UPMC study finds faster stroke transfers and enhanced access to lifesaving care with instant scan sharing across hospitals

 Are you that blitheringly stupid you think survivors want 'care'; NOT RECOVERY?

UPMC study finds faster stroke transfers and enhanced access to lifesaving care with instant scan sharing across hospitals

UPMC’s stroke network is testing new ways to get patients to advanced stroke care(NOT RECOVERY!) faster. In a study published in the Journal of Neurology, Neurosurgery and Psychiatry, UPMC and University of Pittsburgh researchers found that an AI-assisted scan‑sharing and alert app can do just that.

Mohamed (Mo) Doheim, M.D.

Lead author of this research, Dr. Mohamed (Mo) Doheim, research assistant professor of neurology at Pitt and NIH StrokeNet fellow at the UPMC Stroke Institute, answers questions about the study’s findings and what they mean for patients and healthcare providers.

What problem was this study trying to solve?

Dr. Doheim: Each year, nearly 800,000 Americans have a stroke, which is a leading cause of long‑term disability and among the leading causes of death in the United States.

When someone has a severe stroke, it is essential to get them to a major hospital for advanced treatment quickly. For every 15‑minute delay in care(NOT RECOVERY!), the chance of disability‑free survival drops by about 4%. But getting the patient transferred from a smaller hospital to a center that has more extensive stroke care(NOT RECOVERY!) capabilities isn’t instantaneous — it often requires coordinating limited resources, arranging transport and navigating logistical barriers.

The UPMC Stroke Institute team, guided by its director, Dr. Raul Nogueira, wanted to determine if an AI-powered phone app that instantly shares brain scans and alerts the stroke team at the receiving hospital could speed up this process and get patients faster treatment.

What were your most important findings?

Dr. Doheim: We looked at data from over 4,500 stroke patients across UPMC’s network of four stroke centers receiving transfers from 60 community hospitals. Then we compared what happened with the AI system versus without it to see whether it changed timing, transfers and treatment.

Our findings were very encouraging:

• More transferred patients received the life-saving clot-removal procedure.

• Patients transferred from hospitals using the AI system waited about a half hour less before transfer. Once they arrived at the main hospital, their treatment also started sooner.

• • Smaller community hospitals saw the biggest improvements in their treatment times.

• • And, finally, because AI helped doctors easily identify which patients truly needed the clot-removal procedure, it prevented unnecessary transfers.

What do these findings mean for patients and hospitals?

Dr. Doheim: For patients, this means faster, more equal access to life-saving treatments, no matter which hospital they go to first.

For hospitals, this shows that AI could be a powerful tool to make stroke care(NOT RECOVERY!) more efficient by helping doctors communicate instantly and look at scans together on their smart phones, rather than waiting for phone calls or faxes.

Saving time during a stroke is crucial to saving brain tissue, so these faster treatment times should ultimately lead to better, healthier recoveries.

What’s next?

Dr. Doheim: While this is the largest study of its kind in the United States showing that AI improves stroke care(NOT RECOVERY!) times, we still have more to learn. Next, we need to track how patients are doing in the long term after their stroke to prove that these faster times directly lead to better long-term health. We also want to look closer at the outcomes of the patients who weren’t transferred, to make sure that we are making the safest, fastest and most highly informed decisions.

How Gut Bacteria Could Trigger Memory Loss as We Age

 Will your competent? doctor ensure this problem doesn't add onto your memory problems post stroke? 

How Gut Bacteria Could Trigger Memory Loss as We Age

Memory loss and aging go hand-in-hand for most of us, but scientists are getting closer to understanding why. A new study, conducted by researchers at the Arc Institute in Palo Alto, California, and published in Nature, found that a prime suspect may be living in our gut.

“The biggest question that came out of this experiment is: How does the brain know about what’s going on [in the microbiome]?” said Christoph Thaiss, PhD, core investigator at Arc Institute and an assistant professor of pathology at Stanford University, Stanford, California. 

Thaiss focuses his research on how environmental factors, as well as age, predispose individuals to various diseases over the course of their life. When he teamed up with first author Timothy Cox, MD/PhD student at the University of Pennsylvania, Philadelphia, he’d set his sights on the aging gut microbiome. 

The Perfect Test Subjects

“It was previously known that the microbiome changes with age in the same way that we, the host, change with age,” explained Cox. “And so the question was, are there any consequences of that?”

To answer, the researchers took a group of old and young mice and had them live together. When mice cohabitate, “their microbiomes kind of average out because the mice are coprophagic,” said Cox. 

In other words, they eat each other’s poop.

The researchers were surprised by what they observed. After just a month, the young mice that were “otherwise totally healthy” showed signs of severe memory impairment.

Cox had extensive experience conducting memory tests on mice from his previous research on Alzheimer’s disease. “The main test that we use is something called novel object recognition. This takes advantage of the fact that mice are naturally curious and they like to explore new things,” said Cox.

Researchers show mice two identical objects, and the mice get to explore those objects so they learn what they are. Then they remove those objects. An hour later, they put the familiar object back in the cage “along with a new object called the novel object,” said Cox.

Normal mice remember that they’ve seen the familiar object and will spend 2-3 times more time exploring the novel object because it’s new and interesting to them. “Old mice, mice with Alzheimer’s disease, or those that have cognitive impairment forget that they’ve seen the first object before,” said Cox. “When they get exposed to the two objects for the testing phase, instead of spending more time with the new object, they spend equal time with both objects.”

A Surprising Result

The research team was not expecting to see any memory impairment in the young mice, let alone severe memory impairment. “But when we tested the young mice that were living with old mice, they were basically identical to the old mice in terms of performance. They did really poorly on the standard test,” said Cox.

The team was in such disbelief, in fact, that they had multiple people repeat the test to see if they could get the same outcome. “The more experiments we did, the more we got the same thing, and so we became more and more confident in it,” said Cox.

While the research team was surprised by the results, David Hafler, MD, professor of immunobiology and former chairman of the Department of Neurology at Yale School of Medicine, New Haven, Connecticut, was not. “I wasn’t surprised, but I was really very delighted to see more evidence of the gut-brain [connection],” he said (he was not involved in the study).

How This Gut-Brain Connection Works

To find a possible culprit in the gut, the team used germ-free mice. They transplanted the microbiomes of healthy, young mice and old mice and observed the exact same effects: The germ-free mice that received the old microbiomes displayed learning and memory impairment. “This gave us really strong evidence that this was a microbiome phenotype because it was reproduced with a fecal transplant,” said Cox. 

After testing several, they narrowed the search down to a bacterium called Parabacteroides goldsteinii, though Thaiss believes “there are other species that change with age, and there might be other species that have cognitive impact.”

The main function of P goldsteinii is its production of medium-chain fatty acids (MCFAs). High levels of MCFAs accumulate with age and activate gut-resident myeloid immune cells to produce inflammatory signaling molecules. This study allowed researchers to dive into the gut-brain connection, tracing the effects of MCFAs through intestinal immune cells into sensory neurons and up the vagus nerve into the hippocampus of the brain, where memories are formed. The result: “The function of vagal afferent neurons is impaired, the interoceptive signal received by the brain is weakened, and hippocampal function declines,” they write.

“It all fits in with these bigger narratives,” said Hafler. “This is all in mice, and our work has been in both mice and humans, but I think it’s really exciting and suggests the importance of these pathways. I think it just adds to the story of the increasing importance of the gut-brain connection. It’s just becoming increasingly clear.”

Next Steps

A deeper understanding of the gut’s role in cognitive decline could have implications beyond memory impairment. “We did several methods of vagal nerve stimulation. We’re able to restore memory in mice,” said Cox. “Vagal nerve stimulation is already FDA-approved for epilepsy and depression, but it’s now being looked at for many different diseases, including rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis. In the future, we might be able to apply that to cognitive decline.”

“Ultimately, the goal is to do something about cognitive decline in humans,” said Thaiss. “How can we understand and manipulate this communication [between the gut and the brain]? How much of this pathway is active and involved in regulating cognitive decline in humans? These are the two main questions that have come out of this study that I think are going to keep us and others in the field busy for a while.”

David Hafler declared having no competing interests. Disclosure information for all study authors is available in the original study publication.

Stroke Support System Linked to Fewer Vascular Events

 But survivors have only one goal; 100% recovery and you're not measuring that!

Here is your business101 requirements. Not measuring 100% recovery is the height of incompetence!

“What's measured, improves.” So said management legend and author Peter F. Drucker )

Stroke Support System Linked to Fewer Vascular Events

TOPLINE: 

Use of a clinical decision-support system (CDSS) that incorporates AI-assisted imaging analysis was associated with a 25% lower incidence of vascular events and greater adherence to evidence-based stroke care(NOT RECOVERY!) quality measures in adults with acute ischemic stroke compared to usual care(NOT RECOVERY!) in a new open-label study.

METHODOLOGY:

• The multicenter, open-label, cluster randomized Golden Bridge II trial was conducted across 77 hospitals in China. It included more than 21,600 adults (median age, 67 years; 64.5% men) with acute ischemic stroke confirmed using MRI within 7 days of symptom onset between 2021 and 2023.
• The hospitals were randomly assigned to usual care(NOT RECOVERY!) (39 hospitals; n = 10,549) or the stroke CDSS intervention (38 hospitals; n = 11,054), which included AI-assisted imaging analysis, classification of stroke causes, and recommendations for evidence-based treatment.
• The primary outcome was a composite of new vascular events (ischemic stroke, hemorrhagic stroke, myocardial infarction, or vascular death) within 3 months of stroke onset.
• Secondary outcomes included a composite of evidence-based performance indicators for acute ischemic stroke care(NOT RECOVERY!) quality, new vascular events at 6 and 12 months, disability on the modified Rankin Scale (mRS), all-cause mortality at 3, 6, and 12 months, and moderate/severe and all bleeding events after stroke onset.

TAKEAWAY:

• New vascular events at 3 months were significantly less likely in the CDSS group vs control group (2.9% vs 3.9%, respectively; adjusted hazard ratio [aHR], 0.74; P = .01).
• The reduction in new vascular events persisted at 6 months (aHR, 0.71; P = .006) and at 12 months (aHR, 0.73; P = .02).
• The intervention group also had higher adherence to composite measures of evidence-based performance indicators than the control group (adjusted odds ratio, 1.21; P < .001).
• No significant between-group differences were observed for disability (mRS score > 3) at 3, 6, and 12 months; all-cause mortality at any timepoint; or moderate/severe bleeding events.

IN PRACTICE:

“The stroke CDSS offers a promising approach to providing high quality care for patients with acute ischemic stroke admitted to hospital, particularly for resource constrained regions with a heavy burden of cerebrovascular diseases like China,” the investigators wrote. 

SOURCE:

The study was led by Xinmiao Zhang, MD, PhD, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. It was published online on March 21 in The BMJ. 

LIMITATIONS:

The trial randomized hospitals rather than patients and provided limited insight into the effects of the CDSS on patients with severe stroke. The stroke CDSS also did not cover decision-making for endovascular thrombectomy. Additionally, the study did not analyze length of hospital stay or hospital admission costs, limiting understanding of the economic implications of implementing the CDSS. 

DISCLOSURES:

The study was funded by the National Key Research and Development Program of China, the National Natural Science Foundation of China, the Beijing Municipal Administration of Hospitals’ Mission Plan, the Ministry of Industry and Information Technology of the People’s Republic of China, the CAMS Innovation Fund for Medical Sciences, and Beijing Ande Yizhi Technology Co. Disclosure information for study authors is available in the original study publication.

Nasal Brush Biopsy Flags Preclinical Alzheimer’s Disease

 Because of your extra risk of dementia post stroke, you'll want this test so your doctor CAN IMPLEMENT THOSE EXACT ALZHEIMER'S PREVENTION PROTOCOLS THAT WERE WRITTEN AGES AGO! Oh NO, your doctor failed at that! Well, you're screwed, but your doctor is still getting paid for incompetence!

Nasal Brush Biopsy Flags Preclinical Alzheimer’s Disease

A quick, outpatient nasal swab can detect early biological changes linked to Alzheimer’s disease (AD) years before cognitive or memory symptoms present.

Sampling cells in the upper nasal cavity via a minimally invasive brush biopsy may be able to detect AD years before symptoms appear.

Investigators analyzed brush biopsy samples from the olfactory cleft — the narrow upper region of the nasal cavity that houses the olfactory epithelium — and identified immune and neuronal changes that mirror those seen in the brains of people with AD. These signatures distinguished individuals with preclinical and clinical AD from healthy control individuals.

“The nasal biopsy approach is still a research tool rather than something ready for routine care,” study investigator Vincent D’Anniballe, an MD-PhD student with the medical scientist training program at Duke University in Durham, North Carolina, told Medscape Medical News.

“Potentially,” said D’Anniballe, “because the sampling can be repeated and gives us a window into living nerve and immune cells, it could one day help track whether a treatment is changing Alzheimer’s-related biology over time.”

The study was published online on March 18 in Nature Communications.

A Window Into Central Neuropathology

Loss of smell is one of the earliest signs of AD. The olfactory epithelium — located in the upper nasal cavity — harbors olfactory sensory neurons that can accumulate hallmark AD pathology, including amyloid-beta plaques and neurofibrillary tangles, suggesting the olfactory epithelium may “faithfully mirror central AD neuropathology,” the researchers wrote.

To investigate, they profiled olfactory epithelium brush biopsies obtained from healthy control individuals, individuals with cerebrospinal fluid (CSF) biomarker-confirmed AD, and cognitively typical individuals whose positive CSF biomarkers signal a preclinical AD stage.

The biopsy results revealed a “continuum of disease-linked shifts detectable in biomarker-positive, cognitively unimpaired patients and mirrored in the clinical AD.”

Activated CD8 memory T cells and inflammatory myeloid programs were present in adults with preclinical AD and were also present — often at greater magnitude — in adults with clinical AD.

In addition, olfactory sensory neurons in adults with preclinical and clinical AD showed stress-related transcriptional signatures that mirrored those previously reported in postmortem AD brains, suggesting that the olfactory epithelium reflects disease activity occurring deeper in the brain.

A combined gene-expression score derived from the olfactory biopsies was able to distinguish individuals with preclinical and clinical AD from healthy control individuals with about 81% accuracy.

“At this point, our study cannot separate cause from effect. The fact that we see immune cell changes so early suggests they may be a part of the disease process, but we still need follow-up studies to know whether they are driving the disease or reacting to it,” D’Anniballe noted.

Looking ahead, the researchers plan to expand their work to larger patient groups and explore whether olfactory brush biopsy could be used to monitor disease progression or response to therapy over time.

“The biggest hurdles are proving in larger studies that it is reliable and scalable before it can work as a practical clinical test,” said D’Anniballe.

A ‘Compelling’ Early Signal

Reached for comment, Sheena Aurora, MD, vice president of medical affairs at the Alzheimer’s Association, said the results are “intriguing,” given that loss of smell is one of the first symptoms of AD in some people and “targeting the olfactory epithelium is a novel approach.”

However, she noted that the study is very small and preliminary. As a result, the findings need to be replicated and confirmed in larger, more representative study populations before the technique could be considered clinically viable.

Another study limitation is the fact that olfactory cleft biopsies have highly variable rates of success, said Aurora, who wasn’t involved in the research.

If it is eventually validated, this approach could help support diagnosis alongside existing amyloid and tau measures, guide the selection and monitoring of patients for disease-modifying therapies, and provide a way to study early AD-related changes in the brain and adjacent tissues, she noted.

Also weighing in on the findings, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, said this study “turns the nose into a window into the brain. For the first time, we’re seeing Alzheimer’s biology unfold in living neural tissue before symptoms even begin.”

“What’s striking is that the inflammatory signature of Alzheimer’s is already present in people who are cognitively normal. That fundamentally shifts how we think about when this disease begins,” said Lakhan, who was not involved in the research.

“The olfactory epithelium is one of the only places where you can safely sample living human neurons. That’s been the missing piece in Alzheimer’s research. This is not a nasal swab. It’s a targeted biopsy of olfactory neural tissue, which is why it captures real brain biology, not just surface signals,” he added.

Lakhan said the findings point to a potential pharmacodynamic biomarker, offering a way to directly observe how interventions — whether drugs or digital therapeutics — affect neural and immune pathways in living human tissue.

If validated, he added, the approach could transform early detection and clinical trials by providing an earlier, biologically grounded signal of disease activity and treatment response.

He emphasized, however, that the work remains an early proof-of-concept, albeit with a strong and biologically coherent signal.

Funding for the study was provided by the National Institutes of Health. D’Anniballe reported having no disclosures. Duke University and four authors are named inventors on a US patent application related to methods for obtaining olfactory cleft brush biopsy samples and measuring gene-expression biomarker panels to detect/diagnose and guide treatment of preclinical AD. Aurora and Lakhan reported having no relevant disclosures.

Managing Asymptomatic Carotid Stenosis in 2026

 

 I had zero risk factors for this and was totally asymptomatic, except that my Dad had 80% blockage and his doctor failed to tell him that any children had moved into the high risk category for carotid stenosis. So, my stroke was totally preventable except my dads' doctor failed at getting me informed of my risk.

My stroke doctors never diagnosed carotid stenosis in me even though 3 years later the right carotid artery completely closed up which my doctor at the time said it would have been 80% blocked at the time of my stroke, when it dissected. You can easily see the complete failure of my doctors at this! Very luckily, I didn't dissect that plaque again and suffer another stroke, no thanks to my doctors!

Managing Asymptomatic Carotid Stenosis in 2026

Dear colleagues, I am Christoph Diener, from the Faculty of Medicine at the University of Duisburg-Essen in Germany. My video this month concentrates on one important topic only, and this is the management of asymptomatic carotid stenosis. 

Defining Asymptomatic Carotid Stenosis

Asymptomatic stenosis of the internal carotid artery is defined as a stenosis of 50% or more,and these stenoses are usually found at the origin of the internal carotid artery. Asymptomatic carotid stenosis can lead to ischemic strokes caused by embolization from an ulcerated plaque, or very rarely, hemodynamically, if an occlusion of the internal carotid artery occurs.

How are these stenoses identified usually? During screening examinations that people who have coronary artery disease or peripheral arterial disease undergo, or when those older than 60 or 65 years see their internist for a yearly checkup. 

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The first studies comparing optimal drug therapy with carotid endarterectomy were conducted in the 1990s and the early 2000s, and these were the ACAS and ACST studies. At that time, the best possible medical treatment consisted of administrating aspirin and treating arterial hypertension. 

The annual risk for ipsilateral stroke, perioperative stroke, or death over 5 years in the ACAS study was 5% for patients who underwent endarterectomy and 11% for patients who received best medical treatment. This translated to a 53% risk reduction in favor of carotid surgery, and at that time, carotid surgery was recommended. 

Subsequently, a number of additional studies were done comparing surgical treatment with optimal medical therapy. These included between 450 and 3600 patients, and the absolute risk reduction in favor of surgery over best medical treatment was variable, ranging from, in an optimal case, 5.4% to only 3.3%, which was no longer statistically significant. 

In the next 10 years, seven randomized studies involving almost 6000 patients were conducted comparing carotid surgery with carotid stenting. In a meta-analysis, no differences were found for the endpoints of death, stroke, and myocardial infarction. Carotid surgery showed a slight superiority for the endpoint of ipsilateral stroke. 

Since 1990, medical treatment has dramatically improved. In addition to antiplatelet drugs and better antihypertensive drugs, we now have much better medications available for treating elevated glucose levels and diabetes, medications for treating lipid metabolism disorders, obesity treatment, and the management of risk factors, like programs for smoking cessation, regular physical activity, and healthy diet. 

As a result, the 5-year risk for stroke has fallen from 11% in the 1990s to 2.5% in 2026. There are also predictors of increased stroke risk in people with asymptomatic carotid stenosis, and these include high-degree stenosis of more than 80%, evidence of microembolism in transcranial Doppler, plaque ulceration in duplex sonography, progressive stenosis of the internal carotid artery, and clinically silent infarct on MRI of the brain. 

Enter CREST-2 at ISC

The purpose of this video is the publication of the CREST-2 study in The New England Journal of Medicine and the presentation of the study at the International Stroke Congress. This was by far the largest and best planned and -conducted study comparing best medical therapy and carotid stenting in 1245 patients, with carotid endarterectomy in 1240 patients. The primary endpoint was stroke or death, and this was 6% for best medical therapy and 2.8% for stenting. This corresponds to a relative risk reduction of 3.2%, which was statistically significant. 

For carotid surgery, the rate of stroke and death was 5.3% vs 3.7%, so the relative risk reduction was 1.6%, and this was statistically not significant. If we calculate numbers needed to treat, these were 31 for stenting compared to best medical therapy, and 63 for carotid surgery compared to best medical therapy. 

The CREST-2 study also showed that carotid stenting is associated with a slightly higher therapeutic benefit compared to best medical treatment. No superiority for cardiac surgery over optimal medical treatment was observed. The low risk for ipsilateral stroke is noteworthy. This risk ranged between 0.4% and 1.7% per year across all four groups of therapy. 

In contrast to earlier studies, the CREST-2 study excluded myocardial infarction as an endpoint, and this makes sense because carotid surgery or carotid stenting usually has no impact on the risk for myocardial infarction.

Caveats and Limitations of CREST-2

Unfortunately, serious bleeding complications were not reported in the study. And these are relevant because after carotid stenting, dual antiplatelet therapy has to be administered at least for a few weeks. 

It is also important to note that there was a rigorous selection of vascular surgeons and interventionalists, and this might not translate into everyday clinical practice because we can expect that probably most people who do not have a high load of procedures have a higher complication rate. 

The periprocedural risk was 1% for stroke. This study very closely monitored the management of risk factors and the treatment of concomitant diseases, and in everyday clinical practice, this might not always be achieved.

When a physician discusses with a patient with asymptomatic carotid stenosis or the family, then they have to point out that the initial risk for stroke and death from the procedure itself is about 1.3%, and this must be weighed against the long-term benefit of stenting, where the risk reduction over 5 years is 3.2%. The presence of risk factors for an increased risk for stroke that I have mentioned before should also be taken into account when deciding for or against surgery or stenting of the internal carotid artery. 

In summary, the CREST-2 study is by far the best planned and -conducted study for the management of asymptomatic carotid stenosis. If one decides to perform a procedure, then it should be carotid stenting and not carotid surgery. (I would never do either unless YOUR DOCTOR COMPLETELY GUARANTEES NO PROBLEMS!

Here is why you do neither of those options!

Asymptomatic Blocked Carotids Don't Need Surgery, Large Trial Shows

In my non-medical opinion, verify the Circle of Willis is complete, then close up the offending artery. I functioned extremely well for 13 years with only three arteries feeding the Circle of Willis)

Dear colleagues, ladies and gentlemen, this was the management of asymptomatic cardiac stenosis and the status of knowledge in 2026. I'm Christoph Diener from the Faculty of Medicine at the University of Duisburg-Essen. Thank you very much for listening and watching. 

5 Factors May Predict Long-Term Stroke Risk After Minor Event

 Your competent? doctor SHOULD KNOW EXACTLY HOW TO PREVENT THAT STROKE! What excuse are they using to justify failure at that?

5 Factors May Predict Long-Term Stroke Risk After Minor Event

Five factors may predict the long-term risk for another stroke in people who have experienced a transient ischemic attack (TIA) or minor stroke, according to a new study.

The systematic review and meta-analyses examined 28 observational cohort studies, totaling 86,810 patients with a history of TIA or minor stroke, to identify which risk factors affected prognosis for secondary stroke events at 1 year or longer.

Hypertension, smoking, and three subtypes of ischemic stroke — cardioembolism, large artery atherosclerosis, and small vessel disease — were the main factors contributing to long-term secondary stroke risk. Minor stroke accounted for a larger proportion of later strokes than TIA.

Faizan Khan, PhD

“Even though these are known factors for stroke risk, there were some contradictory findings in the literature. We wanted to clarify the associations that had mixed interpretations,” lead author Faizan Khan, PhD, Canadian Institutes of Health Research (CIHR) Banting Postdoctoral Fellow at the University of Calgary in Calgary, Alberta, Canada, told Medscape Medical News.

The study also estimated each risk factor’s population attributable fraction, which quantifies the strength of its association with long-term stroke risk and its prevalence, allowing clinicians to see “which factors are more important and should be prioritized,” Khan said.

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Stroke Risk Beyond 90 Days

The findings build on the earlier PERSIST study, which examined secondary stroke risk in patients with TIA or minor stroke beyond the typical 90-day monitoring window.

“We didn’t have a good understanding of the risk of secondary stroke past 90 days. The PERSIST study found the risk was significant and continued to rise,” Khan said. The results showed about 20% of patients with TIA or minor stroke were likely to have another stroke within 10 years, and more than half of all later strokes occurred a year or more after the initial event.

“The new paper tried to identify, in a systematic way, which factors impact the long-term risk of secondary stroke,” he said.

Modifiable Factors and More

For this study, TIAs were events in which stroke symptoms lasted 24 hours or less or showed no obstructions in imaging, while minor strokes were events with National Institutes of Health Stroke Scale scores of up to 5 and visible obstructions.

Starting with a pool of 14,732 relevant citations from the MEDLINE, Embase, and Web of Science databases, researchers selected studies that examined prognostic factors for later strokes after at least 1 year in patients with TIA or minor stroke. Most had been conducted in Europe, were based on prospectively enrolled cohorts, and had a maximum follow-up of at least 5 years. Twelve studies focused on TIA or minor stroke (19,893 patients), 14 considered only TIA (66,197 patients), and two evaluated only minor stroke (720 patients).

The cohorts were mostly men (median, 57%; interquartile range [IQR], 52-60) with a median age of 69 years (IQR, 65-71). A high percentage (median, 94%; IQR, 86-99) received antithrombotic medications after their hospital discharge.

Older age (adjusted hazard ratio [aHR], 1.04 per year increase; 95% CI, 1.02-1.05) and male sex (aHR, 1.25; 95% CI, 1.15-1.36) were the top non-modifiable risk factors associated with later strokes. Hypertension (aHR, 1.60; 95% CI, 1.31-1.94), smoking (aHR, 1.29; 95% CI, 1.05-1.60), and etiologic stroke subtypes, including cardioembolism (aHR, 2.16; 95% CI, 1.53-3.05), large artery atherosclerosis (aHR, 2.19; 95% CI, 1.68-2.86), and small vessel disease (aHR, 1.69; 95% CI, 1.14-2.49), were the leading modifiable factors. 

High blood pressure and tobacco use had population attributable fractions (PAFs) of 19.3% and 11.2%, respectively, suggesting “hypertension and smoking are worthwhile to focus on when it comes to long-term secondary stroke prevention,” Khan said. “PAF can help tailor strategies…to those patients who can be helped the most.”

The study was presented at the American Heart Association’s EPI Lifestyle Scientific Sessions (AHA-EPI) 2026 on March 18 and simultaneously published in Circulation.