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 cardiovascular events. Show all posts
Showing posts with label cardiovascular events. Show all posts

Thursday, September 4, 2025

Mind-Body-Heart Connection: Anger and Stress Linked to Cardiovascular Events

 

With your massive stress from your incompetent doctor not having 100% recovery protocols, and the fact your doctor doesn't know about this, you are on your own to prevent cardiovascular events! Good luck.

Mind-Body-Heart Connection: Anger and Stress Linked to Cardiovascular Events

Preventive strategies for cardiovascular disease (CVD) have often involved looking into risk factors such as stress, anxiety, hostility, and anger. Stress-related disorders are known to increase risk for atherosclerosis,stroke, and myocardial infarction (MI).1nbsp;An acute experience of anger, as well, has been associated with greater likelihood of CVD onset, though the pathways that underlie the development and progression of CV events are not yet fully known. In addition, lifestyle behaviors, psychosocial variables, personality types, and mental health illnesses may affect the etiology of CVD. However, there is limited information in clinical guidelines for the evaluation and management of this subset of patients.1 We received perspectives from experts in the field regarding the association between anger, stress, and CV events, the potential risk factors and stressors involved, and how providers can address it with their patients. Viola Vaccarino, MD, PhD, is the Wilton Looney Distinguished Professor of Cardiovascular Research in the department of epidemiology at the Rollins School of Public Health, Atlanta, Georgia, and professor in the department of medicine at Emory University School of Medicine, Atlanta, GA. Elizabeth Vella, PhD, is the chair and professor of psychology at the University of Southern Maine.

Research Reveals a Link Between Anger, Stress, and CV Events

“There is a longstanding history of medical science research investigating intersections between anger/stress and CV events,” Dr Vella noted, which goes as far back as 1975 when Rosenman et al coined the term “type A behavior pattern” as a toxic component of trait hostility that predicts CV mortality and morbidity.Recent evidence also revealed the role of a “brain-heart axis” in prognosing CVD and the need for understanding the psychologic impact on CVD, especially among certain population subsets, such as younger women, patients with early-onset MI, and those from racial and ethnic minority groups (owing to disparities in the field).4  Following this research, Dr Vaccarino discussed the impact of acute stressors — environmental disasters or acute emotional states, such as anger, fear, and bereavement — on CV events. She noted the importance of physiologic responses to stress in predicting risk for CVD. “Adverse physiologic responses to acute stress (vascular, ischemic, autonomic, and inflammatory perturbations) can be reproduced in the lab, using a mental stress test/anger recall test, and are associated with adverse CV events in patients with CVD.” To understand the pathways involved, researchers have highlighted the effect of anger on the elevated activity of the sympathetic nervous system, such as blood pressure, heart rate, and reductions in cardiac vagal tone. The association between trait anger/hostility and daily cortisol production is significant in understanding the inflammatory states through elevated proinflammatory cytokines.6 In addition, findings of a recently published research paper by Shimbo and colleagues showed that a brief provocation of anger negatively affected endothelial cell health by way of impairing endothelium-dependent vasodilation.2 There is a longstanding history of medical science research investigating intersections between anger/stress and CV events. Elizabeth Vella, PhD
Influence of Risk Factors and Stressors in CVD Demographic and socioeconomic factors may predict CVD, with these factors interacting with psychosocial factors, such as anger disposition. Dr Vella added that a combination of these factors result in unique patient-specific disease trajectories, including direct effects (eg, stress-induced inflammation that hastens atherosclerotic progression) and indirect effects (eg, stress-induced changes in lifestyle behavior that lead to unhealthy patterns of disrupted sleep, poor diet, excessive alcohol consumption, and smoking).7 Previous studies have indicated clinically significant sex differences in the prevalence, presentation, management, and outcomes of CVD, as well as socioeconomic status being an “unrecognized” risk factor in the primary prevention of CVD.8,9 Dr Vaccarino noted an increased burden of psychosocial stressors, especially in midlife, as well as higher rates of depression and anxiety, in women compared with men. However, “Existing evidence suggests that anger is more strongly associated with CVD in men than in women,” though there are only a few studies that have evaluated sex differences. Referencing a study published in 2022, Dr Vella indicated, “Although the female sex appears to confer benefit as a buffer from CVD, these advantages may disappear in thecontext of underlying traditional risk factors, such as type 2 diabetes, hypertension, central adiposity, and dyslipidemia.” Racial and ethnic minority groups, especially Black American and Hispanic individuals, have a higher burden of psychosocial stressors, such as more adverse life events and discrimination, lower economic resources and access to care, and more chronic stressors.10Both Dr Vaccarino and Dr Vella pointed to socioeconomic factors such as low education levels, lack of financial resources, lack of insurance, and living in poor neighborhoods that are barriers to accessing mental and psychologic care, and thereby, increasing levels of stress among individuals.Exacerbation of already elevated stress levels increases reliance on maladaptive coping responses.8,9,10

Anger Management in Patients: Strategies for Providers

The American Heart Association (AHA) released a statement in 2021 to highlight the association between psychologic health and CV health and disease and to determine steps for clinicians to better screen for and manage this population. The authors noted that CVD should not be treated as a disease but as a system in which the mind, heart, and body are interconnected. They added that the wellness and well-being of patients should not only involve physical factors but also psychologic factors.12 “Because stress and mental health issues are common in the general population and especially in patients with CVD, it is important to consider mental health aspects during routine cardiovascular care,” Dr Vaccarino added. Regular aerobic and resistance exercise have shown to result in better adaptiveness to stress and potentially reduce rates of stress and depression. However, researchers of the HL-PIVOT Network have recommended formal cardiac rehabilitation programs for the reduction of stress-related mortality.>1 “Stress-management training is beneficial to both mental health and CV health. Many cardiologists and primary care providers may feel unprepared to engage in in-depth discussions about stress and mental health with their patients. However, brief targeted conversations can be very useful and are often highly appreciated by patients,” Dr Vaccarino noted. Dr Vella also discussed the efficacy of interventions to lower stress levels among those with anger, such as web-based cognitive behavioral therapy (CBT), which has resulted in significant reductions in anger and hostility, along with states of calm, in patients with coronary artery disease.11 “Physicians may consider referring patients to CBT-based interventions and therapy aimed at enhancing stress management skills and physical activity.” To identify patients who need a referral for anger/stress management or mental health care, the AHA has suggested the use of brief composite screening tools, such as patient questionnaires provided at in-office visits. In addition, cardiology providers and mental health professionals must work together to develop a treatment plan.12

In Summary

Overall, because of increasing evidence to support the relationship between negative emotions, such as anger and stress, and CV events, clinicians must consider psychologic health in the evaluation and management of patients with or at risk for CVD, using a multipronged and multidisciplinary approach. This article originally appeared on The Cardiology Advisor

Wednesday, October 2, 2024

Some Epilepsy Drugs Tied to Cardiovascular Events in Older People

 With your chance of epilepsy and seizures post stroke make sure your competent? doctor is aware of this.


Just maybe you want your doctor to try these solutions.

Cannabidiol May Reduce Seizures by Half in Hard-to-treat Epilepsy

Or maybe the nasal spray referred to in here:

Preventing Seizure-Caused Damage to the Brain

The answers are out there, does your doctor know about them? 

Mozart may reduce seizure frequency in people with epilepsy

 

A dietary supplement dampens the brain hyperexcitability seen in seizures or epilepsy

 The latest here:

Some Epilepsy Drugs Tied to Cardiovascular Events in Older People

Link likely due to enzyme-inducing antiseizure medications

A computer rendering of a transparent body with the heart highlighted.

An association between epilepsy and cardiovascular events (CVEs) in older people was likely largely due to the use of enzyme-inducing antiseizure medications (EIASM), according to a prospective cohort study from Canada.

Among over 27,000 participants, new-onset CVEs were more likely in those with epilepsy than those without (adjusted OR 2.20, 95% CI 1.48-3.27), with the relative contribution to this association highest for "strong" EIASM use (24.6%), reported Mark Keezer, MD, PhD, of Centre de Recherche du Centre Hospitalier de l'Université de Montréal, and colleagues in JAMA Neurology.

"Our study suggests that enzyme-inducing antiseizure medications increase the risk of cardiovascular events," Keezer told MedPage Today. "Future studies will need to study whether this should lead to screening for cardiovascular disease in certain people at greater risk. Our study may also provide healthcare professionals further justification for avoiding enzyme-inducing antiseizure medications, when clinically feasible."

There is a strong association between epilepsy and cardiovascular disease, at least partly because of the overlap in risk factors, Keezer and co-authors noted. Stroke can cause epilepsy, and even in populations without cerebrovascular disease, the risk of developing cardiovascular disease is high, they pointed out. Previous research has suggested that potential damage to the heart and coronary vasculature by repeat seizures may contribute to this connection, along with EIASM use.

For this study, Keezer and team used data from 27,230 participants in the ongoing Canadian Longitudinal Study on Aging (CLSA) with 6 years of follow-up from 2015 to 2021. The CLSA includes adults ages 45 to 85 and excludes residents of long-term care facilities and those with cognitive impairment, among others.

Participants were included in this analysis if they reported no previous history of CVEs (stroke, transient ischemic attack, or myocardial infarction) at baseline. Mean age was 62.3, 52.4% were women, and 94.4% were white. In total, 431 had a lifetime history of epilepsy. Of those included, 86% completed follow-up.

The primary outcome was new-onset CVEs over 6 years, and new-onset strokes, transient ischemic attacks, or myocardial infarctions separately were secondary outcomes. To understand how mediator variables influenced relationships between epilepsy and CVEs, the researchers ran mediation analyses for strong EIASM use, weak EIASM use, Framingham score, Physical Activity Scale for the Elderly (PASE) score, and waist-to-hip ratio.

"Strong EIASM use" included use of carbamazepine, phenytoin, phenobarbital, and primidone, while "weak EIASM use" included use of drugs like oxcarbazepine, eslicarbazepine, topiramate, and rufinamide. Of the CVEs, strong EIASM use appeared to have the largest effect on myocardial infarction, with a proportion-mediated value of 59.1%.

Apart from the mediating effect of strong EIASM use, "more than two-thirds of this association may be due to other factors, such as more prevalent [cardiovascular risk factors] or a direct effect of epilepsy on [cardiovascular disease]," Keezer and colleagues wrote. Weak EIASM use, PASE score, and waist-to-hip ratio also played a role, with proportion-mediated values of 4.0%, 3.3%, and 1.6%, respectively.

The authors noted that they were limited by self-reported data, and by potential effects of the 14% of participants lost to follow-up. They also did not differentiate between ischemic stroke and hemorrhagic stroke, and noted that participants may have begun or stopped EIASM during follow-up, but EIASM data were only available for baseline use.

  • author['full_name']

    Sophie Putka is an enterprise and investigative writer for MedPage Today. Her work has appeared in the Wall Street Journal, Discover, Business Insider, Inverse, Cannabis Wire, and more. She joined MedPage Today in August of 2021. Follow

Disclosures

Data/biospecimens for this study came from the Canadian Longitudinal Study on Aging, which is funded by the Government of Canada through the Canadian Institutes of Health Research and the Canada Foundation for Innovation.

Keezer reported financial relationships with UCB, Eisai, Jazz Pharmaceuticals, and Paladin.

Co-authors reported financial relationships with Fonds de Recherche du Québec-Santé Support, Xenon, Theravance, Novartis, Eisai, Angelini Pharma, LivAssured, UCB, Montreal Heart Institute, and Jazz Pharmaceuticals.

Primary Source

JAMA Neurology

Source Reference: Li J, et al "Antiseizure medications and cardiovascular events in older people with epilepsy" JAMA Neurol 2024; DOI: 10.1001/jamaneurol.2024.3210.

Saturday, February 10, 2024

Vitamin D supplementation and major cardiovascular events: D-Health randomised controlled trial

Ask your doctor what this means for you.

 

Vitamin D supplementation and major cardiovascular events: D-Health randomised controlled trial


BMJ 2023; 381 doi: https://doi.org/10.1136/bmj-2023-075230 (Published 28 June 2023)Cite this as: BMJ 2023;381:e075230
  1. Bridie Thompson, research officer1,  
  2. Mary Waterhouse, statistician epidemiologist1,  
  3. Dallas R English, professor2,  
  4. Donald S McLeod, senior research officer1,  
  5. Bruce K Armstrong, professor3,  
  6. Catherine Baxter, project manager1,  
  7. Briony Duarte Romero, research assistant1,  
  8. Peter R Ebeling, professor4,  
  9. Gunter Hartel, head of statistics5,  
  10. , professor6,  
  11. Sabbir T Rahman, research officer1,  
  12. Jolieke C van der Pols, associate professor7,  
  13. Alison J Venn, professor8,  
  14. Penelope M Webb, professor1,  
  15. David C Whiteman, professor1,  
  16. Rachel E Neale, professor1
    Author affiliations
  1. Correspondence to: R Neale rachel.neale@qimrberghofer.edu.au
  • Accepted 18 May 2023

Abstract

Objective  

To investigate whether supplementing older adults with monthly doses of vitamin D alters the incidence of major cardiovascular events.

 Design  
 
Randomised, double blind, placebo controlled trial of monthly vitamin D (the D-Health Trial). Computer generated permuted block randomisation was used to allocate treatments.
 Setting Australia from 2014 to 2020.
 Participants  
 
21,315 participants aged 60-84 years at enrolment. Exclusion criteria were self-reported hypercalcaemia, hyperparathyroidism, kidney stones, osteomalacia, sarcoidosis, taking >500 IU/day supplemental vitamin D, or unable to give consent because of language or cognitive impairment.
 Intervention 60 000 IU/month vitamin D3 (n=10 662) or placebo (n=10 653) taken orally for up to five years. 16 882 participants completed the intervention period: placebo 8270 (77.6%); vitamin D 8552 (80.2%).

Main outcome measures  

 The main outcome for this analysis was the occurrence of a major cardiovascular event, including myocardial infarction, stroke, and coronary revascularisation, determined through linkage with administrative datasets. Each event was analysed separately as secondary outcomes. Flexible parametric survival models were used to estimate hazard ratios and 95% confidence intervals.

Results  

 

21,302 people were included in the analysis. The median intervention period was five years. 1336 participants experienced a major cardiovascular event (placebo 699 (6.6%); vitamin D 637 (6.0%)). The rate of major cardiovascular events was lower in the vitamin D group than in the placebo group (hazard ratio 0.91, 95% confidence interval 0.81 to 1.01), especially among those who were taking cardiovascular drugs at baseline (0.84, 0.74 to 0.97; P for interaction=0.12), although the P value for interaction was not significant (<0.05). Overall, the difference in standardised cause specific cumulative incidence at five years was −5.8 events per 1000 participants (95% confidence interval −12.2 to 0.5 per 1000 participants), resulting in a number needed to treat to avoid one major cardiovascular event of 172. The rate of myocardial infarction (hazard ratio 0.81, 95% confidence interval 0.67 to 0.98) and coronary revascularisation (0.89, 0.78 to 1.01) was lower in the vitamin D group, but there was no difference in the rate of stroke (0.99, 0.80 to 1.23).

 Conclusions  
Vitamin D supplementation might reduce the incidence of major cardiovascular events, although the absolute risk difference was small and the confidence interval was consistent with a null finding. These findings could prompt further evaluation of the role of vitamin D supplementation, particularly in people taking drugs for prevention or treatment of cardiovascular disease.
 Trial registration ACTRN12613000743763
 Coronary heart disease and stroke are the leading causes of death globally.1 The risk of these events increases with age, and they are more prevalent in men than women.2 The number of cardiovascular disease events will probably continue to increase in developed countries as populations age, and in low to middle income countries as non-communicable diseases become dominant.3 Vitamin D has biological effects which suggest it could influence cardiovascular disease. The vitamin D receptor is expressed in cells throughout the vascular system; many of these also express 1α-hydroxylase, and are therefore able to convert 25-hydroxyvitamin D (25(OH)D) to calcitriol, the active form of vitamin D. Calcitriol reduces inflammation, regulates the renin-angiotensin-aldosterone system, and inhibits proliferation of vascular smooth muscle.4

Meta-analyses of observational studies have found inverse associations between serum 25(OH)D concentration and risk of cardiovascular disease.56789 However, these findings might be due to reverse causality or uncontrolled confounding. Of three Mendelian randomisation studies, which largely overcome these biases, one reported an inverse association between genetically predicted 25(OH)D concentration up to 50 nmol/L and cardiovascular disease.10 The other studies found no association, but did not allow for nonlinear effects.1112 A meta-analysis of randomised controlled trials concluded that vitamin D supplementation does not prevent cardiovascular events.13 However, 45% of the 83 291 participants included in the meta-analysis were from the Women’s Health Initiative Trial, which was restricted to women, used a low dose of vitamin D, and had relatively low compliance.14 Cardiovascular disease was the primary outcome of the Vitamin D Assessment (ViDA) study15 and the Vitamin D and Omega 3 trial (VITAL).16 Despite different outcome definitions, both randomised controlled trials found that vitamin D supplementation had no effect on cardiovascular disease,1516 but VITAL excluded people with a history of cardiovascular disease and the ViDA study had relatively few events.

We launched the D-Health Trial to determine if monthly vitamin D supplementation can improve health outcomes in the older general population. It was a large intermittent dosing trial of vitamin D supplementation (n=21 315). Previous analysis of the D-Health cohort found that vitamin D supplementation did not reduce all cause mortality (the primary outcome of the overall trial) or mortality due to cardiovascular disease,17 but the effect on the incidence of major cardiovascular events has not been analysed.

For the current study we analysed data from the D-Health Trial to examine whether supplementing Australians aged ≥60 years with monthly doses of 60 000 IU of vitamin D altered the incidence of major cardiovascular events.