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 Angiotensin. Show all posts
Showing posts with label Angiotensin. Show all posts

Thursday, December 19, 2024

Blood pressure drug may lower risk for post-stroke epilepsy

 Will your competent? doctor and hospital get this implemented as a protocol in your hospital in the next week? Your risk of epilepsy here and solutions:


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

The latest here:

Blood pressure drug may lower risk for post-stroke epilepsy

Key takeaways:

  • Angiotensin receptor blockers were linked to a reduced risk for post-stroke epilepsy vs. other antihypertension medications.
  • PSE incidence was highest for calcium channel blockers and beta blockers.

LOS ANGELES — Individuals with hypertension and stroke who were prescribed angiotensin receptor blockers had a significantly lower risk for post-stroke epilepsy than those prescribed other antihypertension medications, according to new research.

Patients with hypertension and stroke who were prescribed ARBs had a significantly lower risk for post-stroke epilepsy than those prescribed other antihypertension medications, according to new research. Image: Adobe Stock


“Our study uniquely focused on how effective different blood pressure medications are at

preventing PSE in the real world,” Giacomo Evangelista, MD, PhD, study co-lead author and neurology resident at the Epilepsy Center at G. d’Annunzio University of Chieti-Pescara, Italy, said in a release related to the study, presented at the American Epilepsy Society annual meeting. “Understanding which antihypertensive medications help prevent

complications such as PSE can lead to better patient outcomes.”

According to the European Society of Cardiology, angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) can be considered effective first-line hypertension treatments to protect against seizures; however, it is unknown whether these drugs may assume a preventive role in post-stroke epilepsy (PSE), which occurs in roughly 6% to 8% of those with ischemic stroke.

Evangelista and colleagues investigated the efficacy of ARBs as an antihypertensive treatment for prevention of PSE in a retrospective, observational study. The study was conducted between January 2016 and January 2022 and included 528 individuals (57.2% men) diagnosed with hypertension and ischemic stroke confirmed by clinical and neuroimaging evaluations. The patients did not have epilepsy at the time of stroke but were taking some form of blood pressure medication.

A total of 194 patients were taking two or more antihypertension medications: 164 were prescribed beta-blockers (20 with PSE); 159 were prescribed calcium channel blockers (15 with PSE); 154 were prescribed ACEi (10 with PSE); 136 were prescribed diuretics (8 with PSE), and 109 were prescribed ARBs (3 with PSE), according to the release.

All participants were followed for a mean period of 66 months.

According to the results, 38 (7.2%) individuals developed PSE.

The researchers found that, compared with patients who took ARBs, the likelihood of developing PSE was:

  • 120% higher among those who took beta-blockers;
  • 110% higher among those who took calcium channel blockers;
  • 65% higher among those who took ACEi; and
  • 60% higher among those who took diuretics.

“These findings highlight the importance of personalized medicine, particularly in managing blood pressure in stroke patients,” Fedele Dono, MD, MSc, FEBN, co-lead author of the study and colleague of Evangelista at the Epilepsy Center, G. d’Annunzio University of Chieti-Pescara. “Further research in more patients is necessary to confirm these findings and explore the underlying mechanisms in more detail.”

Reference:

Common Blood Pressure Drug May Help Reduce Increased Risk of Epilepsy after a Stroke. https://aesnet.org/about/aes-press-room/press-releases/common-blood-pressure-drug--may-help-reduce-increased-risk-of-epilepsy-after-a-stroke. Published Dec. 6, 2024. Accessed Dec. 7, 2024.


Monday, December 9, 2024

Could a Hypertension Drug Protect Against Post-Stroke Epilepsy?

 

With your chance of epilepsy and seizures post stroke make sure your competent? doctor has a prevention solution for these.


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:

Could a Hypertension Drug Protect Against Post-Stroke Epilepsy?

      Observational study suggests one antihypertensive class might be preventive

LOS ANGELES -- Use of angiotensin receptor blockers (ARBs) was linked to a lower risk of epilepsy after an acute ischemic stroke, according to an observational study.

Among hypertensive patients, ARB use was the only factor significantly associated with onset of post-stroke epilepsy after multivariate adjustment, reported Giacomo Evangelista, MD, of G. D'Annunzio University of Chieti-Pescara in Chieti, Italy, at the American Epilepsy Society annual meeting.

ARB users accounted for about 5% of those who developed epilepsy (two of 38) and 25% of those who didn't develop epilepsy after their stroke (104 of 409).

The findings match up with observational findings among hypertensive persons without prior stroke, the researchers noted. One large study from Germany showed a hazard ratio of 0.77 (95% CI 0.65-0.90) for epilepsy incidence among ARB users compared with users of other antihypertensive drug classes. An even larger U.S. study showed similar adjusted hazard ratios of 0.70 to 0.75 for ARBs versus other antihypertensive classes, which appeared to be driven by a reduction with losartan.

"In our study, ARBs show a potential protective role in epilepsy development in patients with hypertension and stroke," Evangelista concluded. "These insights can help inform clinical guidelines and therapeutic strategies, emphasizing the need for larger, prospective studies to confirm these results and further elucidate the mechanisms involved."

Ischemic stroke is the most common cause of seizures in patients older than 60 years, Evangelista noted, as it accounts for about 6-8% of new epilepsy diagnoses in elderly patients.

"It has been postulated that the brain's renin-angiotensin-aldosterone system plays a special mediating role in epilepsy pathology and may be associated with the hyperactivation of angiotensin II type 1 receptor and ACE [angiotensin-converting enzyme] signaling in astrocytes, oligodendrocytes, and microglia," the researchers noted.

Potential mechanisms could include reducing neuronal loss and microglia-mediated inflammatory responses or other neuroinflammatory processes. Evangelista's group added that ARBs "downregulate the TGF-beta-mediated signaling cascade displaying numerous neuroprotective benefits, such as diminishing neuroinflammation or reducing epilepsy severity and seizure frequency."

Although the findings corroborate those of prior studies, Alain Lekoubou Looti, MD, of Penn State College of Medicine in Hershey, Pennsylvania, cautioned against overinterpreting the results from observational studies, which cannot account for all possible variables or make any conclusions about causality. He was not involved in the study.

"At this stage it's too premature to just use these results to make a recommendation on antihypertensive medication prescription to prevent late-onset seizures," he told MedPage Today. "I think at this point it's important to start thinking about a randomized clinical trial that would test the impact of ARBs, and more specifically losartan, on preventing seizures in patients with hypertension."

Evangelista's retrospective study used data from 528 patients (mean age 71, 57% men) who had hypertension and a diagnosis of ischemic stroke, which had to be confirmed by clinical and neuroimaging evaluations, and who were seen at the neurology ward of a single center in Italy from January 2016 through January 2022.

All participants were followed up at a median of 24 months with a telephone interview based on a validated seizure detection questionnaire. Those who screened positive for possible epilepsy had an in-person neurological consultation and an electroencephalogram to determine the epileptic etiology of their episodes and to rule out mimic seizures.

Post-stroke epilepsy diagnosis was made according to International League Against Epilepsy criteria in 38 (7.2%) patients.

Most of the patients had pre-existing hypertension before stroke (70.3%), and each antihypertensive class was taken by 20-30% of patients. The same spread was seen post-stroke, with 34% on an ACE inhibitor, 21% on an ARB, 31% on a beta-blocker, and 28% on a calcium channel blocker. Most patients took a single antihypertensive; 37% took two or more drugs.

Unadjusted findings suggested a lower epilepsy risk with a number of the classes. The proportion of patients on each class in the epilepsy versus no-epilepsy groups were significantly lower with:

  • ARBs (P=0.009)
  • Beta-blockers (P=0.008)
  • Calcium channel blockers (P=0.019)

However, the associations of epilepsy incidence with beta-blockers and calcium channel blockers disappeared upon multivariate adjustment.

The observational study could not draw any causal conclusions and was hampered by a limited sample size at a single institution, the researchers noted.

Disclosures

The researchers disclosed no relevant relationships with industry.

Lekoubou Looti reported no relevant relationships with industry.

Primary Source

American Epilepsy Society

Source Reference: Evangelista G "Angiotensin receptor blockers (ARBs) reduce the risk of developing epilepsy in patients with ischemic stroke and hypertension" AES 2024; Abstract 1.34.

Tuesday, July 30, 2024

Vagus nerve stimulation (VNS) inhibits cardiac mast cells activation and improves myocardial atrophy after ischemic stroke

 But you incompetently did not tell us the protocol for that! How the fuck do you expect survivors to be able to tell their stroke medical 'professionals' what to do?

Do you suggest the surgery options or the easier ones?

I think most stroke survivors would rather do the non-invasive approaches. So ask your doctor why surgery; I'm guessing revenue and profits.

Dorset Embarks on Revolutionary Stroke Recovery Trial Utilizing Earpiece Technology February 2024

 

Non-invasive VNS approach could enhance post-stroke recovery outcomes August 2023

The latest here:

Vagus nerve stimulation (VNS) inhibits cardiac mast cells activation and improves myocardial atrophy after ischemic stroke

,
https://doi.org/10.1016/j.intimp.2024.112714
Get rights and content
Under a Creative Commons license
open access

Highlights

  • Vagus nerve stimulation (VNS) can reduce myocardial atrophy after acute ischemic stroke;

  • VNS decreased the amount of Chyamse and inhibited mast cell activation in cardiac tissue after acute ischemic stroke;

  • VNS reduces the expression of angiotensin II (Ang II) after acute ischemic stroke by inhibiting mast cell activity, thereby alleviating cardiac inflammation and autophagy.

Abstract

Background

Ischemic stroke is one of the leading causes of chronic disability worldwide, and stroke-induced heart damage can lead to death. According to research, patients with a variety of brain disease have good clinical results after vagus nerve stimulation (VNS). After ischemic stroke, mast cells (MCs) degranulate and release a large number of mediators, which may cause systemic inflammation. Chymase secreted by MCs can increase the levels of pathological angiotensin II (AngⅡ), which plays a crucial role in the deterioration of heart disease. Our goal was to develop a minimally invasive, targeted, and convenient VNS approach to assess the impact of VNS and to clarify the relationship between VNS and MCs in the prognosis of patients with myocardial atrophy after acute ischemic stroke.

Methods

In this study, we verified the role of VNS in the treatment of myocardial atrophy after stroke and its molecular mechanism using a rat model of middle cerebral artery occlusion (MCAO/r). Behavioral studies were assessed using neurobehavioral deficit scores. Enzyme-linked immunosorbent assays, immunofluorescence staining, Western blotting and qRT-PCR were used to analyze the expression levels of myocardial atrophy, MC and inflammatory markers in rat hearts.

Results

VNS improved myocardial atrophy in MCAO/r rats, inhibited MC activation, reduced the expression of chymase and AngⅡ, and inhibited the expression of proinflammatory factors. The chymase activator C48/80 reversed these effects of VNS. Chymase activation inhibited the effect of VNS on myocardial atrophy in MCAO/r rats, increased AngⅡ expression and aggravated inflammation and autophagy. The myocardial atrophy of MCAO/r rats was improved after chymase inhibition, and AngⅡ expression, inflammation and autophagy were reduced. Our results suggest that VNS may reduce the expression of chymase and AngⅡ by inhibiting MC activation, thereby improving myocardial atrophy and reducing inflammation and autophagy in MCAO/r rats. Inhibition of MC activation may be an effective strategy for treating myocardial atrophy after stroke.

Conclusions

VNS inhibits MC activation and reduces the expression of chymase and AngII, thereby alleviating myocardial atrophy, inflammation and autophagy after stroke.

Thursday, July 7, 2022

Angiotensin receptor blockers may lower risk for progression to dementia

I had to look up mine separately; nifediprine, is in a class of medications called calcium-channel blockers, but I am also taking Losartan.

 
Examples of angiotensin II receptor blockers include:
  • Azilsartan (Edarbi)
  • Candesartan (Atacand)
  • Eprosartan.
  • Irbesartan (Avapro)
  • Losartan (Cozaar)
  • Olmesartan (Benicar)
  • Telmisartan (Micardis)
  • Valsartan (Diovan)

 

Angiotensin receptor blockers may lower risk for progression to dementia

Angiotensin receptor blockers may reduce progression from mild cognitive impairment to dementia in patients undergoing antihypertensive treatment, researchers wrote in Hypertension.

Compared with ACE inhibitors, beta-blockers, calcium channel blockers, diuretic and no treatment at all, antihypertensive treatment using angiotensin receptor blockers (ARBs) was associated with lower risk for progression to dementia during a median of 3 years follow-up among patients with mild cognitive impairment and hypertension, according to the researchers.

Man trying to think
Source: Adobe Stock

“The angiotensin hypothesis has recently been proposed that the renin-angiotensin system plays a role in brain function. ... Medications that increase angiotensin-mediated activity at the angiotensin II and angiotensin IV receptors (eg, ARBs) may provide better brain protection compared with those decreasing activity at these receptors (eg, ACE inhibitors),” Zhenhong Deng, of the department of neurology at Sun Yat-sen Memorial Hospital, Sun Yat-sen University in Guangzhou, China, and colleagues wrote. “It remains unclear whether and to what extent ARBs are superior to ACE inhibitors in reducing progression to dementia in patients with mild cognitive impairment.”

Researchers investigated whether ARBs, compared with ACE inhibitors and other antihypertensive medications, may lower risk for progression from mild cognitive impairment to dementia in patients with hypertension.

Researchers used the Alzheimer’s Disease Neuroimaging Initiative, developed by the Laboratory of Neuro Imaging at University of Southern California, to identify 403 patients with hypertension and mild cognitive impairment at baseline (mean age, 74 years; 38% women). Data on antihypertensive medications received during a median follow-up of 3 years were self-reported.

During follow-up, 39.2% of participants progressed to dementia and the 3-year rate of progression-free survival was 67%.

In patients with hypertension and mild cognitive impairment, ARBs were associated with lower risk for progression to dementia compared with ACE inhibitors (adjusted HR = 0.45; 95% CI, 0.25-0.81; P = .023).

Compared with beta-blockers, calcium channel blockers and diuretics, ARB use was associated with lower risk for progression of mild cognitive impairment to dementia (aHR = 0.49; 95% CI, 0.27-0.89; P = .037).

Hypertension treatment with ARBs was also associated with lower risk for progression to dementia in patients with hypertension and mild cognitive impairment compared with no treatment (aHR = 0.31; 95% CI, 0.16-0.58; P = .001).

In adjusted analyses, treatment with ACE inhibitors did not affect progression of cognitive impairment compared with beta-blockers, calcium channel blockers and diuretics (P = .685) nor compared with no treatment (P = .179).

Moreover, antihypertensive treatment with beta-blockers, calcium channel blockers and diuretics did not prevent cognitive decline compared with no treatment in this cohort (P = .121).

“Overall, angiotensin II and IV may provide neuroprotection through angiotensin II and angiotensin IV receptors, although most evidence was based on experimental studies and the mechanisms were not fully understood,” the researchers wrote. “ARBs, which selectively block the angiotensin I receptors without inhibiting ACE and result in the relatively upregulated activities of angiotensin II and angiotensin IV receptors, and keep the pathway of amyloid beta degradation mediated by ACE intact, may offer superior protection than simultaneously lowering all the angiotensin receptors’ activities with ACE inhibitors.”

Monday, December 7, 2020

ACE inhibitors, ARBs do not pose additional risk in COVID-19 in two meta-analyses

Great since I'm on Nifedipine is in a class of medications called calcium-channel blockers.

ACE inhibitors, ARBs do not pose additional risk in COVID-19 in two meta-analyses

Use of ACE inhibitors and angiotensin receptor blockers was not associated with an increased rate of COVID-19 infection or mortality, according to two meta-analyses reported at the virtual American Heart Association Scientific Sessions.

Yujiro Yokoyama, MD, surgeon at St. Luke’s University Health Network’s Easton Hospital, Bethlehem, Pennsylvania, and colleagues conducted two meta-analyses to compare mortality and susceptibility to COVID-19 infection between patients treated and not treated with ACE inhibitors and/or angiotensin receptor blockers. The first meta-analysis evaluated the impact on rate of positive COVID-19 testing and the second meta-analysis evaluated the impact on in-hospital mortality for patients with COVID-19.

Source: Adobe Stock

Researchers examined MEDLINE and EMBASE databases to identify studies that detailed patients treated with ACE inhibitors and/or angiotensin receptor blocks. Their search yielded three eligible studies for the first meta-analysis and 14 eligible studies for the second meta-analysis.

Positive COVID-19 testing rates were similar for patients treated with ACE inhibitors compared with those who did not receive ACE inhibitors (OR = 0.96; 95% CI, 0.88-1.04; P = .69) and for patients treated with angiotensin receptor blockers compared with those not treated with angiotensin receptor blockers (OR = 0.99; 95% CI, 0.91-1.08; P = .35), according to the abstract.

Rates of in-hospital mortality for patients who tested positive for COVID-19 infection were similar between patients treated with ACE inhibitors and/or angiotensin receptor blockers and those who did not receive either medication (HR = 0.88; 95% CI, 0.64-1.2; P = .42), according to the abstract.

In a subanalysis restricted to studies that only investigated patients with hypertension, use of ACE inhibitors and/or angiotensin receptor blockers was associated with a significant reduction in in-hospital mortality compared with no use of either medication (HR = 0.65; 95% CI, 0.48-0.87), according to the abstract.

“Our study results confirm that patients already taking ACE inhibitors and angiotensin receptor blockers should not discontinue takin them due to COVID-19 infection,” Yokoyama said in a press release. “Both medications have proven benefits for heart and kidney disease, and this further confirms previous findings that ACE inhibitors do not pose additional risk with COVID-19.”

Earlier this year, the AHA, Heart Failure Society of America and American College of Cardiology issued a joint statement calling for the continuation of ACE inhibitors and angiotensin receptor blockers during the COVID-19 pandemic in patients prescribed these medications for HF, hypertension and/or ischemic heart disease, and recommended that patients with COVID-19 should be fully evaluated before any treatment changes.

Reference:

Press Release.

 

Wednesday, April 1, 2020

Clinical review of COVID-19 and CVD: What the cardiovascular practitioner needs to know

You will want to talk to your doctor if you are using ACE inhibitors or angiotensin receptor blockers.

Hypertension is on the risk list but doesn't say whether controlled or not. I have no idea if the definition of CVD here is old and thus includes stroke or is new and just heart stuff.

Found the most common comorbidities were hypertension (19%), diabetes (8.2%) and CVD (2.7%; Zhao X, et al. MedRxIV. 2020;doi:10.1101/2020.03.17.20037572).

 

ace inhibitor medications

angiotensin receptor blockers list 

This is on the second page; Currently, the American College of Cardiology and American Heart Association have recommended against preemptively stopping or starting an ACE inhibitor or angiotensin receptor blocker in the setting of COVID-19.

The latest here:

Clinical review of COVID-19 and CVD: What the cardiovascular practitioner needs to know


by Eamon Duffy, MD, MBA; Andrew Ayers; Miguel Caínzos-Achirica, MD, MPH, PhD; and Roger S. Blumenthal, MD

Eamon Duffy
The novel coronavirus disease, or COVID-19, is now a global pandemic. Clinicians, scientists and public health officials around the world are racing to define the molecular pathway and clinical presentation of the virus, identify risk factors for infection and poor clinical outcomes, and develop effective treatments and preventive interventions.
Although the data on each of these ventures continue to develop on a daily basis across the globe, several trends have emerged showing that CV comorbidities are common in patients with COVID-19 and are independently associated with a greater risk for morbidity and mortality.
This summary reviews the evolving molecular and clinical data on COVID-19, with a focus on the intersection of this virus with CVD and its potential impact on patients with CV and professionals.
The molecular pathway

Andrew Ayers
COVID-19 is caused by the pathogen SARS-CoV-2, a novel enveloped RNA betacoronavirus that is thought to originate in bats (Zhou P, et al. Nature. 2020;doi:10.1038/s41586-020-2012-7). Infection with SARS-CoV-2 is caused by binding of a spike protein on the viral surface to the ACE2 receptor. The virus is then internalized and propagated with viral replication (Walls AC, et al. Cell. 2020;doi:10.1016/j.cell.2020.02.058). This ACE2 receptor is found on type 2 pneumocytes in the lungs, the primary route of infection, but it is also found in high levels in the heart, arteries, kidneys and intestines (Hamming TW, et al. J Pathol. 2014;doi:10.1002/path.1570). ACE2, when activated, converts angiotensin 2 to angiotensin 1-7, leading ultimately to vasodilation, diuresis and reduced oxidative stress. When SARS-CoV-2 binds to ACE2, it leads to ACE2 downregulation, increased angiotensin II, and increased pulmonary vascular permeability as well as the clinical state of acute respiratory distress syndrome (ARDS) seen in so many severely ill patients with COVID-19 (Zhang H, et al. Intensive Care Med. 2020;doi:10.1007/s00134-020-05985-9).
The potential impact of ACE inhibitors and angiotensin receptor blockers, ubiquitously used in patients with CVD, on this pathway has so far been studied primarily in rodent models. These models have shown that ACE inhibitors lead to an increase in ACE2 (Ferrario CM, et al. Circulation. 2005;doi:10.1161/CIRCULATIONAHA.104.510461). This raises that concern that these medications could, by increasing the viral target, increase a patient’s susceptibility to the virus. 
4 more pages at link.

Monday, October 21, 2019

Top News in Internal Medicine Certain blood pressure meds tied to suicide risk in study

So ask your doctor about this. Mine is Nifedipine is in a group of drugs called calcium channel blockers. So not listed here.

Certain blood pressure meds tied to suicide risk in study

MedicalXpress Breaking News-and-Events | October 18, 2019
A common type of blood pressure medication might be associated with an increased risk of suicide, a new study suggests.
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People taking angiotensin receptor blockers (ARBs) appear to be more likely to die by suicide, compared to those who take another type of blood pressure drug called ACE inhibitors, researchers found.
Patients using ARBs had a 63% increased risk of death by suicide over people on ACE inhibitors, the findings showed. But the study could not prove a cause-and-effect relationship.
"There is reason for some concern," said lead researcher Muhammad Mamdani, director of the Applied Health Research Center of the Li Ka Shing Knowledge Institute at St. Michael's Hospital, in Toronto. "Now would I be going en masse and change everybody's prescriptions? No, not just yet. We should have more work done in this area."
"But certainly if I had a choice as a patient, I would be choosing the ACE inhibitor over the ARB," Mamdani concluded.
ARBs and ACE inhibitors both work by interfering with the action of angiotensin II, a hormone in the body that causes blood vessels to constrict.
ARBs work by blocking the ability of angiotensin II to bind with receptors and command blood vessels to narrow, while ACE inhibitors actually lower the amount of the hormone produced within the body.
Both drugs are widely used to treat high blood pressure, chronic kidney disease, heart failure and diabetes, the study authors said in background notes.
Mamdani and his colleagues pursued their new research based on earlier studies suggesting ARBs might be linked to suicide risk.
Using Canadian health databases, the investigators identified 964 people who died by suicide within 100 days of being prescribed either an ARB or an ACE inhibitor. They then compared those people to a control group of just over 3,000 people also taking either type of blood pressure medication.
The results showed that people taking ARBs had a statistically significant higher risk of suicide than those on an ACE inhibitor.
"It is a fairly commonly used set of drugs, and lots of people would be affected by it. Certain people, especially if you're susceptible to mood disorders, may be even more at risk," Mamdani said.
He noted that ARBs might cause levels of angiotensin II to increase in the brain.
"That could be related to mood disorders, and that could trigger suicidal-type behavior," Mamdani suggested.
However, there's currently no evidence that angiotensin II has anything to do with moods or suicidal intent, said Dr. Robert Carey, dean emeritus of the University of Virginia School of Medicine.
"I think those speculations are exactly that," Carey said. "There is no realistic mechanism to which one could attribute that difference in suicide risk."
Carey noted that other factors that could influence suicide risk might have come into play with these patients. For example, some were taking antidepressants or benzodiazepines, "which might have had an influence on the suicide rate," he said.
The study also didn't assess underlying substance abuse, prior mental health hospitalizations, or previous emergency department visits, said Dr. Suzanne Steinbaum, a cardiologist with the Mount Sinai Hospital in New York City.
The study was published online Oct. 16 in JAMA Network Open.
"I don't think this could be construed as evidence to switch from ARBs to ACE inhibitors," Carey concluded. "The mechanism is absolutely up in the air and needs more basic study."
—Dennis Thompson
To read more, click here.

Monday, November 5, 2018

Some hypertension drugs linked to reduced Alzheimer's risk

Followup needed so don't expect anything for decades. Unless you really really think your doctors and stroke hospital are competent enough to get followup research started and completed.  Nah, that will never occur.

Some hypertension drugs linked to reduced Alzheimer's risk


University of Washington Medicine | November 02, 2018
Medical researchers are increasingly exploring medications used to treat chronic illnesses to see whether they also might stave off cognitive decline. A study published today in PLOS ONE suggests that some older adults who take a class of blood pressure medication called angiotensin-II receptor blockers, or ARBs, might be reducing their risk of Alzheimer’s disease.
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Doug Barthold of the University of Washington and Julie Zissimopoulos of the University of Southern California, the study’s lead authors, compared different blood pressure medications and examined their potential cognitive benefits within subgroups of people based on race, ethnicity, and sex.
The researchers found that use of ARBs was associated with a lower rate of Alzheimer’s among black women and white women and men. Evidence of the reduced risk, however, was inconclusive among black men and Hispanic men and women.
“Repurposing existing drugs could be an inexpensive means to reduce the large and disparate burden of Alzheimer’s disease,” said Barthold, a UW research assistant professor in the School of Pharmacy. “By analyzing commonly used prescription drugs in Medicare claims data, we can identify relationships with Alzheimer’s disease onset across diverse populations,”
Strong evidence exists, he said, that managing high blood pressure is an important step to lowering the risk of Alzheimer’s disease and that some antihypertensive drugs may be more protective than others.
The research included records of more than 1 million Medicare enrollees. ARBs containing valsartan, candesartan, and losartan were found to be more protective against Alzheimer’s than other antihypertensives, such as angiotensin-converting enzyme (ACE) inhibitors and four other classes of drugs.
The results merit additional observational studies and randomized control trials that include men and women from diverse racial and ethnic groups, to investigate whether the drugs are causing the effect, the researchers suggested.
Alzheimer’s disease is a growing public health problem. About 5.7 million Americans, most over 65, live with Alzheimer’s disease; that number is expected to grow to 7.1 million in 2025 and 13.8 million in 2050, according to the US Centers for Disease Control and Prevention.
At that incidence, even small delays in disease onset could substantially reduce the financial and caregiving burden facing Americans—pegged at $277 billion and 18 billion hours, respectively, in 2018.
The building crisis also reflects the higher incidence of Alzheimer’s disease among women and racial and ethnic minorities, who are more likely to require high-intensity care and have unmet care needs.
“Alzheimer’s disease is an enormous public health concern, and while more than a hundred potential drug treatments are in clinical trials, there are still no treatments available to prevent or slow the progression of the disease,” wrote Zissimopoulos. She directs the aging research program at the USC Schaeffer Center. “All else being equal, for patients who are already being prescribed antihypertensives, these findings highlight a potential differential effect on their risk of acquiring Alzheimer’s, which a clinician may want to take into account.”
To read more, click here.

Wednesday, October 11, 2017

Generic BP medication may be linked to higher adverse event rates

Be careful out there. 

Generic BP medication may be linked to higher adverse event rates


Paul Poirier
Generic angiotensin II receptor blockers may be associated with increased risk for adverse events compared with brand-name counterparts, according to data published in Circulation: Cardiovascular Quality and Outcomes.
After generic commercialization of three antihypertensive drugs, higher adverse event rates were observed in generic users vs. brand-name users, according to the study.

“For generic users, we observed differences in rates of adverse events after generics commercialization using time series analysis,” Paul Poirier, MD, PhD, professor of the faculty of pharmacy at Laval University in Quebec, and colleagues wrote. “To our knowledge, this is the first ecological study assessing clinical outcomes with time series analysis after generics commercialization using a specific variable distinguishing between generic and brand-name users.”
The researchers used the Quebec Integrated Chronic Disease Surveillance System to observe the adverse event rates of losartan, valsartan and candesartan on 136,177 patients aged at least 66 years at 24 months prior and 12 months after generic commercialization.
Using negative binomial-segmented regression models, Poirier and colleagues compared periods before and after generic commercialization.
Among all angiotensin II receptor blocker users, there was a monthly mean rate of 100 adverse events for 1,000 users before and after generic commercialization.
Increase in adverse events
On the month of generic commercialization, there was an increase of adverse event rates of 8% among users of losartan (difference of proportions vs. brand names, 7.5%; 95% CI, –0.9 to 15.9), of 11.7% among valsartan users (difference of proportions, 17.1%; 95% CI, 9.9-24.3) and of 14% candesartan users (difference of proportions, 16.6%; CI, 7.9-25.3).

According to the study results, less than a year after generics commercialization, the monthly trend of adverse events was only affected among those treated with losartan (difference of proportions, 2%; 95% CI, 0.7-3.4).
Incremental risks
“More likely than not, the incremental risks observed by Poirier and colleagues were not entirely attributable to the use of generic drug preparations,” David Alter, MD, PhD, from the department of medicine at the University of Toronto, wrote in an accompanying editorial.
The use of segmentation analyses may not be the best approach because “systematic differences may have existed that explained why some patients received their generic drugs earlier than others,” Alter wrote.
“Poirier et al are ... correct in advising caution when interpreting their findings. They advocate instead, for further research,” he wrote. “However, what sort of future research also remains unclear. The methodological techniques the authors themselves employed and promoted underscores uncertainty about the optimal research methods that may be most appropriate when conducting drug surveillance research.”
Poirier told Cardiology Today that the findings underwent a rigorous review process.
There are some limitations for the study, but ... at the end of the day, we ended up with the same conclusions,” Poirier said. “We're glad that the reviewer was so hard on us because it made us more confident in the data and I hope someone will run the same analysis with the same design in the United States. It could be a huge dataset to show if there is something there or not, and if it is there, then the next step will try to identify the patients who should not be changed to a generic.” – by Dave Quaile
For more information:
Paul Poirier, MD, PhD, can be reached at paul.poirier@criucpq.ulaval.ca.

Friday, April 7, 2017

Angiotensin II Receptor Blockers May Reduce Age-Related Cognitive Decline

Any followup at all to see if this might help stroke cognitive decline? Or will nothing occur because we have NO STROKE LEADERSHIP?  

Angiotensin II Receptor Blockers May Reduce Age-Related Cognitive Decline


By Thomas S. May
FLORENCE, Italy -- April 5, 2017 -- Individuals treated with angiotensin II receptor blockers (ARBs), including losartan, valsartan, and candesartan, experience a decreased risk for age-related cognitive decline and dementia, according to results of a cross-sectional analysis presented at the 25th European Congress of Psychiatry (EPA).
Lead author Dominik Wincewicz, MD, Medical University of Bialystok, Bialystok, Poland and colleagues observed a significant decrease in the risk for cognitive decline in subjects who received ARB treatment over the course of approximately 9 years of follow up (odds ratio [OR] = 0.445, 95% confidence interval [CI] = 0.22 to 0.90, P = .024). The risk of dementia also was decreased significantly in participants treated with ARBs (hazard ratio [HR] = 0.621, 95% CI = 0.40 to 0.98, P = .038), added Dr. Wincewicz, speaking here on April 2.
He and his fellow investigators analysed data from the population-based, longitudinal Kuopio Ischemic Heart Disease (KIHD) Risk Factor Study, an extensive epidemiologic research project launched in the 1980s, which initially involved nearly 3,000 middle-aged men from the Kuopio region in Eastern Finland. A decade later, over 1,000 women of the same age were recruited to the study. A major part of the original cohorts have been re-examined 4, 11, and 20 years after the baseline.
The researchers included a total of 1,774 subjects (920 females; baseline age range: 42 to 61 years). They utilised a cut-off score of ≥ 2 point decrease in the Mini-Mental-State Examination over a 9-year follow-up period to detect age-related cognitive decline, and a hospital discharge diagnosis of dementia as the outcome variable for dementia.
Using logistic regression, the investigators determined cross-sectional relationships, and conducted prospective analyses with the Cox proportional hazards model. The team adjusted analyses for all relevant background variables.
ARBs modulate the brain renin-angiotensin system (RAS), and have been shown to improve cognitive functioning in animal models of neuropsychiatric disorders. The brain RAS also has been considered as a new target for the treatment of Alzheimer’s Disease.
[Preserved Cognition and Reduced Age Related Cognitive Decline During Treatment with Angiotensin II Receptor Blockers: a 20-year Follow-up Study. Abstract ED773]

Tuesday, March 14, 2017

The complex of PAMAM-OH dendrimer with Angiotensin (1–7) prevented the disuse-induced skeletal muscle atrophy in mice

You'll have to ask your doctor what protocols are being used to prevent muscle atrophy. This will require lots more research that will never occur in humans before being useful. I could tell my calf muscle was atrophying because my AFO was getting looser. It wasn't even checked during any exam.

The complex of PAMAM-OH dendrimer with Angiotensin (1–7) prevented the disuse-induced skeletal muscle atrophy in mice

Authors Márquez-Miranda V, Abrigo J, Rivera JC, Araya-Durán I, Aravena J, Simon F, Pacheco N, González-Nilo FD, Cabello-Verrugio C
Received 23 October 2016
Accepted for publication 1 February 2017
Published 13 March 2017 Volume 2017:12 Pages 1985—1999
DOI https://doi.org/10.2147/IJN.S125521
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Alexander Kharlamov
Peer reviewer comments 2
Editor who approved publication: Dr Thomas J. Webster
Valeria Márquez-Miranda,1,2,* Johanna Abrigo,3,4,* Juan Carlos Rivera,3,4 Ingrid Araya-Durán,1 Javier Aravena,3,4 Felipe Simon,3,4 Nicolás Pacheco,1 Fernando Danilo González-Nilo,1,2,5 Claudio Cabello-Verrugio3,4

1Center for Bioinformatics and Integrative Biology (CBIB), Facultad de Ciencias Biologicas, Universidad Andres Bello, Santiago, 2Fundación Fraunhofer Chile Research, Las Condes, 3Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas & Facultad de Medicina, Universidad Andres Bello, 4Millennium Institute on Immunology and Immunotherapy, Santiago, 5Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Valparaíso, Chile

*These authors contributed equally to this work

Abstract: Angiotensin (1–7) (Ang-(1–7)) is a bioactive heptapeptide with a short half-life and has beneficial effects in several tissues – among them, skeletal muscle – by preventing muscle atrophy. Dendrimers are promising vehicles for the protection and transport of numerous bioactive molecules. This work explored the use of a neutral, non-cytotoxic hydroxyl-terminated poly(amidoamine) (PAMAM-OH) dendrimer as an Ang-(1–7) carrier. Bioinformatics analysis showed that the Ang-(1–7)-binding capacity of the dendrimer presented a 2:1 molar ratio. Molecular dynamics simulation analysis revealed the capacity of neutral PAMAM-OH to protect Ang-(1–7) and form stable complexes. The peptide coverage ability of the dendrimer was between ~50% and 65%. Furthermore, an electrophoretic mobility shift assay demonstrated that neutral PAMAM-OH effectively bonded peptides. Experimental results showed that the Ang-(1–7)/PAMAM-OH complex, but not Ang-(1–7) alone, had an anti-atrophic effect when administered intraperitoneally, as evaluated by muscle strength, fiber diameter, myofibrillar protein levels, and atrogin-1 and MuRF-1 expressions. The results of the Ang-(1–7)/PAMAM-OH complex being intraperitoneally injected were similar to the results obtained when Ang-(1–7) was systemically administered through mini-osmotic pumps. Together, the results suggest that Ang-(1–7) can be protected for PAMAM-OH when this complex is intraperitoneally injected. Therefore, the Ang-(1–7)/PAMAM-OH complex is an efficient delivery method for Ang-(1–7), since it improves the anti-atrophic activity of this peptide in skeletal muscle.

Keywords: muscle wasting, peptide delivery, carrier, anti-atrophic peptide
Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.
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Thursday, February 18, 2016

Vaccine shows potential to protect the brain before a stroke

This should be added to other pretreatment possibilities: 



Vaccine shows potential to protect the brain before a stroke

A type of vaccine previously studied to treat high blood pressure may have the potential to protect the brain when administered before a stroke, according to an animal study presented at the American Stroke Association’s International Stroke Conference 2016.
Japanese researchers tested a peptide vaccine targeting the hormone angiotensin II (Ang II) a key player in high blood pressure. Members of the research team previously had found that their peptide vaccine decreased blood pressure in a mouse model of hypertension, while the blood pressure of mice with normal readings was unaffected. The hormone also has been linked to patients’ prognosis after a ischemic (clot-caused) stroke.
In the new study, researchers injected 53 male rats with the vaccine three times, at ages 4, 6 and 7 weeks old, and administered a second group of 41 with saline at the same intervals. Stroke was induced in vaccinated rats and rats that were given saline.
The team then measured levels of anti-Ang II antibody in the blood and brains of the rats that received the vaccine and had a stroke. Compared with rats that had low blood levels of antibody, the animals with high levels in the blood had more anti-Ang II antibodies in functional tissue at the side of the brain where the stroke occurred. Researchers also noted that vaccinated rats that produced high blood levels of antibody had less damage to the brain and fewer degenerated neurons.
Because the Ang II peptide vaccine is long-lasting, has anti-inflammatory effects and appears able to protect the brain after a blood vessel blockage, it has potential to be a therapy for high blood pressure and stroke prevention, researchers said.

http://newsroom.heart.org/news/basic-science-tip-sheet-3127213?preview=288bf38a9020a77868a1001b3426486c

Wednesday, May 27, 2015

Future vaccine may help lower blood pressure long-term

And it is even needleless, although you would have to be a rat right now. 

Future vaccine may help lower blood pressure long-term 


Study Highlights
  • A DNA vaccine helped lower blood pressure for up to six months, reduced tissue damage to the heart and blood vessels associated with hypertension in rats.
  • If future research shows the vaccine is a viable treatment option in humans, it could improve high blood pressure levels.  

DALLAS, May 26, 2015 – A vaccine may one day help lower blood pressure for up to six months, according to new research in the American Heart Association’s journal Hypertension.
The study in rats may eventually provide a novel alternative to treat high blood pressure in people, who would not need to take a pill everyday.
“The potential of a vaccine for hypertension offers an innovative treatment that could be very effective for the control of non-compliance which is one of the major problems in the management of hypertensive patients,” said Hironori Nakagami M.D., Ph.D., study co-author and professor at Osaka University in Japan.
Researchers have designed a DNA vaccine that targets angiotensin II ― a hormone that raises blood pressure by causing blood vessels to constrict. This narrowing can increase your blood pressure and force your heart to work harder.
In the study, researchers immunized hypertensive rats three times at two-week intervals with needleless injections. The vaccine not only lowered blood pressure for up to six months, but also reduced tissue damage to the heart and blood vessels associated with hypertension. There were no signs of damage to other organs such as the kidney or liver.
The DNA vaccine works similar to common ACE inhibitor blood pressure medications which help blood vessels relax and open up, which, in turn, lowers blood pressure. Other types of vaccines have been tested for hypertension (e.g. a peptide vaccine), but didn’t have lasting effects and some had undesirable side effects.
The ultimate goal of an anti-hypertensive vaccine is to achieve perfect blood pressure control by improving drug compliance through the vaccine. In addition, in the developing countries like Africa and south Asia, anti-hypertensive drugs such as ARB (angiotensin receptor blockade) are expensive. A DNA vaccine may provide cheaper and effective anti-hypertensive treatments in such countries, researchers said.
“Further research on this DNA vaccine platform, including increasing the longevity of blood pressure reduction, may eventually provide a new therapeutic option to treat hypertensive patients,” Nakagami said.
The technology can also be applied to generate other vaccines.
Co-authors are Hiroshi Koriyama M.D., Ph.D; Futoshi Nakagami; M.D., Ph.D; Mariana Kiomy Osako, Ph.D; Mariko Kyutoku, Ph.D; Munehisa Shimamura M.D.; Ph.D; Hitomi Kurinami M.D., Ph.D; Tomohiro Katsuya M.D., Ph.D; Hiromi Rakugi M.D., Ph.D; and Ryuichi Morishita M.D., Ph.D. Author disclosures are on the manuscript.
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