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

What this blog is for:

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

Showing posts with label Arterial stiffness. Show all posts
Showing posts with label Arterial stiffness. Show all posts

Monday, May 11, 2026

Arterial Stiffness Changes Linked to Development of Dementia in SPRINT Post Hoc Analysis

 Your competent doctor already knows how to prevent this problem, right? Oh NO, your doctor and everyone is incompetent? Say it isn't so.

Arterial Stiffness Changes Linked to Development of Dementia in SPRINT Post Hoc Analysis

Persistent elevations or rapid increases in arterial stiffness were linked to incident dementia in adults with hypertension, a SPRINT MIND trial post hoc analysis showed.

In the analysis, each 1 m/s increase in estimated pulse wave velocity was associated with more than twofold higher likelihood of developing probable dementia (adjusted hazard ratio [HR], 2.11; 95% CI, 1.93-2.30) compared with individuals with more stable vascular profiles.

Estimated pulse wave velocity — a marker of vascular aging calculated from blood pressure and age as a surrogate for arterial stiffness — has previously been linked to cardiovascular outcomes, stroke, and cognitive impairment.

A Practical Measure

However, arterial stiffness is difficult to directly measure, said Sula Mazimba, MD, MPH, of the University of Virginia in Charlottesville, Virginia, whose group reported the findings ahead of presentation at American College of Cardiology (ACC) Scientific Session 2026 in New Orleans.

“Estimated pulse wave velocity is to dementia as calcium score is to coronary artery disease,” Mazimba said. “This is one tool that can be used to assess risk and to try and shoot toward treating patients to lower their risk.”

photo of Newton Nyirenda, MD
Newton Nyirenda, MD

As a noninvasive index derived from routine vitals, this measure could be clinically useful to motive more aggressive blood pressure lowering, said presenter Newton Nyirenda, MD, of Georgetown University in Washington, DC.

The SPRINT trial included 9361 adults aged 50 years or older with a systolic blood pressure between 130 and 180 mm Hg and an increased risk for cardiovascular disease but did not have a history of diabetes or stroke. It randomly assigned them to an aggressive systolic blood pressure treatment target below 120 mm Hg or then-standard 140 mm Hg, showing superiority of an intensive target for risk for heart disease, stroke, and related deaths, as well as death from all causes. The MIND substudy followed cognitive endpoints for 7670 participants, showing a reduction in mild cognitive impairment and similar but nonsignificant trend for less dementia with a tight blood pressure control target.

In the post hoc analysis, the intensive treatment arm had fewer participants with a rapidly increasing trajectory of estimated pulse wave velocity than in the standard management arm (13.6% vs 30.8%).

Study Implications

“We know that both the US and world population is underdiagnosed and undertreated from a hypertension perspective,” said Beth Abramson, MD, MSc, of St. Michael’s Hospital in Toronto, Ontario, Canada, and a spokesperson for the American College of Cardiology. Abramson was not involved in the study.“This analysis of the SPRINT trial would suggest…wide ranging impact on our patients,” she told Medscape Medical News. However, estimated pulse wave might not be a go-to for routine clinical practice, she said.

“The take-home message is not that we should all be checking the pulse wave velocity, but we should be paying attention to the components of it,” she said. “We can’t turn back the clock when it comes to age, but we can certainly treat blood pressure in our patients and treat it appropriately.”

Analysis Findings

The top and bottom quartiles for estimated pulse wave velocity change over the trial follow-up period had more than 10-fold difference in dementia-free survival probability (HR, 10.86; 95% CI, 6.88-17.16; P < .0001). The findings were adjusted for sex, race or ethnicity, smoking, chronic kidney disease, clinical and subclinical cardiovascular disease, and treatment arm in the trial.

The risk appeared to be concentrated in the top quartile of estimated pulse wave velocity, as the other quartiles did not differ significantly from the bottom quartile, which the researchers said “supports a clinically meaningful threshold.”

Their analysis included 8536 adults aged 50 years or older with hypertension from the SPRINT trial who had repeated blood pressure follow-up visits. During the trial, 324 participants developed probable dementia.

Limitations

Although SPRINT was a randomized controlled trial, the post hoc analysis could not establish causality in its findings. Rather, the “findings should be interpreted as risk stratification signals,” the researchers said.

Other limitations included omission of age from models to avoid overadjustment and unknown generalizability to lower risk populations, as all SPRINT participants had both hypertension and cardiovascular risk factors that put them at higher risk for adverse events like dementia.SPRINT was funded by the National Heart, Lung, and Blood Institute. The researchers and Abramson disclosed having no relevant financial relationships.

Friday, March 27, 2026

Arterial Stiffness Changes Linked to Development of Dementia in SPRINT Post Hoc Analysis

 You competent? doctor has been creating protocols to address arterial stiffness for stroke for over a decade, right? Oh NO, DOING NOTHING!

Not being able to provide them means your board of directors is so incompetent they can't recognize incompetence in their hospital! 

Arterial Stiffness Changes Linked to Development of Dementia in SPRINT Post Hoc Analysis

Persistent elevations or rapid increases in arterial stiffness were linked to incident dementia in adults with hypertension, a SPRINT MIND trial post hoc analysis showed.

In the analysis, each 1 m/s increase in estimated pulse wave velocity was associated with more than twofold higher likelihood of developing probable dementia (adjusted hazard ratio [HR], 2.11; 95% CI, 1.93-2.30) compared with individuals with more stable vascular profiles.

Estimated pulse wave velocity — a marker of vascular aging calculated from blood pressure and age as a surrogate for arterial stiffness — has previously been linked to cardiovascular outcomes, stroke, and cognitive impairment.

A Practical Measure

However, arterial stiffness is difficult to directly measure, said Sula Mazimba, MD, MPH, of the University of Virginia in Charlottesville, Virginia, whose group reported the findings ahead of presentation at American College of Cardiology (ACC) Scientific Session 2026 in New Orleans.

“Estimated pulse wave velocity is to dementia as calcium score is to coronary artery disease,” Mazimba said. “This is one tool that can be used to assess risk and to try and shoot toward treating patients to lower their risk.”

Suggested for you
photo of Newton Nyirenda, MD
Newton Nyirenda, MD

As a noninvasive index derived from routine vitals, this measure could be clinically useful to motive more aggressive blood pressure lowering, said presenter Newton Nyirenda, MD, of Georgetown University in Washington, DC.

The SPRINT trial included 9361 adults aged 50 years or older with a systolic blood pressure between 130 and 180 mm Hg and an increased risk for cardiovascular disease but did not have a history of diabetes or stroke. It randomly assigned them to an aggressive systolic blood pressure treatment target below 120 mm Hg or then-standard 140 mm Hg, showing superiority of an intensive target for risk for heart disease, stroke, and related deaths, as well as death from all causes. The MIND substudy followed cognitive endpoints for 7670 participants, showing a reduction in mild cognitive impairment and similar but nonsignificant trend for less dementia with a tight blood pressure control target.

In the post hoc analysis, the intensive treatment arm had fewer participants with a rapidly increasing trajectory of estimated pulse wave velocity than in the standard management arm (13.6% vs 30.8%).

Study Implications

“We know that both the US and world population is underdiagnosed and undertreated from a hypertension perspective,” said Beth Abramson, MD, MSc, of St. Michael’s Hospital in Toronto, Ontario, Canada, and a spokesperson for the American College of Cardiology. Abramson was not involved in the study.

“This analysis of the SPRINT trial would suggest…wide ranging impact on our patients,” she told Medscape Medical News. However, estimated pulse wave might not be a go-to for routine clinical practice, she said.

“The take-home message is not that we should all be checking the pulse wave velocity, but we should be paying attention to the components of it,” she said. “We can’t turn back the clock when it comes to age, but we can certainly treat blood pressure in our patients and treat it appropriately.”

Analysis Findings

The top and bottom quartiles for estimated pulse wave velocity change over the trial follow-up period had more than 10-fold difference in dementia-free survival probability (HR, 10.86; 95% CI, 6.88-17.16; P < .0001). The findings were adjusted for sex, race or ethnicity, smoking, chronic kidney disease, clinical and subclinical cardiovascular disease, and treatment arm in the trial.

The risk appeared to be concentrated in the top quartile of estimated pulse wave velocity, as the other quartiles did not differ significantly from the bottom quartile, which the researchers said “supports a clinically meaningful threshold.

Their analysis included 8536 adults aged 50 years or older with hypertension from the SPRINT trial who had repeated blood pressure follow-up visits. During the trial, 324 participants developed probable dementia.

Limitations

Although SPRINT was a randomized controlled trial, the post hoc analysis could not establish causality in its findings. Rather, the “findings should be interpreted as risk stratification signals,” the researchers said.

Other limitations included omission of age from models to avoid overadjustment and unknown generalizability to lower risk populations, as all SPRINT participants had both hypertension and cardiovascular risk factors that put them at higher risk for adverse events like dementia.

SPRINT was funded by the National Heart, Lung, and Blood Institute. The researchers and Abramson disclosed having no relevant financial relationships.

Crystal Phend is an award-winning medical journalist with decades of experience reporting on clinical research and healthcare developments across specialties. When not walking the halls at a medical conference, she can be found at a keyboard in upstate New York.

Friday, March 20, 2026

Blood pressure readings may help identify future dementia risk

Described a potential problem but offered NO SOLUTION! In the business world describing a problem with not even a hint of a solution would be immediate grounds for firing!

You've known of arterial stiffness problems for well over a decade AND DONE NOTHING!

Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHY you aren't solving blood pressure management protocols with NO EXCUSES! I've never received any communications from any stroke association. You'd think they would want to talk to their fiercest critic, but no, they are hiding under a rock someplace, probably don't even know I exist! Swearing at me is allowed, I'll return the favor. Don't even attempt to use the excuse that brain research is hard.

Blood pressure readings may help identify future dementia risk

Measures of blood vessel health derived from routine blood pressure readings may help identify adults at increased risk for dementia, according to research being presented at the American College of Cardiology's Annual Scientific Session (ACC.26). The findings from two studies that tracked patterns of arterial stiffness over time align with growing evidence that uncontrolled hypertension contributes to the development of dementia by accelerating the aging and stiffening of blood vessels.

Rates of dementia and aging-related cognitive decline are expected to increase as populations age. At the same time, nearly half of U.S. adults have high blood pressure, known as the "silent killer" because many people don't know they have it. Efforts to better address hypertension-a key contributor to heart disease and a risk factor for dementia-could impact both heart and brain health. The 2025 ACC/AHA Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults names blood pressure as the most prevalent and modifiable risk factor for the development of cardiovascular diseases, as well as dementia due to damage to blood vessels in the brain.

Blood pressure management(There are NO protocols to address this problem, so stop your fucking blathering and CREATE EXACT PROTOCOLS ON THIS!) isn't just about preventing heart attacks and strokes; it may also be one of the most actionable strategies for preserving cognitive health. We need to start thinking about hypertension management much earlier than we typically have in order to address this in younger adults before damage starts to accumulate."

Newton Nyirenda, MD, epidemiologist at Georgetown University, Washington and lead author of the studies

The two studies, by the same research team, highlight risk scores that identify patients who may be more likely to develop dementia. One study showed that pulse pressure-heart rate index-calculated from heart rate and blood pressure measurements-independently predicted the risk of dementia among adults over age 50. In a separate study, researchers found adults with persistently elevated or rapidly increasing estimated pulse wave velocity-a marker of vascular aging calculated from age and blood pressure-were significantly more likely to develop dementia compared with those with more stable vascular profiles.

"Our findings suggest that vascular aging patterns may provide meaningful insight into future dementia risk," said Nyirenda, MD. "This reinforces the idea that managing vascular health earlier in life may influence long-term brain health."

The studies analyzed 8,536 participants from the SPRINT trial, a large, multicenter study of adults aged 50 years and older with hypertension. Over follow-up, 323 participants developed probable dementia. Researchers examined pulse pressure-heart rate index and estimated pulse wave velocity patterns over five years.

The results showed that participants with higher pulse pressure-heart rate index before age 65 years had a significantly higher risk of developing probable dementia or mild cognitive impairment, with each unit increase in pulse pressure-heart rate index being associated with a 76% higher risk. Participants with a higher estimated pulse wave velocity profile also had a higher risk of developing dementia, even after accounting for clinical risk factors such as age, sex, kidney disease, cardiovascular history, smoking and other factors.

Since the components of pulse pressure-heart rate index and estimated pulse wave velocity are routinely measured at primary care visits, researchers said that risk scoring based on either of these metrics should be relatively easy to integrate into clinical workflows. Discussing dementia risk in these terms could encourage more patients to reduce their risk by making lifestyle changes and taking medications if needed to lower blood pressure, Nyirenda said.

"Clinicians should focus on individualizing risk assessments and then tailoring treatment strategies that help patients improve cardiovascular health while preventing neurocognitive decline," said Sula Mazimba MD, associate professor at the University of Virginia and senior author. "You don't want to wait until a patient starts manifesting cognitive decline before you act."

As a post hoc analysis of clinical trial data, researchers said that the study cannot establish causation. Participants were adults with hypertension and elevated cardiovascular risk, so the findings may not generalize to lower-risk populations. Further studies are needed to validate clinically actionable thresholds and determine whether modifying vascular aging trajectories reduces dementia risk.

Friday, October 31, 2025

High blood pressure variability linked to brain atrophy in older adults

 How exactly is your doctor addressing arterial stiffness and neurofilament light chain problems? Oh, has DONE NOTHING, LIKE USUAL!    

Let's see how long your doctor has been incompetent!

  • blood pressure variability (7 posts to July 2016)
  • Arterial stiffness (31 posts to December 2014)
  • Neurofilament light chain (12 posts to January 2019)
  • High blood pressure variability linked to brain atrophy in older adults

    The combination of high beat-to-beat blood pressure variability (BPV) and elevated pulse pressure variability -- a marker of arterial stiffness -- was linked to medial temporal lobe atrophy and increased plasma neurofilament light chain (NfL), both key markers of neurodegeneration, according to a study published in the Journal of Alzheimer’s Disease.

    The findings suggest that haemodynamic instability may play a significant role in age-related brain decline, highlighting the importance of monitoring and managing BPV to protect cognitive health.

    “Our findings show that even when average blood pressure is normal, instability from one heartbeat to the next may place stress on the brain,” said senior author Daniel A. Nation, PhD, University of Southern California, Los Angeles, California. “These moment-to-moment swings appear to be associated with the same kinds of brain changes we see in early neurodegeneration.”

    The researchers recruited 105 older adults without major neurological or systemic diseases to investigate the relationship between BPV and markers of neurodegeneration. Participants underwent continuous blood pressure monitoring to quantify beat-to-beat variability using systolic average real variability (ARV) and pulse pressure variability via an arterial stiffness index (ASI). Brain MRI assessed medial temporal lobe atrophy, while plasma samples measured NfL and glial fibrillary acidic protein (GFAP) as biomarkers of neuronal and glial injury.

    Analysis revealed that participants with both high ARV and high ASI exhibited significant left-sided medial temporal lobe atrophy, including in the hippocampus and entorhinal cortex, confirmed through region-of-interest and voxel-based morphometry analyses. This combination was also associated with elevated plasma NfL levels, indicating increased neurodegenerative activity, though GFAP levels were unaffected.

    “Traditionally, we’ve focused on lowering average blood pressure numbers,” said Trevor Lohman, PhD, University of Southern California. “But this study suggests we should also be looking at how stable blood pressure is from moment to moment. Reducing these fluctuations could help protect the brain, even in people whose average readings look fine.”

    The authors noted that because this was a cross-sectional study, it cannot prove cause and effect, necessitating larger, long-term studies that closely examine the links between cardiovascular and brain health.

    Reference: https://journals.sagepub.com/doi/10.1177/13872877251386443

    SOURCE: University of Southern California

    Wednesday, January 29, 2025

    Ozone exposure may contribute to reduced oxygen levels and arterial stiffness

    Your competent? doctor should have monitoring in your hospital and give you EXACT INSTRUCTIONS on how to monitor at home. You really think your doctor is capable of that?

    Ozone exposure occurs in the air when harmful ground-level ozone forms through chemical reactions between pollutants like nitrogen oxides (NOx) and volatile organic compounds (VOCs) emitted from sources like vehicles, factories, and certain consumer products, primarily in the presence of sunlight and warm temperatures; this process is most prevalent on hot, sunny days, leading to increased ozone levels in the air we breathe. 
     Ozone exposure may contribute to reduced oxygen levels and arterial stiffness

    Ozone (O3) exposure may reduce the availability of oxygen in the body, resulting in arterial stiffening due to the body's natural response to create more red blood cells and hemoglobin, according to a study published today in JACC, the flagship journal of the American College of Cardiology.

    Researchers found that even brief exposure to elevated ozone levels reduced blood oxygen saturation, triggered hypoxia-related biomarkers, and increased arterial stiffness, highlighting the novel connection between ozone exposure and arterial stiffness, demonstrated through comprehensive biomarker analysis in a high-altitude setting. This study uniquely isolates ozone's effects from other pollutants, providing a critical step forward in understanding its independent role in cardiovascular injury."

    Dr. Harlan Krumholz, MD, SM, Editor-in-Chief of JACC

    Ozone pollution is becoming a worldwide health issue. Recent studies have linked O3 exposure with an increased risk of cardiovascular diseases (CVDs), including ischemic heart disease, stroke, heart failure, and atherosclerosis. Hypoxia, or the deficiency of oxygen in the body, is recognized as a pivotal factor in O3-associated CVDs.

    Source:
    Journal reference:

    Hua, Q., et al. (2025) Associations of Short-Term Ozone Exposure With Hypoxia and Arterial Stiffness. Journal of the American College of Cardiology. doi.org/10.1016/j.jacc.2024.11.044.

    Thursday, October 26, 2023

    Relationship of arterial stiffness and baseline vascular burden with new lacunes and microbleeds: A longitudinal cohort study

    I bet your doctor doesn't have a protocol for testing your arterial stiffness and certainly not one for  reducing it. 

    So if you have arterial stiffness what the fuck is your doctor's protocol to address the problem? Maybe something in one of these?

    Or does your doctor incompetently not even know about testing for and correcting this problem?

     

    Relationship of arterial stiffness and baseline vascular burden with new lacunes and microbleeds: A longitudinal cohort study

    Abstract

    Introduction:

    Arterial stiffness may have a significant impact on the development of cerebral small vessel disease (cSVD).

    Patients and methods:

    We obtained pulse wave velocity (24-h PWV) by means of ambulatory blood pressure monitoring (ABPM) in patients with a recent small subcortical infarct (RSSI). Patients with known cardiac or arterial embolic sources were excluded. Lacunes, microbleeds, white matter hyperintensities and enlarged perivascular spaces at baseline were assessed in a brain MRI and included in a cSVD score. A follow-up MRI was obtained 2 years later and assessed for the appearance of new lacunes or microbleeds. We constructed both unadjusted and adjusted models, and subsequently selected the optimal models based on the area under the curve (AUC) of the predicted probabilities.

    Results:

    Ninety-two patients (mean age 67.04 years, 69.6% men) were evaluated and 25 had new lacunes or microbleeds during follow-up. There was a strong correlation between 24-h PWV and age (r = 0.942, p < 0.001). cSVD was associated with new lacunes or microbleeds when adjusted by age, 24-h PWV, NT-proBNP and hypercholesterolemia (OR 2.453, CI95% 1.381–4.358). The models exhibiting the highest discrimination, as indicated by their area under the curve (AUC) values, were as follows: 1 (AUC 0.854) – Age, cSVD score, 24-h PWV, Hypercholesterolemia; 2 (AUC 0.852) – cSVD score, 24-h PWV, Hypercholesterolemia; and 3 (AUC 0.843) – Age, cSVD score, Hypercholesterolemia.

    Conclusions:

    cSVD score is a stronger predictor for cSVD progression than age or hemodynamic parameters in patients with a RSSI.

    Monday, June 19, 2023

    Arterial stiffness and its influence on cerebral morphology and cognitive function

     

    So if you have arterial stiffness what the fuck is your doctor's protocol to address the problem? Maybe something in one of these?

    Or does your doctor incompetently not even know about testing for and correcting this problem?

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

    Arterial stiffness and its influence on cerebral morphology and cognitive function

    Abstract

    Background:

    Recently, arterial stiffness has been associated with cerebral small vessel disease (SVD), brain atrophy and vascular dementia. Arterial stiffness is assessed via pulse wave velocity (PWV) measurement and is strongly dependent on arterial blood pressure. While circadian blood pressure fluctuations are important determinants of end-organ damage, the role of 24-h PWV variability is yet unclear.

    Objectives:

    We here investigated the association between PWV and its circadian changes on brain morphology and cognitive function in community-dwelling individuals.

    Design:

    Single-centre, prospective, community-based follow-up study.

    Methods:

    The study cohort comprised elderly community-based participants of the Austrian Stroke Prevention Family Study which was started in 2006. Patients with any history of cerebrovascular disease or dementia were excluded. The study consists of 84 participants who underwent ambulatory 24-h PWV measurement. White matter hyperintensity volume and brain volume were evaluated by 3-Tesla magnetic resonance imaging (MRI). A subgroup of patients was evaluated for cognitive function using an extensive neuropsychological test battery.

    Results:

    PWV was significantly related to reduced total brain volume (p = 0.013), which was independent of blood pressure and blood pressure variability. We found no association between PWV with markers of cerebral SVD or impaired cognitive functioning. Only night-time PWV values were associated with global brain atrophy (p = 0.005).

    Conclusions:

    This study shows a relationship of arterial stiffness and reduced total brain volume. Elevations in PWV during night-time are of greater importance than day-time measures.

    Introduction

    In recent studies, arterial stiffness has been related to cerebral small vessel disease (SVD), brain volume and cognitive function. With increasing age, the elasticity of the aortic wall is reduced, resulting in an increased aortic pulse wave transmitted to the cerebral microvasculature and consecutive brain tissue damage.1 This process is accelerated by exposure to vascular risk factors such as arterial hypertension, diabetes mellitus and cardiac disease.2,3
    Arterial stiffness has been related to higher burden of white matter hyperintensities (WMHs).4,5 In addition, recent studies investigated a possible association between arterial stiffness and microstructural changes of the white matter captured by diffusion tensor imaging (DTI) techniques. Arterial stiffness related to lower fractional anisotropy and to higher mean diffusivity, suggesting that increased arterial stiffness exerts widespread detrimental effects on microstructural integrity of the white matter.68
    Current literature also indicates an association of arterial stiffness and reduced brain volume as well as impaired cognitive abilities, including executive function and processing speed.2,9,10
    The gold standard of measurement of arterial stiffness is assessment of carotid-femoral pulse wave velocity (PWV).11 New technological approaches of PWV measurements, however, have been developed. These include pulse wave analysis which can easily be combined with a blood pressure measurement device allowing repetitive evaluation in an ambulatory 24-h setting.12,13 As arterial stiffness is highly depending on arterial blood pressure, a circadian rhythm of PWV is assumed.14,15 Data on circadian changes of PWV and its associations to cerebral structural damage and impairment of cognitive function, however, are lacking.
    Therefore, this study aims to investigate the associations between PWV and its circadian fluctuations and focal SVD-related brain lesions, the peak width of skeletonized mean diffusivity (PSMD), brain volume and cognitive functioning.
     
    More  at link.

    Friday, March 17, 2023

    One-Year Aerobic Exercise Reduced Carotid Arterial Stiffness and Increased Cerebral Blood Flow in Amnestic Mild Cognitive Impairment

    You want both of these benefits, so demand your doctor get you recovered enough to easily do the exercises. And find out exactly what those exercises were.

    Hypoperfusion is a term that describes "a reduced amount of blood flow".

    One-Year Aerobic Exercise Reduced Carotid Arterial Stiffness and Increased Cerebral Blood Flow in Amnestic Mild Cognitive Impairment 

    Affiliations

    Abstract

    Background: Central arterial stiffness and brain hypoperfusion are emerging risk factors of Alzheimer's disease (AD). Aerobic exercise training (AET) may improve central arterial stiffness and brain perfusion.

    Objective: To investigate the effects of AET on central arterial stiffness and cerebral blood flow (CBF) in patients with amnestic mild cognitive impairment (MCI), a prodromal stage of AD.

    Methods: This is a proof-of-concept, randomized controlled trial that assigned 70 amnestic MCI patients into a 12-month program of moderate-to-vigorous AET or stretching-and-toning (SAT) intervention. Carotid β-stiffness index and CBF were measured by color-coded duplex ultrasonography and applanation tonometry. Total CBF was measured as the sum of CBF from both the internal carotid and vertebral arteries, and divided by total brain tissue mass assessed with MRI to obtain normalized CBF (nCBF). Episodic memory and executive function were assessed using standard neuropsychological tests (CVLT-II and D-KEFS). Changes in cardiorespiratory fitness were measured by peak oxygen uptake (VO2peak).

    Results: Total 48 patients (29 in SAT and 19 in AET) were completed one-year training. AET improved VO2peak, decreased carotid β-stiffness index and CBF pulsatility, and increased nCBF. Changes in VO2peak were associated positively with changes in nCBF (r = 0.388, p = 0.034) and negatively with carotid β-stiffness index (r = -0.418, p = 0.007) and CBF pulsatility (r = -0.400, p = 0.014). Decreases in carotid β-stiffness were associated with increases in cerebral perfusion (r = -0.494, p = 0.003). AET effects on cognitive performance were minimal compared with SAT.

    Conclusion: AET reduced central arterial stiffness and increased CBF which may precede its effects on neurocognitive function in patients with MCI.