with diabetes.
  • However, the trial was halted prematurely and the data should be interpreted with caution.

The GLP-1 liraglutide showed potential benefit in reducing stroke recurrence and improving functional outcomes after minor stroke or transient ischemic attack, a speaker reported.

However, the LAMP study, presented at the International Stroke Conference, was terminated early due to slow enrollment and cost.

Graphical depiction of data presented in article
Data were derived from Zhu H, et al. LB44. Presented at: International Stroke Conference; Feb. 5-7, 2025; Los Angeles (hybrid meeting).

Diabetes increases the [incidence] and recurrence of stroke by two to four times. But insulin or sulfonylurea-based treatment for glycemic control did not reduce the risk of microvascular complications such as myocardial infarction and ischemic stroke. Even with 3 weeks of dual antiplatelet therapy, 12.8% of diabetic patients with minor acute ischemic stroke experienced recurrence within 90 days,” Hui-Li Zhu, MD, associate professor at The First Affiliated Hospital of Jinan University, Guangzhou, China, said during a presentation. “Liraglutide is a synthetic long-acting GLP-1 receptor agonist, and has the ability to cross the blood-brain barrier. Our previous study showed liraglutide decreased the infarct volume and improved neurologic deficits in a rat model of [middle cerebral artery] occlusion. ... Both basic research and clinical studies have suggested that GLP-1 receptor agonists may have the potential to improve stroke recurrence and prognosis.”

LAMP was a multicenter, randomized controlled, prospective trial designed to evaluate the efficacy and safety of liraglutide (Victoza/Saxenda, Novo Nordisk) for the prevention of recurrent stroke after minor ischemic stroke or high-risk TIA in patients with diabetes.

The LAMP study was terminated early due to a lower-than-expected enrollment and financial constraints, which prevented completion within the planned timeframe or target sample size, according to the presentation.

Overall, 636 patients hospitalized with minor ischemic stroke or high-risk TIA within 24 hours of symptom onset were included in the study and were randomly assigned to liraglutide or usual care.

Individuals assigned to liraglutide were provided ascending daily doses of the drug, starting with 0.6 mg and rising to 1.8 mg by day 30.

The primary endpoint was occurrence of new strokes within 90 days of index stroke.

Baseline characteristics were balanced between the liraglutide and usual care groups (mean age, 64 years; 36% women; 91% with history of diabetes; mean baseline HbA1c, 8.2%). The average BMI was approximately 24 kg/m2 and one-third of patients were currently smoking.

Subsequent new stroke occurred in 13.8% of the usual care arm compared with 7.9% of the liraglutide arm, which in the intention-to-treat analysis translated to a hazard ratio of 0.56 favoring liraglutide (95% CI, 0.34-0.91; P = .02). However, due to insufficient sample size, statistical power was only 67%.

In secondary analysis, the researchers reported that after minor ischemic stroke or high-risk TIA, individuals with diabetes assigned to liraglutide were more likely to achieve a modified Rankin score of 1 or less at 90 days compared with usual care (OR = 1.95; 95% CI, 1.28-3; P = .002). Similarly, liraglutide was associated with greater likelihood to achieve a modified Rankin score of 2 or less compared with usual care (OR = 1.77; 95% CI, 1.06-3.02; P = .032).

“Among Chinese patients with minor acute ischemic stroke or high-risk TIA who were diagnosed with type 2 diabetes, treatment with liraglutide probably reduced the risk of stroke recurrence and improved outcomes at 90 days,” Zhu said during the presentation. “Careful interpretation of these early terminated study results is warranted, and additional research is required to confirm these potential benefits. The LAMP study is the first and largest-scale trial investigating GLP-1 receptor agonists in patients with ischemic stroke, offering some valuable insights into their potential benefits for improving patient outcomes.”

Thursday, February 13, 2025

GLP-1 may have potential to improve poststroke outcomes, prognosis

 I'm not diabetic and I'm 19 years posts stroke but because my doctor COMPLETELY FAILED at getting me recovered, I'm overweight at 28.4 BMI.

For weight loss, healthcare professionals may prescribe GLP-1 agonists for people with an initial BMI of 30 or higher or people who have a BMI of 27 or higher and at least one weight-related health condition, such as: type 2 diabetes. prediabetes. high blood pressure.

 I fall into this category:  I now have a BMI of 28 because my doctor failed to get me 100% recovered so I could continue my active life that kept my weight in check. High blood pressure is controlled by drugs.

My cardiologist agrees I could be on it but in June I'll ask my regular doctor for it.

GLP-1 may have potential to improve poststroke outcomes, prognosis


Key takeaways:

  • Liraglutide may improve outcomes and prognosis after minor stroke/transient ischemic attack in patients with diabetes.
  • However, the trial was halted prematurely and the data should be interpreted with caution.

The GLP-1 liraglutide showed potential benefit in reducing stroke recurrence and improving functional outcomes after minor stroke or transient ischemic attack, a speaker reported.

However, the LAMP study, presented at the International Stroke Conference, was terminated early due to slow enrollment and cost.Graphical depiction of data presented in article

Data were derived from Zhu H, et al. LB44. Presented at: International Stroke Conference; Feb. 5-7, 2025; Los Angeles (hybrid meeting).

Diabetes increases the [incidence] and recurrence of stroke by two to four times. But insulin or sulfonylurea-based treatment for glycemic control did not reduce the risk of microvascular complications such as myocardial infarction and ischemic stroke. Even with 3 weeks of dual antiplatelet therapy, 12.8% of diabetic patients with minor acute ischemic stroke experienced recurrence within 90 days,” Hui-Li Zhu, MD, associate professor at The First Affiliated Hospital of Jinan University, Guangzhou, China, said during a presentation. “Liraglutide is a synthetic long-acting GLP-1 receptor agonist, and has the ability to cross the blood-brain barrier. Our previous study showed liraglutide decreased the infarct volume and improved neurologic deficits in a rat model of [middle cerebral artery] occlusion. ... Both basic research and clinical studies have suggested that GLP-1 receptor agonists may have the potential to improve stroke recurrence and prognosis.”

LAMP was a multicenter, randomized controlled, prospective trial designed to evaluate the efficacy and safety of liraglutide (Victoza/Saxenda, Novo Nordisk) for the prevention of recurrent stroke after minor ischemic stroke or high-risk TIA in patients with diabetes.

The LAMP study was terminated early due to a lower-than-expected enrollment and financial constraints, which prevented completion within the planned timeframe or target sample size, according to the presentation.

Overall, 636 patients hospitalized with minor ischemic stroke or high-risk TIA within 24 hours of symptom onset were included in the study and were randomly assigned to liraglutide or usual care.

Individuals assigned to liraglutide were provided ascending daily doses of the drug, starting with 0.6 mg and rising to 1.8 mg by day 30.

The primary endpoint was occurrence of new strokes within 90 days of index stroke.

Baseline characteristics were balanced between the liraglutide and usual care groups (mean age, 64 years; 36% women; 91% with history of diabetes; mean baseline HbA1c, 8.2%). The average BMI was approximately 24 kg/m2 and one-third of patients were currently smoking.

Subsequent new stroke occurred in 13.8% of the usual care arm compared with 7.9% of the liraglutide arm, which in the intention-to-treat analysis translated to a hazard ratio of 0.56 favoring liraglutide (95% CI, 0.34-0.91; P = .02). However, due to insufficient sample size, statistical power was only 67%.

In secondary analysis, the researchers reported that after minor ischemic stroke or high-risk TIA, individuals with diabetes assigned to liraglutide were more likely to achieve a modified Rankin score of 1 or less at 90 days compared with usual care (OR = 1.95; 95% CI, 1.28-3; P = .002). Similarly, liraglutide was associated with greater likelihood to achieve a modified Rankin score of 2 or less compared with usual care (OR = 1.77; 95% CI, 1.06-3.02; P = .032).

“Among Chinese patients with minor acute ischemic stroke or high-risk TIA who were diagnosed with type 2 diabetes, treatment with liraglutide probably reduced the risk of stroke recurrence and improved outcomes at 90 days,” Zhu said during the presentation. “Careful interpretation of these early terminated study results is warranted, and additional research is required to confirm these potential benefits. The LAMP study is the first and largest-scale trial investigating GLP-1 receptor agonists in patients with ischemic stroke, offering some valuable insights into their potential benefits for improving patient outcomes.”


Wednesday, September 18, 2024

Association between intensive blood pressure lowering and stroke-free survival among patients with and without Diabetes

 Wow, lot of words but couldn't make heads or tails if a protocol was in there someplace. So useless.

Association between intensive blood pressure lowering and stroke-free survival among patients with and without Diabetes

Abstract

This study pooled data from SPRINT (Systolic Blood Pressure Intervention Trial) and ACCORD-BP (Action to Control Cardiovascular Risk in Diabetes Blood Pressure) trial to estimate the treatment effect of intensive BP on stroke prevention, and investigate whether stroke risk score impacted treatment effect. Of all the potential manifestations of the hypertension, the most severe outcomes were stroke or death. A composite endpoint of time to death or stroke (stroke-free survival [SFS]), whichever occurred first, was defined as the outcome of interest. Participants without prevalent stroke were stratified into stroke risk tertiles based on the predicted revised Framingham Stroke Risk Score. The stratified Cox model was used to calculate the hazard ratio (HR) for the intensive BP treatment. 834 (5.92%) patients had SFS events over a median follow-up of 3.68 years. A reduction in the risk for SFS was observed among the intensive BP group as compared with the standard BP group (HR: 0.76, 95% CI: 0.65, 0.89; risk difference: 0.98([0.20, 1.76]). Further analyses demonstrated the significant benefit of intensive BP treatment on SFS only among participants having a high stroke risk (risk tertile 1: 0.76 [0.52, 1.11], number needed to treat [NNT] = 861; risk tertile 2: 0.87[0.65, 1.16], NNT = 91; risk tertile 3: 0.69[0.56, 0.86], NNT = 50). Intensive BP treatment lowered the risk of SFS, particularly for those at high risk of stroke.

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Introduction

Elevated blood pressure (BP) has been identified as the major modifiable risk for stroke development with an estimated population-attributable risk of 48%1. Thus, strict and aggressive BP lowering is deemed the most important prevention strategy for both primary and secondary stroke prevention2,3,4,5. A significant benefit of intensive BP lowering the risk of stroke was observed in the ACCORD-BP trial (Action to Control Cardiovascular Risk in Diabetes Blood Pressure Trial)6. On the contrary, this treatment benefit was not found in the SPRINT (Systolic Blood Pressure Intervention Trial) trial with a similar study design but a larger sample size in comparison to the ACCORD-BP trial7.

Although this observed difference could be attributed to the trial population or the study power, treatment heterogeneity on all-cause mortality from the two trials should be otherwise noted. We observed a significant reduction in death from any cause in the SPRINT trial, which contrasted with the ACCORD-BP trial6,7. Clearly, it is known that the occurrence of death would preclude the observation of a stroke. As such, further analyses are needed to account for the presence of this terminal competing risk. Meanwhile, many researchers have identified that individual patients vary from one another in many ways that can affect the potential for benefit, which cannot be captured by conventional one-variable-at-a-time subgroup analyses8,9,10. However, the heterogeneity of treatment effect (HTE) of intensive BP lowering based on individual stroke risk has not been explored.

As such, the aims of this study were (1) to estimate the treatment effect of intensive BP lowering on stroke prevention using the pooled patient data of SPRINT and ACCORD-BP after considering the presence of competing risks from death; (2) to further investigate whether stroke risk score was associated with differential treatment effect.