LVADs Linked to Concerning Neurologic Events, Strokes Aside

 If your doctors suggest this, have THEM GUARANTEE no complications! Can't do that, what is the backup plan?

An LVAD (left ventricular assist device) is a surgically implanted mechanical pump that helps a weakened heart pump blood to the rest of the body.

LVADs Linked to Concerning Neurologic Events, Strokes Aside

 Subarachnoid hemorrhage, subdural hemorrhage, encephalopathy emerge in registry data

Key Takeaways

• A registry study found an 8% incidence of stroke at 1.4 years after LVAD placement, accompanied by another 8% incidence of nonstroke neurologic adverse events.
• Pre-LVAD extracorporeal membrane oxygenation (ECMO) and concomitant surgery may be modifiable targets to reduce neurologic dysfunction.
• A more complete view of neurologic dysfunction is needed to inform decision-making, researchers said.

It's not all about stroke: Various neurologic events boded poorly for survival on the contemporary magnetically levitated HeartMate 3 left ventricular assist device (LVAD) in a retrospective registry study.

Based on the U.S. INTERMACS database, there was an 8% incidence of both stroke and nonstroke neurologic adverse events (NAEs) over a median 1.4 years among nearly 12,000 people with advanced heart failure who got the contemporary magnetically levitated LVAD.

Two-year survival rates were 45% in LVAD recipients who had a stroke and 56% in peers with nonstroke neurologic events (P<0.001). Compared with no neurologic event, there was an elevated risk of death after a stroke (HR 7.3, 95% CI 6.6-8.1) or a nonstroke neurologic event, the latter associated with:

• Highest mortality risk where there is overt central nervous system (CNS) injury (HR 12.58, 95% CI 10.39-15.23)
• High risk with covert CNS injury detected by neuroimaging (HR 9.19, 95% CI 6.75-12.51)
• Lower but still elevated risk with neurologic dysfunction without CNS injury, such as encephalopathy (HR 3.69, 95% CI 3.20-4.25)

"Stroke and nonstroke NAEs are incurred by a similar proportion of patients, and both are associated with substantially reduced survival. Consequently, stroke and nonstroke NAEs should be given comparable weight with universal nomenclature when evaluating the safety of durable LVADs," concluded a group led by Omar Saeed, MD, MSc, of Montefiore Medical Center, Albert Einstein College of Medicine in New York City, reporting in JACC: Heart Failure.

In their study, there were two potentially modifiable targets to reduce neurologic dysfunction from LVAD therapy: pre-LVAD extracorporeal membrane oxygenation (ECMO) and concomitant surgery.

A Long List of Neglected Neurologic Complications?

Much attention has centered strokes as the neurologic complication of concern in LVAD recipients. Prior work established that strokes may arise due to thromboembolism from various sources, while preexisting cerebrovascular disease, uncontrolled hypertension, and anticoagulation therapy may also contribute to stroke burden, Saeed and colleagues noted.

Other clinically significant neurologic complications, such as encephalopathy, have consequently been less well described.

"Neurological assessment after LVAD implantation should extend beyond focal stroke symptoms," commented Sung-Min Cho, DO, MHS, of Johns Hopkins University School of Medicine in Baltimore, who was not involved with the study.

Of note, Cho told MedPage Today, it may not be the case that encephalopathy itself causes death, as it may reflect underlying infection, shock, or multiorgan dysfunction. "Altered mental status/encephalopathy may warrant clinicians' attention both to possible brain injury and to the systemic illness that may be causing it, both of which increase the risk of death."

There is also an issue with attributing deaths to covert brain injury, as scans are ordered usually when a patient is already doing poorly, according to Mandeep Mehra, MD, MSc, of Brigham and Women's Hospital and Harvard Medical School in Boston, who was also not involved with the study.

Cho and Mehra both stressed the clinical heterogeneity of the so-called "nonstroke" endpoint in the study, which included overt CNS injury from subarachnoid hemorrhage (SAH), hypoxic-ischemic injury, subdural hemorrhage (SDH), or traumatic brain injury; covert CNS injury detected by neuroimaging; and neurologic dysfunction without CNS injury including encephalopathy, delirium, seizures, and transient ischemic attacks (TIA).

"SAH is a cerebrovascular event ordinarily considered a hemorrhagic stroke; SDH is generally classified separately, but grouping both under 'nonstroke neurological dysfunction' obscures the distinction between structural brain injury and conditions such as delirium in my opinion," Cho said.

"The nonstroke category needs dissecting before we give it equal weight with stroke. Seventy percent of these events are encephalopathy, delirium, seizures, or TIA. None of them were adjudicated, and in a very sick postoperative patient they are often a consequence of sepsis or multiorgan failure rather than a device-related brain injury," warned Mehra. "What we need is rigorous, adjudicated, device-attributable neurological endpoints. Lumping heterogeneous, unadjudicated events into a safety endpoint for future device trials could obscure rather than clarify device performance."

Can Neurologic Events Be Prevented?

Saeed's group performed a retrospective cohort study using the nationwide Society of Thoracic Surgeons INTERMACS database. Included were 11,739 patients who got a HeartMate 3 LVAD from 2017 to 2023.

The authors reported that pre-LVAD ECMO was associated with more stroke (HR 1.70, 95% CI 1.35-2.16) and nonstroke events (HR 1.45, 95% CI 1.11-1.90); concomitant surgery was also tied to stroke (HR 1.23, 95% CI 1.08-1.41) and nonstroke events alike (HR 1.17, 95% CI 1.03-1.34).

"Patients coming to implant on ECMO or temporary support, or undergoing concomitant procedures, carry higher neurological risk. That calls for careful thrombus screening, attention to stasis, and early neurological assessment after surgery," Mehra said.

Cho and Mehra both cautioned against calling ECMO a "modifiable" risk factor based on these findings, however. "Patients are on ECMO because they are in shock. ECMO marks severity of illness more than it represents a choice we can simply avoid," Mehra said.

It also remains to be shown that "avoiding ECMO would reduce neurological injury," according to Cho.

In any case, there is already some improvement on the neurologic safety of LVADs, as Saeed and colleagues reported that stroke and nonstroke NAEs occurred at an incidence of 0.044 and 0.049 events per patient-year, respectively, in this real-world cohort. In contrast, in the MOMENTUM3 trial, the incidence of any stroke was 0.050 events per patient-year across HeartMate 3 and HeartMate II LVAD recipients, while other neurologic events were logged at 0.073 events per patient-year.

The contemporary HeartMate 3 is already an improvement over its predecessor HeartMate II in terms of staving off neurologic complications. In a prespecified analysis of MOMENTUM 3, stroke rates were 10.1% and 19.2% in the first 2 years between the two LVAD groups, respectively (P=0.02).

"I was not at all surprised by this analysis which is itself reassuring(I'm not reassured at all, you are not the one under the knife!)," and "confirms that neurological complications have fallen substantially in the magnetically levitated era," said Mehra. "The device itself is no longer the dominant driver of neurological risk; the surgery and peri-implant factors are the issue."

The report found that the independent predictors of death after stroke were older age, pre-LVAD implantable cardioverter-defibrillator, higher pre-LVAD blood urea nitrogen level, and pre-LVAD dialysis. Predictors of death after nonstroke NAE were higher pre-LVAD body mass index, higher pre-LVAD serum creatinine, greater pre-LVAD international normalized ratio, and lower pre-LVAD albumin.

"Awareness of these patient-level characteristics may help direct resources to those who are most vulnerable after the occurrence of NAEs," the study authors suggested.

Saeed and colleagues nevertheless acknowledged that their retrospective study left room for bias and did not account for variables such as blood pressure management, anticoagulation management, or atrial fibrillation. Additionally, NAE events may be underestimated due to the lack of reporting of recurrent events and the classification of patients experiencing both stroke and nonstroke NAEs as stroke only.

Microglia Rescue Vulnerable Dopamine Neurons in Parkinson’s

 With your risk of Parkinsons' poststroke. How is your competent? doctor ensuring these microglia are working in your case?

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here: 

Microglia Rescue Vulnerable Dopamine Neurons in Parkinson’s

Summary:

Researchers at the University of Oxford have discovered that human microglia can selectively prune away toxic alpha-synuclein aggregates from dopamine-producing neurons without destroying the host nerve cells. Utilizing co-cultures of human induced pluripotent stem cell (iPSC)-derived neurons and microglia, the team demonstrated that microglia employ “trogocytosis”, a precise cellular nibbling mechanism, regulated by GPNMB, P2RY12, and CD22 signaling pathways, along with an IL-10 molecular brake. The findings identify a distinct, neuroprotective microglial subtype that shields neurons in Parkinson’s disease.

Key Facts:

• Selective Pruning via Trogocytosis: Human microglia selectively extract and dispose of aggregated alpha-synuclein clumps by “nibbling” specific segments of living dopamine neurons while preserving overall neuronal viability and connectivity.
• GPNMB Identified as Functional Driver: Glycoprotein non-metastatic melanoma protein B (GPNMB), a protein previously linked to Parkinson’s risk via genome-wide association studies (GWAS), binds directly to alpha-synuclein and is required for microglia to effectively clear aggregates.
• Fine-Tuned Immune Brakes: The protective clearance mechanism is controlled by sensing receptors (P2RY12), inhibitory checkpoints (CD22), and an interleukin-10 (IL-10) autocrine brake that prevents runaway neurotoxic inflammation.

Source: University of Oxford

Beyond the Double-Edged Sword: A Precision Immune Defense

In neurodegenerative diseases, microglia, the central nervous system’s resident immune sentinels, are typically framed through a conflicted narrative. Under physiological conditions, they survey brain tissue, prune synapses, and clear cellular debris; during chronic neurodegeneration, their persistent activation drives inflammatory signaling cascades that accelerate neuronal death.

Nowhere has this paradox been more evident than in Parkinson’s disease, a condition affecting more than 10 million individuals globally. The disease is defined by the selective death of dopamine-producing neurons within the substantia nigra, driven largely by the misfolding and aggregation of alpha-synuclein into toxic intracellular clumps.

Whether human microglia can intervene constructively to rescue dopamine neurons from this proteinaceous burden, without destroying the neurons in the process, has remained an open question.

Now, a team of neuroscientists at the University of Oxford has revealed an unexpected, highly targeted defense mechanism.

The researchers established that a specialized population of human microglia actively extracts and destroys harmful alpha-synuclein aggregates directly from living dopamine neurons via trogocytosis (from the Greek trogo, meaning “to gnaw” or “to nibble”).

“What is striking is the precision of this response,” said first author Hung-Ju Chueh, Ph.D., of the University of Oxford. “The microglia were not simply engulfing damaged neurons but instead removing parts of the neuron containing aggregated alpha-synuclein, suggesting that, at certain stages of disease, microglia help neurons dispose of potentially harmful material.”

Engineering Human iPSC Co-Cultures to Model Live Interactions

To investigate interactions between human brain cells in real time, the Oxford investigators generated human induced pluripotent stem cell (iPSC) lines, co-culturing authentic human dopamine neurons alongside human microglia.

The team modeled alpha-synuclein pathology through two complementary methods: by introducing genetic alpha-synuclein gene dosage elevations (triplication), and by seeding the cultures with exogenous preformed alpha-synuclein fibrils that template the misfolding of native neuronal protein.

High-resolution cellular imaging revealed that rather than engulfing entire dying neurons via standard phagocytosis, the microglia selectively nibbled off membrane pockets enclosing the aggregated protein. This process of trogocytosis eliminated the toxic pathology while leaving the broader axonal network and cell body intact.

Single-cell RNA sequencing showed that this clearance was driven by a distinct, transcriptionally defined subpopulation of activated microglia. This subset was kept from over-activating through a balanced signaling network:

• Surveillance and Guidance: Governed by P2RY12 purinergic receptor sensing.
• Cellular Checkpoints: Regulated by CD22 inhibitory surface interactions between neurons and microglia.
• Inflammatory Suppression: Maintained by an autocrine interleukin-10 (IL-10) brake that halted secondary, collateral inflammatory tissue injury.

Solving the GPNMB Genetic Mystery in Parkinson’s

The investigation also cracked a longstanding genetic puzzle. Multiple large-scale genome-wide association studies (GWAS) had previously flagged variants in the GPNMB (glycoprotein non-metastatic melanoma protein B) gene locus as significant risk factors for Parkinson’s disease, but its mechanistic function in the brain remained unknown.

The Oxford team discovered that GPNMB is directly upregulated in human microglia when exposed to aggregate-bearing neurons, where it physically interacts with pathological alpha-synuclein within the microglial machinery.

Furthermore, post-mortem analysis of human brain tissue from patients with incidental Lewy body disease and confirmed Parkinson’s disease revealed elevated GPNMB levels within substantia nigra microglia.

To confirm causality, the team used CRISPR interference (CRISPRi) to knock down GPNMB expression in human microglia. Deprived of GPNMB, the microglia lost their ability to clear alpha-synuclein aggregates from the neighboring dopamine neurons, establishing GPNMB as an essential driver of the neuroprotective response.

“Our findings highlight that the immune response in Parkinson’s disease is more nuanced than simply being beneficial or harmful,” noted senior author George Tofaris, M.D., Ph.D., Professor of Neurology and Translational Neuroscience at the University of Oxford. “We have identified a population of human microglia that can actively remove pathological alpha-synuclein from neurons. Understanding how to enhance and monitor such beneficial microglial functions, without triggering damaging inflammation, could open up new avenues for developing disease-modifying treatments.”

Editorial Notes:

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

About this Neurology Research:

• Media Contact: Christopher McIntyre
• Source: University of Oxford
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Science Translational Medicine (Oct 7, 2026). “Human microglia clear intraneuronal alpha- synuclein aggregates by GPNMB-mediated trogocytosis.” Authors: Hung-Ju Chueh, Antigoni Katsikoudi, Ana Aragón-González, Chor Lai Lam, Liezel Tamon, Ashwin Jainarayanan, Devika Agarwal, Sally A. Cowley, David Sims, and George K. Tofaris.
• DOI: 10.1126/scitranslmed.adz9258

Statins Linked to Reduced Glaucoma Risk and Slower Progression

 

 Your competent? doctor immediately prescribed statins post stroke based on earlier research, right? NO? And still hasn't been fired yet?

1. Statins.

tested in rats from 2003

http://Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke  

Simvastatin Attenuates Stroke-induced Splenic Atrophy and Lung Susceptibility to Spontaneous Bacterial Infection in Mice

Or,

Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons 

October 2012

tested in humans, March 2011

http://www.medwirenews.com/39/91658/Stroke/Acute_statin_therapy_improves_survival_after_ischemic_stroke.html

And now lost even to the Wayback Machine

So, I think this below is the actual research.

Association Between Acute Statin Therapy, Survival, and Improved Functional Outcome After Ischemic Stroke April 2011 

The latest here: 

Statins Linked to Reduced Glaucoma Risk and Slower Progression

Summary:

A massive real-world epidemiological investigation from the UC San Diego School of Medicine reveals that statin medications are associated with a significantly reduced risk of developing open-angle glaucoma and a lower rate of surgical escalation in those already diagnosed.

Analyzing health records from more than 420,000 propensity-matched individuals across a 20-year cohort in the British Journal of Ophthalmology, researchers discovered that statin users had a 15% lower incidence of glaucoma and up to a 55% to 60% reduction in the need for laser or surgical interventions.

Key Facts:

• Lower Glaucoma Incidence: Statin use was associated with a 15% relative risk reduction in developing open-angle glaucoma compared to matched non-users over five years.
• Significant Reduction in Surgical Escalation: Among patients with established glaucoma, statin therapy was linked to a 36% lower risk of incisional surgery, a 55% reduction in minimally invasive glaucoma surgery (MIGS), and a 60% reduction in selective laser trabeculoplasty (SLT).
• Massive International Cohort: The study evaluated electronic health records from a global registry spanning 165 million patients, examining over 210,000 matched pairs followed between August 2006 and August 2026.

Source: UC San Diego School of Medicine / British Journal of Ophthalmology

Glaucoma is one of the leading global causes of irreversible blindness, marked by the progressive and permanent degeneration of retinal ganglion cells and optic nerve axons. While current clinical management focuses almost exclusively on lowering intraocular pressure (IOP) via topical eye drops, laser procedures, or invasive filtering surgeries, mechanical pressure reduction does not always halt neurodegenerative progression.

Statins, the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors taken by tens of millions of adults to manage cardiovascular disease, are increasingly recognized for their pleiotropic properties. Beyond reducing low-density lipoprotein (LDL) cholesterol, statins exhibit potent anti-inflammatory, antioxidant, endothelial-stabilizing, and neuroprotective activities across the central nervous system.

Whether these systemic actions translate into measurable clinical protection for the human optic nerve has remained an unresolved question in ophthalmic medicine.

Now, an observational study led by researchers at the University of California San Diego School of Medicine provides robust population-scale evidence that statins protect against both the development and the clinical progression of glaucoma.

Published online in the British Journal of Ophthalmology, the study shows that statin users not only develop open-angle glaucoma less frequently, but those already living with the condition are significantly less likely to require advanced interventions, such as laser therapy or operating room surgery.

“Glaucoma is one of the leading causes of irreversible blindness, and statins are among the most common medications used to lower cholesterol and reduce the risk of heart disease,” said senior study author Robert Weinreb, M.D., Distinguished Professor in the Viterbi Family Department of Ophthalmology at UC San Diego School of Medicine and Director of both the Hamilton Glaucoma Center and the Gleiberman Center for Glaucoma Research at the Shiley Eye Institute. “If this association is confirmed in future studies, it could have implications for a very large number of people.”

Mining 20 Years of Global Patient Data

To resolve conflicting conclusions from smaller prior trials, the UC San Diego team, collaborating with researchers from the University of South Florida and the University of Southern California, queried a federated global database covering 165 million individuals.

The investigators structured two targeted clinical cohorts:

• Primary Incidence Cohort: The team compared 210,000 adults with a confirmed record of statin use between August 2006 and August 2026 against a meticulously matched control group of 210,000 individuals with no history of statin exposure. Both groups had documented longitudinal ophthalmological examinations. Over five years, 2.3% of the statin cohort developed open-angle glaucoma compared to 2.6% of the control group, representing a statistically significant 15% reduction in incident disease.
• Disease Progression Cohort: In a secondary analysis, researchers tracked more than 30,000 individuals with pre-existing glaucoma taking statins compared with nearly 250,000 glaucoma patients not taking statins.

Shielding the Optic Nerve from Escalating Interventions

In patients already managing glaucoma, statin use was tied to a marked decrease in the need for escalating treatments across both five- and ten-year follow-up windows.

At the five-year mark, statin therapy was associated with:

• A 60% lower risk of undergoing selective laser trabeculoplasty (SLT), a laser procedure that enhances aqueous outflow.
• A 55% reduced risk of requiring minimally invasive glaucoma surgery (MIGS), keyhole microsurgical implants designed to reduce intraocular pressure.
• A 36% lower risk of undergoing traditional, incisional glaucoma surgeries (such as trabeculectomy or tube-shunt drainage implants).
• A 12% reduced risk of needing additional prescription intraocular pressure-lowering eye drops.

These protective associations persisted out to a decade of follow-up, suggesting sustained therapeutic benefit over time.

“Statins are known to have pleiotropic effects beyond cholesterol lowering, including anti-inflammatory and potential neuroprotective properties,” Dr. Weinreb explained. “This study suggests those effects could be relevant to optic nerve health, and future studies will be able to tell us if this is a causal, clinically actionable relationship.”

Caveats and the Path to Randomized Clinical Trials

Because this investigation was retrospective and observational, the authors emphasize that it cannot demonstrate direct causality. Residual confounding factors, such as socioeconomic status, exercise, diet, or overall medication adherence, could influence the observed outcomes.

Furthermore, the database lacked granular physiological metrics, such as baseline intraocular pressure measurements, visual field mean deviation scores, or specific surgical rationales, precluding researchers from verifying whether surgeries were omitted due to milder disease or patient choice.

Nevertheless, given the high safety profile, affordability, and widespread accessibility of statins, the findings provide a strong clinical rationale for prospective, randomized controlled clinical trials to test whether targeted statin regimens can serve as adjuvant neuroprotective therapies to preserve eyesight in glaucoma patients.

Funding: The research was funded, in part, by Research to Prevent Blindness.

Editorial Notes:

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

About this Visual Neuroscience and Neuropharmacology Research:

• Media Contact: Miles Martin
• Source: UCSD
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: British Journal of Ophthalmology (Oct 1, 2026). “Statin use is associated with lower risk of open-angle glaucoma incidence and treatment escalation.” Authors: Forest Lin, Alexander T. Hong, and Robert N. Weinreb.
• DOI: 10.1136/bjo-2026-330339

Post-stroke checklist survey launched

 The proper checklist is one question! Are you fully recovered? Y/N? 

Anything more that that is useless and trying to justify incompetence in not getting survivors recovered!

Post-stroke checklist survey launched

The World Stroke Organization (WSO) has launched a global survey to find out how the Post-Stroke Checklist is being used in practice and what is stopping it from being used more widely. SAFE encourages healthcare professionals and stroke support organisations across Europe to take part.

 

The Post-Stroke Checklist is a validated screening tool that helps professionals and stroke survivors talk through unmet needs at follow-up appointments and when moving between services. It was developed through international collaboration, is endorsed by WSO, and covers the areas of life most affected by stroke: mood and emotional wellbeing, cognition and communication, fatigue and sleep, pain and sensory changes, mobility and daily activities and carer strain and social support.

 

Yet little is known about how often the checklist is used in routine care, or what helps and hinders its use. The survey, led by WSO’s Stroke Support Organization Committee, aims to close that gap. It will also look at whether the checklist has been translated or adapted for different languages and cultures, a question that matters greatly across Europe’s many health systems.

 

Who should take part

The survey is open to stroke physicians, rehabilitation professionals, clinical and health system leaders, stroke programme leads, and representatives of stroke organisations worldwide. You don’t need to have used the checklist, the researchers want to hear from regular users, people who have tried it once and people who have never heard of it.

 

It takes around 15 minutes and asks about your familiarity with the checklist, how it is used in your setting, the barriers and enablers you see, and what would support wider uptake.

There is one open box at the end when you can inform them of their incompetence at 100% recovery

 

Click the link below to take part, it closes on the 30 November 2026.

 

Click to take survey

This One Exercise 3x a Week Could Keep Your Blood Pressure Down – And It Doesn't Take Long

 What EXACT non-pharmaceutical methods does your doctor have to lower blood pressure? 

NONE? So, INCOMPETENT THEN?

This One Exercise 3x a Week Could Keep Your Blood Pressure Down – And It Doesn't Take Long

We all know exercise is good for us – but we don't all have the time, motivation, or mobility to put in regular workout sessions. Researchers are trying to help by looking for activities that bring the most benefits for the least amount of time and effort.

In a new study published in BMJ Open Sport & Exercise Medicine, a team led by researchers from Canterbury Christ Church University in the UK has identified isometric exercise training (IET) as a way of reducing blood pressure with just a couple of sessions a week.

That's any training where one position is held for a few minutes at a time. Staying in a squat, holding a plank pose, or doing a hand grip exercise would all count.

These exercises are simple and quick to do, require no equipment, and the researchers suggest they're a worthwhile option for those who can't manage longer, more comprehensive workouts.

Over the course of the study period, IET was linked to drops in systolic blood pressure – the top number in a reading like 130/85, showing peak artery pressure as your heart pumps blood out, and the average pressure in the arteries overall.

"Lower-frequency IET can help maintain short-term blood pressure reductions, providing a pragmatic option for individuals with limited time or adherence challenges," write the researchers in their published paper.

IET has already been associated with lowering blood pressure in previous studies, but before now no one had really investigated how much of it was needed – the duration and frequency required for the biggest benefits.

Here, the researchers recruited 100 adults with an average age of 37, who weren't meeting minimum exercise guidelines and had normal to high-normal systolic blood pressure (that's in the range 120–140 mm Hg).

For four weeks, 80 of these volunteers were asked to do wall squats three times a week (four squats each session), while the other 20 acted as a control group. For the four weeks after that, the exercise participants were asked to keep up the three weekly sessions, or drop down to two, one, or none.

After the first four weeks, systolic blood pressure in the exercising group had dropped by an average of 9.45 mm Hg, compared to the control group. For those who kept up the three sessions for eight weeks, the average drop increased to 13.73 mm Hg.

For those who went down to a couple of sessions or a single session, the overall average drop after eight weeks was around 6.5–7 mm Hg. The blood pressure of those who gave up the exercises after four weeks, meanwhile, was back to its previous level after four weeks.

Three weekly sessions of wall squats significantly reduced systolic blood pressure. (Swift et al., BMJ Open Sport Exerc. Med., 2026)

"For optimal blood pressure reductions and the maintenance of a broader range of physiological adaptations, a frequency of three times per week may be recommended," write the researchers.

It's strong evidence for the benefit of IET when it comes to blood pressure: systolic, diastolic, and mean arterial pressure all improved significantly compared to the control group after four weeks, though how often participants did the training didn't make a meaningful difference to the results.

The researchers think that the exercises may be relaxing and widening blood vessels, and putting the nervous system into a calmer mode – but more detailed, longer-term studies will be needed to know for sure.

"While causality cannot be confirmed, the observed alignment between the mechanistic decline and the loss of blood pressure reduction suggests that training frequency plays a critical role in sustaining the cardiovascular adaptations necessary for blood pressure control following IET," write the researchers.

The team also suggests that extending the IET beyond a couple of months may lead to actual structural changes in blood pressure, meaning the benefits wouldn't disappear as soon as the exercise stopped, as happened here.

It's another reminder that when it comes to staying healthier through exercise, you don't always need a lot of activity to improve your fitness.

"[The study] may inform policy discussions around feasible, scalable exercise interventions for populations with low adherence or limited exercise tolerance," write the researchers.

The research has been published in BMJ Open Sport & Exercise Medicine.