How to Work Effectively With Stroke Survivors Throughout the Research Process

 How the fuck do none of you know about me?  I'm boldly proclaiming you are all blithering idiots because you don't know a goddamn thing about stroke survivors. Or even minimally how to solve stroke to 100%recovery.

How to Work Effectively With Stroke Survivors Throughout the Research Process

Elizabeth A. Lynch, PhD https://orcid.org/0000-0001-8756-1051 elizabeth.lynch@flinders.edu.au, Brenda Booth, Adrian O’Malley, Kathryn S. Hayward, PhD, Gillian Mason, BPhysio https://orcid.org/0000-0003-4060-3132, Ciara Shiggins, PhD https://orcid.org/0000-0003-3263-5038, and Dana Wong, PhD https://orcid.org/0000-0001-9619-1929Author Info & Affiliations

Stroke

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https://doi.org/10.1161/STROKEAHA.124.047193

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Two researchers to receive first-ever Ralph L. Sacco Scholarships for Brain Health

 I see nothing here that even remotely suggests they are working on the only goal in stroke: 100% RECOVERY! As such they really need to change the criteria for the award.

Two researchers to receive first-ever Ralph L. Sacco Scholarships for Brain Health

Two researchers to receive first-ever Ralph L. Sacco Scholarships for Brain Health

American Academy of Neurology and American Heart Association award $150,000 scholarships to researchers from Texas, Connecticut

DALLAS and MINNEAPOLIS, July 2, 2024 — The American Academy of Neurology and the American Heart Association have awarded the first-ever Ralph L. Sacco Scholarships for Brain Health to two researchers, Patrick Devlin, Ph.D., of Houston, Texas, and Cyprien Rivier, M.D., M.Sc., of New Haven, Connecticut. Each will receive a $150,000 two-year scholarship to support continuing scientific research in brain health. Devlin and Rivier also receive the professional distinction of being named the inaugural “Sacco Scholars.”

The Ralph L. Sacco Scholarships in Brain Health, also known as the Sacco Scholars program, are made possible by a generous bequest to the American Academy of Neurology and the American Heart Association from the late Ralph L. Sacco, M.D., M.S., FAAN, FAHA. Sacco was the only neurologist to have served as president of both organizations. He passed away in 2023 from a brain tumor.

“For more than 20 years, Dr. Ralph Sacco served as a dedicated volunteer for the American Heart Association, particularly leading the acceleration of our investment into and emphasis on brain health. He was the first neurologist to ever serve as our volunteer president,” said Nancy Brown, the American Heart Association’s chief executive officer. “He had big ideas and put them into action in ways that improved and saved the lives of all people. One of his greatest joys was mentoring young scientists, boosting their careers the same way icons of previous generations did for him. I am so proud to be able to welcome our first-ever Sacco Scholars in memory of my very dear friend.”

“It was important to Dr. Ralph Sacco to support continued research in brain health because, as he said, each and every one of us only has one brain, and it is critical to keep it as healthy as possible,” said American Academy of Neurology President Carlayne E. Jackson, M.D., FAAN. “We look forward to the inaugural year of this scholarship program with the first two Sacco Scholars and the vital research they will do to help find ways for all of us to improve our brain health.”

“Ralph was a personal friend and mentor, and I am grateful that his legacy of influencing the careers of countless physicians, researchers and health care professionals will live on through this unique scholarship program,” said Mitchell S.V. Elkind, M.D., M.S., FAAN, FAHA, chief clinical science officer and past volunteer president of the American Heart Association. “These research projects will build upon his decades of work in saving and improving the lives of people with stroke and will break new ground in our knowledge of how vascular disease impacts cognitive decline, dementia and brain health more broadly. I look forward to seeing what our awardees learn about the mechanisms of brain aging, both before and after stroke. I know Ralph would have been very interested in their projects.”

“Physicians who had the privilege of training under my dear friend Dr. Ralph Sacco knew he was a remarkable human being with a kind and generous heart,” said Orly Avitzur, M.D., M.B.A., FAAN, immediate past president of the American Academy of Neurology. “With the Sacco Scholars program, his mentorship continues as we begin creating a community of researchers focused on brain health.”

Devlin is a postdoctoral research fellow in the Ritzel Lab at the University of Texas Health Science Center at Houston. He is being awarded the scholarship for his research on the after-effects of stroke, specifically how the brain may age more quickly after a stroke, including the aging process of immune cells in the brain. The goal of Devlin’s research is to increase understanding of cognitive decline and dementia after stroke so that new treatments can be developed for people who have had a stroke, resulting in fewer complications such as memory loss. This is especially important to improve long-term quality of life as more people are surviving strokes thanks to advances in stroke diagnosis, treatment and care.

Rivier is a postdoctoral research fellow in the Falcone Lab in the Department of Neurology at Yale University. A significant portion of his work is conducted in collaboration with the Sheth Lab and the Yale Center for Brain and Mind Health. He is being awarded the scholarship for his research on how biological age—as opposed to chronological age—impacts the brain. Rivier is exploring whether people with younger biological age are less likely to develop dementia and stroke. By gaining a better understanding of biological age, Rivier’s research could lead to finding better ways for people to take care of their brain, lowering the risk of major health problems so they can live longer, healthier lives.

Devlin and Rivier began their two-year research projects on July 1.

About the American Heart Association 

The American Heart Association is a relentless force for a world of longer, healthier lives. We are dedicated to ensuring equitable health in all communities. Through collaboration with numerous organizations, and powered by millions of volunteers, we fund innovative research, advocate for the public’s health and share lifesaving resources. The Dallas-based organization has been a leading source of health information for a century. During 2024 - our Centennial year - we celebrate our rich 100-year history and accomplishments. As we forge ahead into our second century of bold discovery and impact our vision is to advance health and hope for everyone, everywhere. Connect with us on heart.org, Facebook, X or by calling 1-800-AHA-USA1.    

About the American Academy of Neurology

The American Academy of Neurology is the world's largest association of neurologists and neuroscience professionals, with over 40,000 members. The AAN’s mission is to enhance member career fulfillment and promote brain health for all. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer's disease, stroke, concussion, epilepsy, Parkinson's disease, multiple sclerosis, headache and migraine. For more information about the American Academy of Neurology, visit AAN.com or find us on Facebook, X, Instagram, LinkedIn and YouTube.

For Media Inquiries: 214-706-1173

AHA - Cathy Lewis: cathy.lewis@heart.org

AAN - Renee Tessman: rtessman@aan.com

For Public Inquiries: 1-800-AHA-USA1 (242-8721)

heart.org and stroke.org

Adding just a few ultraprocessed foods to a healthy diet raised risk of cognitive decline and stroke, study says

Absolutely useless crapola, give us an EXACT EXAMPLES!

Adding just a few ultraprocessed foods to a healthy diet raised risk of cognitive decline and stroke, study says 

Eating more ultraprocessed foods is linked to a higher risk of cognitive decline and stroke, even if a person is trying to adhere to a Mediterranean diet, the DASH diet or the MIND diet, a new study found.

All three diets are plant-based, focused on consuming more fruits and vegetables, whole grains, beans and seeds while limiting sugar, red meat and ultraprocessed foods.

Related article You may be eating predigested food. Here’s why

“If you increased your ultraprocessed food intake by 10% in the study, it increased your risk of cognitive impairment by 16%,” said cardiologist Dr. Andrew Freeman, director of cardiovascular prevention and wellness at National Jewish Health in Denver. He was not involved in the study.

“You can always extrapolate and say, ‘Well, if someone increases their ultraprocessed food consumption by 100%, then they have 160% chance of cognitive impairment,’” he said. “Of course, this study can only show an association, not a direct cause and effect.”

On the flip side, eating more unprocessed or minimally processed foods was linked with a 12% lower risk of cognitive impairment, according to the study published Wednesday in the journal Neurology.

Eating more ultraprocessed foods such as hot dogs is linked to a higher risk of stroke and cognitive decline, according to a new study.

LauriPatterson/E+/Getty Images

Unprocessed foods include fresh fruits and vegetables, eggs and milk. Minimally processed foods include culinary ingredients such as salt, herbs and oils and foods such as canned goods and frozen vegetables that combine culinary ingredients with unprocessed foods.

Ultraprocessed foods include prepackaged soups, sauces, frozen pizza, ready-to-eat meals and pleasure foods such as hot dogs, sausages, French fries, sodas, store-bought cookies, cakes, candies, doughnuts, ice cream and many more.(EXACT EXAMPLES!)

Such foods are typically high in calories, added sugar and salt and low in fiber, all of which can contribute to cardiometabolic health problems, weight gain, obesity, type 2 diabetes and high blood pressure, experts say.

Related article Just how bad are ultraprocessed foods? Here are 5 things to know

An increased risk of stroke

The study analyzed data on 30,000 people participating in the REGARD, or REasons for Geographic and Racial Differences in Stroke study, made up of 50% Whites and 50% Blacks in a nationally diverse group of people who have been followed for up to 20 years.

The risk of stroke was 8% higher for people who added the most ultraprocessed foods to their diet as compared with those who ate minimally processed foods, said study author and neurologist Dr. W. Taylor Kimberly, chief of the division of neurocritical care at Massachusetts General Hospital in Boston.

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That risk rose to 15% for Black participants, likely due to the impact of ultraprocessed foods on high blood pressure in that population, Kimberly said. However, if a person ate more unprocessed or minimally processed foods, the risk of stroke dropped by 9%, the study found.

Related article Ultraprocessed foods now account for two-thirds of calories in the diets of children and teens

What is it about ultraprocessed foods that may allow them to sabotage efforts to follow a healthy diet? It could be their poor nutrient composition and tendency to spike blood sugars, which can lead to type 2 diabetes, obesity, elevated blood pressure and high cholesterol, said Peipei Gao and Zhendong Mei in an editorial published with the study.

Mei is a research fellow in medicine at Brigham and Women’s Hospital in Boston, while Gao is a graduate student in nutrition visiting Harvard T.H. Chan School of Public Health, also in Boston. Neither was involved in the study.

Type 2 diabetes, obesity, elevated blood pressure and high cholesterol are all key risk factors for vascular disease in the heart and brain, they wrote.

The impact on blood vessels that leads to stroke and cognitive decline may also be due “to the presence of additives including emulsifiers, colorants, sweeteners, and nitrates/nitrites, which have been associated with disruptions in the gut microbial ecosystem and inflammation,” they added.

Growing dangers of ultraprocessed foods

Studies on the dangers of eating ultraprocessed foods are piling up. According to a February review of 45 meta-analyses on almost 10 million people, eating 10% more ultraprocessed foods raised the risk of developing or dying from dozens of adverse health conditions.

That 10% increase was considered “baseline,” and adding even more ultraprocessed foods might increase the risk, experts say.

There was strong evidence that a higher intake of ultraprocessed foods was associated with about a 50% higher risk of cardiovascular disease-related death and common mental disorders, according to the review.

Related article Experts find cardiometabolic risk signs in kids young as 3. Here is the food they say is linked

Researchers also found highly suggestive evidence that eating more ultraprocessed foods raised the risk of obesity by 55%, sleep disorders by 41%, development of type 2 diabetes by 40% and the risk of depression by 20%.

“We really need to put a sign in the ultraprocessed food section, or on the packaging like they do on cigarettes, saying, ‘Warning, this food may be detrimental to your health,’” Freeman said.

“What we think of as ‘convenient food’ really needs to change from a package of chips to an apple or carrot that is also shelf-stable and can travel in your purse or backpack,” he said. “And we need to make that kind of stuff more readily available, especially to our kids and in food deserts where often all the available food is ultraprocessed.”

Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

 We've known about this problem a long time! LEADERS SOLVE PROBLEMS! We have NO leaders in stroke!

• Delayed cerebral ischemia (6 posts to November 2016)

Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

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Michael Veldeman, MD, PhD https://orcid.org/0000-0003-3648-6842, Tobias Rossmann, MD, Roel Haeren, MD, PhD, Laura V. Vossen, MD cand, Miriam Weiss, MD https://orcid.org/0000-0001-8820-0805, Catharina Conzen, MD, Jari O. Siironen, MD, PhD, … Show All … , and Rahul Raj, MD, PhD https://orcid.org/0000-0003-4243-9591Authors Info & Affiliations

August 13, 2024 issue

103 (3)

https://doi.org/10.1212/WNL.0000000000209607

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Abstract

Background and Objectives

Delayed cerebral ischemia (DCI) is one of the main contributing factors to poor clinical outcome after aneurysmal subarachnoid hemorrhage (SAH). Unsuccessful treatment can cause irreversible brain injury in the form of DCI-related infarction. We aimed to assess the association between the location, distribution, and size of DCI-related infarction in relation to clinical outcome.

Methods

Consecutive patients with SAH treated at 2 university hospitals between 2014 and 2019 (Helsinki, Finland) and between 2006 and 2020 (Aachen, Germany) were included. Size of DCI-related infarction was quantitatively measured as absolute volume (in milliliters). In a semiquantitative fashion, infarction in 14 regions of interest (ROIs) according to a modified Alberta Stroke Program Early CT Score (ASPECTS) was noted. The association of infarction in these ROIs along predefined regions of eloquent brain, with clinical outcome, was assessed. For this purpose, 1-year outcome was measured by the Glasgow Outcome Scale (GOS) and dichotomized into favorable (GOS 4–5) and unfavorable (GOS 1–3).

Results

Of 1,190 consecutive patients with SAH, 155 (13%) developed DCI-related infarction. One-year outcome data were available for 148 (96%) patients. A median overall infarct volume of 103 mL (interquartile range 31–237) was measured. DCI-related infarction was significantly associated with 1-year unfavorable outcome (odds ratio [OR] 4.89, 95% CI 3.36–7.34, p < 0.001). In patients with 1-year unfavorable outcome, vascular territories more frequently affected were left middle cerebral artery (affected in 49% of patients with unfavorable outcome vs in 30% of patients with favorable outcome; p = 0.029), as well as left (44% vs 18%; p = 0.003) and right (52% vs 14%; p < 0.001) anterior cerebral artery supply areas. According to the ASPECTS model, the right M3 (OR 8.52, 95% CI 1.41–51.34, p = 0.013) and right A2 (OR 7.84, 95% CI 1.97–31.15, p = 0.003) regions were independently associated with unfavorable outcome.

Discussion

DCI-related infarction was associated with a 5-fold increase in the odds of unfavorable outcome, after 1 year. Ischemic lesions in specific anatomical regions are more likely to contribute to unfavorable outcome.

Trial Registration Information

Data collection in Aachen was registered in the German Clinical Trial Register (DRKS00030505); on January 3, 2023.

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The association between ferritin levels and all-cause mortality in stroke patients

 Who approved this useless research that predicts mortality rather than prevents it? They need to be fired!

The association between ferritin levels and all-cause mortality in stroke patients

Xuefen Xia¹Jiongjiong Liu²Wenqiang Fang¹Zhibo Chen¹Jie Wang^3*Huiqin Xu^1*

• ¹Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
• ²Department of General Practice, Fuyang Hospital Affiliated to Anhui Medical University, Anhui, China
• ³Department of Endocrinology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

Purpose: The purpose of study was to describe the association between ferritin and all-cause mortality of cases with stroke.

Methods: Clinical data derived from Multiparameter Intelligent Monitoring in Intensive Care were analyzed. The primary endpoint was 30-day mortality. The potential prognostic roles of Ferritin L were analyzed by Cox proportional hazard models. The independent prognostic roles of Ferritin L in the cases were analyzed by smooth curve fitting.

Results: Concerning 30-day mortality, the HR (95% CI) for a high Ferritin (≥373) was 1.925 (1.298, 2.854; p = 0.00113), compared to a low ferritin (< 373). After adjusting for multiple confounders, the HR (95% CI) for a high Ferritin (≥373) was 1.782 (1.126, 2.820; p = 0.01367), compared to a low Ferritin (< 373). A non-linear association between Ferritin and 30-day mortality was found. Using recursive algorithm and two-piecewise linear regression model, inflection point (IP) was calculated, which was 2,204. On the left side of the IP, there was a positive relationship between Ferritin and 30-day mortality, and the effect size, 95% CI and p value were 1.0006 (1.0004, 1.0009) p < 0.0001, respectively. On the right of the IP, the effect size, 95% CI and p value were 1.0000 (1.0000, 1.0000) and 0.3107, respectively.

Conclusion: Ferritin was associated with increased risk of stroke; it is important to further examine the association if the increased uric acid would increase the outcome of stroke in a longitudinal study. The non-linear relationship between Ferritin and all-cause mortality of stroke was observed. Ferritin was a risk factor for the outcome of stroke when ferritin was <2204.

1 Introduction

Stroke, a neurological deficit originating from cerebrovascular causes, disrupts blood supply to part of the brain, potentially inducing irreversible damage to deprived neural tissues and consequently triggering substantial morbidity and mortality worldwide (1–3). With various subtypes, including ischemic and hemorrhagic strokes, each presenting unique pathophysiology, risk factors, and outcomes, stroke management demands rigorous attention to detail, a comprehension of its multifaceted nature, and often, a patient-centric approach to care (4). While acute phase interventions, both medical and/or surgical, followed by rehabilitative strategies, remain fundamental to stroke management, a prudent understanding and investigation of potential prognostic markers are pivotal to interpret, forecast, and possibly enhance patient outcomes (3–5).

Ferritin, a cellular protein that binds and sequesters iron, is traditionally recognized as an indicator of iron stores within the body (6, 7). Elevated serum ferritin levels, aside from implications in iron metabolism disorders, have also been acknowledged as an acute-phase reactant, often elevating in situations of systemic inflammation, cellular injury, and specific disease states (8). Within cardiovascular diseases, elevated ferritin levels have been associated with adverse outcomes, highlighting its potential utility as a prognostic marker (9). Furthermore, emerging data insinuate that ferritin, through its involvement in iron metabolism and its capacity to induce oxidative stress, might participate in the pathophysiological cascade following ischemic cell death and in propagating secondary injury mechanisms post-stroke. Nevertheless, the explicit association between ferritin levels and outcomes in stroke patients warrants further elucidation. While stroke instigates a complex interplay of inflammatory, oxidative, and neurodegenerative processes, defining the role of ferritin—both as a marker and a participant in this cascade—requires meticulous investigation (10, 11). Given the pathophysiological complexity and heterogeneity among stroke patients, it is imperative to discern whether ferritin levels maintain a consistent, independent association with outcomes or simply reflect the inflammatory and oxidative processes that prevail following cerebral ischemia or hemorrhage (12, 13).

This study commences an exploration into the association between serum ferritin levels and all-cause mortality in stroke patients, delving into the complexities of stroke subtypes and coexisting variables that could potentially influence this relationship. By unraveling these associations, we aim to enhance our understanding of stroke pathophysiology, potentially facilitating the development of novel prognostic and therapeutic strategies aimed at mitigating the profound impact of this formidable neurological challenge. In this study, we utilized real-world data obtained from the latest Multiparameter Intelligent Monitoring in Intensive Care (MIMIC) database to assess the association between ferritin and stroke patient outcomes, adjusting for various potential confounders.

More at link.

Serum uric acid as a predictor of mortality in patients with stroke: results from National Health and Nutrition Examination Survey 2007–2016

 Who approved this useless research that predicts mortality rather than prevents it? They need to be fired!

Serum uric acid as a predictor of mortality in patients with stroke: results from National Health and Nutrition Examination Survey 2007–2016

Xinyu Tong¹Chuxin Lyu²Minjie Guo¹Jianxiong Gu¹Yichun Zhao^1*

• ¹Department of Neurology, Wuxi Traditional Chinese Medicine Hospital, Wuxi, China
• ²First Clinical Medical School, Nanjing University of Chinese Medicine, Nanjing, China

Objective: This research endeavors to explore the relationship between serum uric acid (SUA) concentration and all-cause mortality in stroke patients.

Methods: We undertook a cross-sectional analysis utilizing data derived from the National Health and Nutrition Examination Survey (NHANES) spanning 2007 to 2016. The concentrations of SUA served as the independent variable, while the dependent variable was defined as all-cause mortality in stroke patients. The quartile method was utilized to classify uric acid levels into four distinct categories. Subsequently, three models were developed, and Cox proportional hazards regression was used to assess the effect of varying uric acid concentrations on the risk of all-cause mortality among stroke patients.

Results: The study included a total of 10,805 participants, of whom 395 were stroke patients. Among all populations, the group with elevated levels of uric acid (Q4) exhibited a significant association with the overall mortality risk among stroke patients in all three models (model 1 p < 0.001, model 2 p < 0.001, model 3 p < 0.001). In the male population, there was no significant correlation observed between uric acid levels and the overall mortality risk among stroke patients in model 3 (Q2 p = 0.8, Q3 p = 0.2, Q4 p = 0.2). However, within the female population, individuals with high uric acid levels (Q4) demonstrated a noteworthy association with the overall mortality risk among stroke patients across all three models (model 1 p < 0.001, model 2 p < 0.001, model 3 p < 0.001).

Conclusion: This cross-sectional investigation reveals a significant correlation between SUA levels and all-cause mortality in stroke patients, with a noticeable trend observed among females. Consequently, SUA may serve as a promising biomarker for assessing the prognosis(Why? So you can tell your patients they are going to DIE!) of individuals affected by stroke.

Introduction

Stroke, a term encompassing sudden localized or diffuse neurological deficits, is attributed to the disturbance of blood circulation. Sometimes stroke is covert. According to the Global Burden of Diseases, Injuries and Risk Factors Study (GBD) 2017, stroke is ranked as the third leading cause of mortality and disability, quantified by disability-adjusted life years (DALY). Furthermore, it is the second most significant contributor to death and disability (1, 2). In 2017, the global incidence of acute ischemic strokes was approximately 950 per 100,000 individuals (3).

Following a significant long cessation of oxygen supply resulting from blood inflow or outflow disturbance, a sequence of cascading events (4) is initiated, which includes ATP depletion, alterations in sodium, potassium, and calcium ion concentrations, an increase in lactic acid, acidosis, the accumulation of oxygen free radicals, cell edema, and proteolysis. These processes ultimately result in cell death and neurological deficits. Prior research has identified numerous contributing factors to these neurological deficits after a stroke. It has been found that hypertension, suboptimal blood glucose control, smoking, alcohol consumption, and other unhealthy lifestyle habits significantly influence neurological deficits following a stroke (5–9). Serum uric acid (SUA) serves as a prevalent index in serological tests. Its impact on blood pressure and renal function is notable, particularly due to its role in generating oxidative stress via xanthine oxidase. This enzyme binds with endothelial cells, thereby inhibiting the activity of nitric oxide (NO), which results in vascular damage. Inflammation and damage of blood vessels lead to atherosclerosis, thereby promoting the occurrence and development of stroke.

Several prior meta-analyses have demonstrated that hyperuricemia marginally elevates the risk of stroke morbidity and mortality (10, 11). However, contrasting findings suggest the potential beneficial effects of SUA on the central nervous system (12, 13). Reactive oxygen species, induced by ischemia/reperfusion injury, play a significant role in neuronal cell death. Consequently, the antioxidant properties of SUA may be advantageous for neuronal survival. Currently, only a handful of small-scale studies have indicated that a reduction in serum uric acid (SUA) levels is independently linked to adverse outcomes following acute ischemic stroke (14). Therefore, further research is required to substantiate whether SUA levels can effectively influence the prognosis of stroke patients.

However, limited research has been conducted to explore the relationship between SUA levels and all-cause mortality. The optimal range of SUA levels that could prevent death remains ambiguous, necessitating substantial evidence from the general population to fill these knowledge gaps. Consequently, this study will utilize the public NHANES database, which boasts a large sample size. We conducted a cross-sectional study utilizing pooled data from the NHANES spanning 2007 to 2016, aiming to elucidate the specific association between SUA levels and all-cause mortality in patients with stroke.

More at link.

Differential distribution of plasma apoA-I and apoB levels and clinical significance of apoB/apoA-I ratio in ischemic stroke subtypes

 I can't see any explanation here that even remotely suggests this does ANYTHING AT ALL for stroke recovery. Totally useless.

Differential distribution of plasma apoA-I and apoB levels and clinical significance of apoB/apoA-I ratio in ischemic stroke subtypes

Nguyen Van Tuyen^1,2Nguyen Hoang Ngoc¹Phan Quoc Hoan³Nguyen Thi Yen⁴Nghiem Xuan Hoan^3,5*†Nguyen Cam Thach^4*†

• ¹Department of Stroke, Institute of Neurology, 108 Institute of Clinical Medical and Pharmaceutical Sciences, Hanoi, Vietnam
• ²VNU University of Medicine and Pharmacy, Hanoi, Vietnam
• ³Department of Molecular Biology, 108 Institute of Clinical Medical and Pharmaceutical Sciences, Hanoi, Vietnam
• ⁴Department of Biochemistry, 108 Institute of Clinical Medical and Pharmaceutical Sciences, Hanoi, Vietnam
• ⁵Vietnamese-German Center for Medical Research (VG-CARE), Hanoi, Vietnam

Background and purpose: Ischemic stroke (IS) is classified into clinical subtypes and likely influenced by various lipid components. Nevertheless, the roles of apolipoprotein A-I (apoA-I), apolipoprotein B (apoB), and apoB/apoA-I ratio in different IS subtypes remain underexplored. This study aimed to investigate the differential distribution of plasma apoA-I and apoB levels among IS subtypes and to evaluate the predictive value(Does nothing for recovery!) of the apoB/apoA-I ratio in assessing IS subtypes and disease severity.

Methods: In this study, 406 IS patients were categorized into three IS-subtypes based on clinical manifestations and imaging assessment, including intracranial atherosclerosis-related IS patients (ICAS, n = 193), extracranial atherosclerosis-related IS patients (ECAS, n = 111), and small artery occlusion-related IS patients (SAO, n = 102). Plasma apoA-I and apoB levels were measured upon hospital admission. Random forest (RF) models were performed to assess predictive values of these apolipoproteins apoB, apoA-I and their ratio in assessing IS subtype stratification and disease severity.

Results: Serum apoA-I levels were significantly lower in ICAS compared to ECAS and SAO patients (p < 0.0001), while apoB levels were higher in ICAS patients (p < 0.0001). The apoB/apoA-I ratio was significantly higher in ICAS compared to ECAS and SAO patients (p < 0.0001). Correlation analyses found a significant correlation between the apoB/apoA-I ratio and conventional lipid components. Additionally, RF models and plots of variable importance and distribution of minimal depth revealed that the apoB/apoA-I ratio played the most influential predictor in predicting IS subtypes and stenosis severity.

Conclusion: Our study shows the differential distribution of apoA-I and apoB IS subtypes and reveals the significance of the apoB/apoA-I ratio in assessing IS subtypes and arterial stenosis severity. Further studies are warranted to validate these findings and enhance their clinical applicability.

Introduction

Globally, stroke stands as the second leading cause of mortality globally, contributing to 11.6% of all deaths (1). In which, ischemic stroke (IS) prevails as the most prevalent, constituting 62.4% of all stroke incidents worldwide in 2019 (1, 2). Despite significant advances in treatment and therapy for IS, mortality rates remain high. The critical factor is the time elapsed between symptom onset and seeking medical attention. This underscores the importance of swift action in stroke management. Among survivors, the recurrence rate of stroke patients after the acute event is very high, with approximately 15–30% at risk within the first 2 years, 25% within 5 years, and doubling after 10 years (3). Importantly, IS can inflict profound neurological impairment and persistent disability in these survival individuals, thereby imposing significant health and economic burdens on societies.

Ischemic stroke is a vascular disorder of the brain’s circulatory system, with multiple causes leading to this condition, such as arterial atherosclerosis, cardiac emboli or blood clots originating from the heart, and coagulation disorders. Among which arterial atherosclerosis is a known strong risk factor for IS (4). Arterial atherosclerosis can occur both intracranially and extracranially, with intracranial atherosclerosis (ICAS) is more prevalent in Asian patients and is associated with a high risk of recurrence, whereas extracranial atherosclerosis (ECAS) is more common in individuals from western countries (4, 5). Meanwhile, a distinct IS subtype, known as small-artery occlusion (SAO), resulting in small (<15 mm in axial diameter) subcortical infarcts, is well categorized by the Trial of ORG10172 in Acute Stroke Treatment (TOAST classification) (6). This subtype is prevalent in developing nations, particularly accounting for 27.3% of IS cases in China (7, 8).

Atherosclerosis is a chronic lipid-driven and maladaptive inflammatory disease of arterial intima. Several factors were considered to contribute to pathogenesis of artery atherosclerosis formation. It is characterized by the dysfunction of lipid homeostasis and signaling pathways that control the inflammation. High-risk factors, such as hypertension, diabetes, and smoking, cause vascular endothelial dysfunction and increased permeability. This leads to accumulation of cholesterol-containing low-density lipoproteins (LDL) in the intima, which initiates a complex series of inflammatory and biochemical reactions involving accumulation of extracellular matrix, activation of the endothelium, infiltration of monocytes and T cells, intimal thickening, fibrous cap formation, and angiogenesis (9–11).

In clinical practice, one of the important measures in the prevention and treatment of arterial atherosclerotic disease is the control of lipoproteins (cholesterol, HDL, LDL). These are commonly measured parameters that help clinicians assess metabolic disorders and identify risk factors for arterial atherosclerosis (12–14). Nonetheless, apolipoproteins, in particular, apolipoprotein B (apoB) may be more useful clinically than LDL cholesterol because it captures greater information about atherogenic particles and is not influenced by heterogeneity of particle cholesterol content (15). Apolipoproteins are integral components of lipoproteins and play essential roles in lipid metabolism and transport. Unlike lipoproteins, apolipoproteins are directly involved in the pathophysiology of atherosclerosis. ApoB is present on atherogenic lipoproteins (such as LDL and VLDL) and is directly involved in their interaction with arterial endothelial cells, promoting the formation of atherosclerotic plaques. Additionally, apolipoprotein A-I (apoA-I), the major protein component of HDL particles, is associated with reverse cholesterol transport and has protective effects against atherosclerosis. In recent years, several investigations have shed light on the significance of apoA-I, apoB, and the apoB/apoA-I ratio in predicting and assessing susceptibility to cardiovascular diseases (16–20). These metrics serve as indicators of the balance between atherogenic and anti-atherogenic lipoproteins, offering insights into the status of arterial atherosclerotic disease.

While apoA-I and apoB hold promise as biomarkers, potentially traditional lipoproteins in terms of enhanced accuracy and practicality in predicting arterial atherosclerosis in cardiovascular diseases. However, to date, research on apolipoproteins and their application in monitoring, prognostication, and preventive treatment of IS has garnered scant attention. To the best of our knowledge, only a few studies have investigated apolipoproteins in IS patients (21–23). Therefore, exploring the potential roles of apoA-I and apoB in IS patients holds significant value, particularly in the Vietnamese population where IS represents a substantial medical concern. In addition to these reasons, we conducted this study aimed to investigate the differential distribution of plasma apoA-I and apoB levels among IS subtypes and to evaluate the predictive value of the apoB/apoA-I ratio in assessing IS subtypes and disease severity.