UVA Stroke Center earns national certification - CHARLOTTESVILLE, Va.

You'll notice that nowhere in here do they refer to RESULTS. Excellent stroke care means absolutely nothing. We don't give a shit about care, care and service doesn't solve any of the problems in stroke  or get you to 100% recovery. Call that leader - Executive Vice President for Health Affairs, University of Virginia (

Richard P. Shannon, MD

general number  ( 434.924.2946  and demand to know what the RESULTS are; tPA efficacy, 30 day deaths, 100% recovery, rehab protocol efficacy.

Big f*cking whoopee.

You can check out Joint Commission standards here:

 http://www.jointcommission.org/assets 

 I saw absolutely nothing about what should be done the first week or anything about measuring 30-day deaths and 100% recovery.  God, these people are worse than worthless. Complacent good-for-nothings.

    
The puffery article here:
http://www.newsplex.com/content/news/UVA-Stroke-Center-earns-national-certification-442258443.html

CHARLOTTESVILLE, Va. (NEWSPLEX) -- The Stroke Center at the University of Virginia Health System has been certified as a Comprehensive Stroke Center.
According to a release, the certification comes from the Joint Commission, an accrediting group for hospitals that works with the American Heart Association and the American Stroke Association.
The UVA Stroke Center is one of just three in Virginia to earn the national certification, which follows a site visit by surveyors measuring how well the center complies with stroke care standards and using evidence-based guidelines to provide care.
The release says about three percent of hospitals across the country earn this certification.
"This is a tremendous honor for our Stroke Center physicians and team that highlights their dedication to providing excellent care whenever it is needed, using the most advanced procedures and imaging," said Pamela M. Sutton-Wallace, the CEO of the UVA Health System.
According to the release, the services available at a Comprehensive Stroke Center include a dedicated intensive care unit that is staffed around the clock, care for patients with strokes caused by blocked blood vessels in the brain and by brain bleeding, advanced imaging to help with diagnosis, quick delivery of intravenous tissue plasminogen activator or tPA that is used to break up clots, and advanced surgical procedures such as coiling and clipping to treat aneurysms that may cause strokes due to bleeding in the brain.
Such centers can also help coordinate care for patients after they are discharged from the hospital and conduct research to help improve care for stroke patients.

Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats

Don't do this without a doctors prescription.
https://link.springer.com/article/10.1007/s12035-017-0732-y

• Authors
• Authors and affiliations

• Taiza H. Figueiredo
• Carolina L. Harbert
• Volodymyr Pidoplichko
• Camila P. Almeida-Suhett
• Hongna Pan
• Katia Rossetti
• Maria F. M. Braga
• Ann M. MariniEmail author

• Taiza H. Figueiredo
  • 1
• Carolina L. Harbert
  • 1
• Volodymyr Pidoplichko
  • 1
• Camila P. Almeida-Suhett
  • 1
• Hongna Pan
  • 2
• Katia Rossetti
  • 1
• Maria F. M. Braga
  • 1
• Ann M. Marini
  • 2
  Email author

1. 1.Department of Anatomy, Physiology and GeneticsUniformed Services University of the Health SciencesBethesdaUSA
2. 2.Department of Neurology and Program in NeuroscienceUniformed Services University of the Health SciencesBethesdaUSA

Article

First Online:

26 August 2017

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• 24 Downloads

Abstract

Approximately, 1.7 million Americans suffer a TBI annually and TBI is a major cause of death and disability. The majority of the TBI cases are of the mild type and while most patients recover completely from mild TBI (mTBI) about 10% result in persistent symptoms and some result in lifelong disability. Anxiety disorders are the second most common diagnosis post-TBI. Of note, TBI-induced anxiety disorders are difficult to treat and remain a chronic condition suggesting that new therapies are needed. Previous work from our laboratory demonstrated that a mild TBI induced an anxiety-like phenotype, a key feature of the human condition, associated with loss of GABAergic interneurons and hyperexcitability in the basolateral amygdala (BLA) in rodents 7 and 30 days after a controlled cortical impact (CCI) injury. We now confirm that animals display significantly increased anxiety-like behavior 30 days after CCI. The anxiety-like behavior was associated with a significant loss of GABAergic interneurons and significant reductions in the frequency and amplitude of spontaneous and miniature GABA_A-receptor-mediated inhibitory postsynaptic currents (IPSCs) in the BLA. Significantly, subchronic treatment with alpha-linolenic acid (ALA) after CCI prevents the development of anxiety-like behavior, the loss of GABAergic interneurons, hyperexcitability in the BLA and reduces the impact injury. Taken together, administration of ALA after CCI is a potent therapy against the neuropathology and pathophysiological effects of mTBI in the BLA.

Only 20 minutes less sitting per day is enough to maintain good health and muscle mass

Will your doctors let you know of this study and setup a protocol to accomplish this for you?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=178478&CultureCode=en

30 August 2017 University of Jyväskylä

Finnish researchers conducted one of the largest and longest studies to find out if it is possible to reduce sedentary time and if the reduction will result in any health benefits during one year. A tailored counseling helped busy office workers with young children to decrease their sedentary leisure time 21 minutes per day, which was enough to improve some biomarkers and to maintain muscle mass during one year.
A total of 133 office workers with young children participated in the study conducted at the University of Jyväskylä, Finland. The participants were randomized in two groups. The participants of the intervention group were provided with tailored counseling in order to discuss strategies to reduce sitting at work and leisure time. The participants set personal goals that they found feasible for the everyday lives of their families. The most common goal for work time was to break up sitting periods while working and at coffee breaks. For leisure time, the most common goals were active commuting and an increase in active time with the family.
At the baseline, the participants were sedentary (assessed objectively by accelerometers) for 5.6 hours per day at work, and 3.8 hours per day during leisure time. After the counseling session, sedentary leisure time decreased by 21 minutes per day while light activity and breaks in sedentary time increased. At the end of the year, the intervention group still had 8 minutes less sedentary leisure time, whereas that of the control group tended to increase slightly. Women, but not men, were able to increase light activity time and breaks in sitting also at work.
Several health markers were monitored during the one-year period. After the counseling session, the intervention group’s fasting glucose levels decreased slightly. The Apolipoprotein B-to-Apolipoprotein A-1 ratio, which is a novel biomarker of cholesterol transport capacity and related to cardiovascular risk, improved during the year. At the same time, leg muscle mass was maintained in the intervention groups, whereas the control group’s muscle mass decreased by a half percent.
The first author, Doctor of Sport Sciences Arto Pesola finds the results preliminary but promising:
– This study shows that it is possible to reduce the sedentary time of people in a busy phase of life. Even though the effect of tailored counseling diluted during the year, the intervention was effective in preventing an increase in sitting. This is important, because sedentary time tends to increase while we age. The effect was most visible during leisure time, where the sedentary time was already lower. This may reflect the demands of working life and that counseling targeted at individuals and their families is ineffective in changing the sitting time at work, at least in men. Instead, people may find more opportunities and freedom to reduce sedentary time and to participate in enjoyable family activities out of working hours. Parents may think at first that spending time with their children is away from their own physical exercise. However, that way they can reduce sitting time and show a good example to their offspring about a physically active lifestyle. This is motivating, and as shown in the study, may be beneficial for health in the long run.
Epidemiological studies have shown that increased sitting time is associated with type 2 diabetes, cardiovascular diseases and premature mortality.
The present study was among the first ones to show that it is possible to reduce sedentary time and that even a small decrease in sedentary time can be beneficial for initially healthy people. Reductions in sedentary time may be easier to achieve when they are incorporated in common family activities and other everyday tasks during leisure time. Future studies should investigate if it would be possible to reduce sitting at work by changing the physical or social environment, and what are the physiological mechanisms that explain the health benefits of reduced sitting time.
The study was part of the InPACT project led by Professor Taija Juutinen Finni and funded by the Finnish Ministry of Education and Culture. Other financers were the Juho Vainio Foundation, the Yrjö Jahnsson Foundation and the Ellen and Artturi Nyyssönen Foundation.
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0183299

• Full bibliographic informationThe original paper was published in the PLOS ONE journal on 24 August 2017:
  Arto J. Pesola, Arto Laukkanen, Risto Heikkinen, Sarianna Sipilä, Arja Sääkslahti, Taija Finni. Accelerometer-assessed sedentary work, leisure time and cardio-metabolic biomarkers during one year: effectiveness of a cluster randomized controlled trial in parents with a sedentary occupation and young children.

MRI scan that can predict stroke risk has 'promise to save lives'

But is intravascular photoacoustic (IVPA) imaging better? 

Or sodium fluoride that had been tagged with a tiny amount of a radioactive tracer and then using PET scans?

I expect your doctor and hospital should be monitoring and updating their protocols to identify stroke risks from unstable plaque. That is if your doctor and hospital are not incompetent.  Do they even know about IVPA and sodium fluoride tracing?  A fucking protocol is needed rather than thousands of doctors trying to analyze stuff they know nothing about.

MRI scan that can predict stroke risk has 'promise to save lives'

Scientists at Oxford University develop non-invasive technique to measure amount of cholesterol in carotid plaques

There are an annual 100,000 strokes in the UK. Photograph: Peter Byrne/PA 

Haroon SiddiqueWednesday 23 August 2017 19.01 EDT Last modified on Wednesday 23 August 2017 19.45 EDTA new type of MRI scan can predict the risk of having a stroke, researchers have said in a study.The non-invasive technique, developed by scientists at the University of Oxford, predicts whether plaques in the carotid arteries are rich in cholesterol and therefore more likely to cause a stroke.  Carotid arteries supply the brain with blood. The rupture of fatty plaques can block them and possibly starve the brain of oxygen, causing potentially debilitating and life-threatening strokes. A quarter of the more than 100,000 strokes in the UK each year are caused by carotid plaques. Dr Luca Biasiolli, the co-author of the study, said: “When someone goes to hospital having suffered a minor stroke, it’s vital that doctors know whether the patient might be at risk of a further stroke, which could be fatal. “Being able to quantify cholesterol in carotid plaques is a really exciting prospect, as this new MRI technique could help doctors to identify patients at higher risk of stroke and make more informed decisions on their treatments.” The study, published in the journal JACC: Cardiovascular Imaging on Thursday, created a test that produces a quantitative result, whereas traditionally the risk of stroke is measured by the size of the plaque in the carotid artery. At present, if a plaque is deemed too big it is removed, but the researchers say fatty plaques that are not large yet have a high risk of rupturing can be missed. 

Number of strokes in UK predicted to rise by 44% in next 20 years

Read more

The scientists used the new MRI scan to measure the amount of cholesterol in the carotid plaques of 26 patients scheduled for surgery. After the plaques were surgically removed, the team looked at the actual cholesterol content in each plaque and found that the new technique was accurate – the more cholesterol they detected within the plaque, the greater the risk of a stroke. The same team confirmed and extended their findings in another study on 50 people published in PLOS ONE.
Prof Sir Nilesh Samani, medical director at the British Heart Foundation, which part-funded the study, said: “This exciting research opens up the possibility that in the future we may be able to more accurately identify people with carotid plaques that are likely to rupture and cause a stroke.
“These patients can then be treated earlier – for example, with surgery to remove the plaque – while others might be spared surgery altogether. More research is now necessary before this advance can come into routine clinical practice. However, if successful this technique has the promise to save lives.”

Injecting stem cells into the brain reverses Parkinson’s symptoms in monkeys

You might very well need this so you better hope that this is followed up better than any stroke research is.

Parkinson’s Disease May Have Link to Stroke

Injecting stem cells into the brain reverses Parkinson’s symptoms in monkeys 

 

By Kate Sheridan @sheridan_kate

August 30, 2017

Injecting neurons created from stem cells into the brain may relieve Parkinson’s symptoms, according to a new study in monkeys.

Why it matters:

Parkinson’s disease can happen when some of a person’s dopamine-producing brain cells die, so replacing those neurons could be an effective treatment. Administering dopamine is part of currently accepted treatment, but over time the treatment has less effect as neurons die off and the side effects become difficult to manage. So scientists have begun studying approaches using stem cells, primarily in rodents. A clinical trial is also underway at the Royal Melbourne Hospital to inject neural stem cells into the brains of people with Parkinson’s as part of a Phase I clinical trial. Results are expected in 2019, and preliminary results were presented at the American Academy of Neurology meeting this year.

The nitty-gritty:

Researchers collected skin or blood cells from seven humans, some who had Parkinson’s disease and some who did not. (The people with Parkinson’s did not have any of the genes thought to be associated with the disease.) Next, using sets of proteins, they “reprogrammed” some of those cells and encouraged them to grow up as neurons — specifically, neurons that could produce dopamine. Finally, they injected the stem cells into the brains of monkeys that were treated with a neurotoxin, which made them act like they had the condition.

Researchers found that the symptoms of the monkeys treated with stem cells from either group improved more over the course of a year than monkeys treated with a placebo injection. To determine if the monkey’s symptoms had improved, the team evaluated their tremors, movements, and posture, among other things. The team published its results in Nature on Wednesday.

Read More

Mighty morphed brain cells cure Parkinson’s in mice, but human trials still far off

“I think that a stem cell-based therapy will bring more benefits than conventional treatments can do now,” said Dr. Jun Takahashi, a professor at Kyoto University and one of the authors of the paper.

You should know:

Among conventional treatments for Parkinson’s is a medication called L-DOPA, which ultimately helps patients replace some of the dopamine they can no longer produce. Another accepted procedure is deep brain stimulation, which sparked Takahashi’s interest in this project, he said.
Takahashi and his team did not run tests comparing their results to those seen after deep-brain stimulation and L-DOPA treatment, but they did compare their findings to published statistics. They concluded that the transplants “should exert [similar] effects.”

What they’re saying:

Dr. Lorenz Studer, director of the center for stem cell biology at Memorial Sloan Kettering Cancer Center, said Takahashi’s work was “a very impressive study,” especially given the number of animals, the length of time they were followed, and the similarity of the protocols used to those that might be used in human trials. “In this regard, it was a really interesting test run,” he said.

“It is probably the best study to date using the induced pluripotent stem cells,” said Studer, who was not involved in the research.

Rivaroxaban Plus Aspirin More Effective Than Aspirin Alone for Secondary Cardiovascular Prevention

How up-to-date is your doctor and when will you be told about this? You'll have to decide if the risk of bleeding is worse than the risk of death
http://dgnews.docguide.com/rivaroxaban-plus-aspirin-more-effective-aspirin-alone-secondary-cardiovascular-prevention?overlay=2&

August 30, 2017

By Walter Alexander
BARCELONA, Spain -- August 30, 2017 -- After 1 year, the majority of patients with cardiovascular disease (CVD) who were given twice-daily rivaroxaban 2.5 mg plus daily aspirin reduced their risk of cardiovascular death, stroke, and myocardial infarction (MI), compared with patients who only received daily aspirin.
However, the combination therapy was associated with higher rates of major bleeding, reported John Eikelboom, MD, McMaster University, Hamilton, Ontario, and colleagues at the 2017 Annual Meeting of the European Society of Cardiology (ESC).
In the COMPASS study, patients (n = 27,395) with CVD from 33 countries were randomised 1:1:1 to rivaroxaban 2.5 mg twice daily plus aspirin 100 mg once daily, rivaroxaban 5 mg twice daily, or standard therapy with aspirin 100 mg once daily.
The primary endpoint was a composite of cardiovascular death, stroke, and MI.
Clear superiority of the arm receiving rivaroxaban plus aspirin at interim analysis led the Data Safety Monitoring Board (DSMB) to recommend cessation of treatment in both monotherapy arms.
The primary endpoint was experienced by 4.1%, 4.9%, and 5.4% of patients in the combination, rivaroxaban alone, and aspirin alone arms, respectively. The hazard ratio (HR) for the rivaroxaban/aspirin versus aspirin arm was 0.76 (P< .0001). The rivaroxaban versus aspirin arm comparison showed no differences (HR = 0.90; P = .12).
Major bleeding rates were 3.1%, 2.8%, and 1.9%, respectively, with significant increases for both rivaroxaban-containing arms versus aspirin (P< .0001).
Net clinical benefit analysis taking into account primary and severe bleeding events found a significantly lower rate for the combination arm (4.7% vs 5.9%; HR = 0.80; P = .0005).
“The substantial benefits seen with rivaroxaban and aspirin support the approach of using low doses of the 2 treatments in combination,” said Dr. Eikelboom. “Recent trials in other disease areas have demonstrated substantial benefits from using low doses of a combination of drugs, and this concept is now further supported by the results of COMPASS.”
“Many of these bleeds were not serious and despite the increase in bleeding the results clearly show a net benefit for patients, as highlighted by an 18% reduction in mortality,” added co-author Stuart Connolly, McMaster University.
[Presentation title: Rivaroxaban With or Without Aspirin in Stable Cardiovascular Disease]

Physical Activity in Midlife Not Linked to Cognitive Fitness in Later Years

To improve your cognitive functioning post-stroke your doctor should tell you the exact amount of physical activity needed. We need a fucking protocol, get your doctor to write up one rather than 10 million yearly stroke survivors  looking for the same damn thing.

Physical Activity in Midlife Not Linked to Cognitive Fitness in Later Years

Moving When Young May Strengthen the Adult Brain

Stroke Rehabilitation: Exercise Improves Cognitive Function

 

 

Consuming Cannabis Could Slash Your Chances Of Blood Clots, Stroke: Study

Now we just need to know what delivery method and how much. Increased blood flow sounds like an excellent intervention immediately post-stroke. DEMAND your doctor figure out how to get some, how much and how delivered. I'm not medically trained so I obviously don't know how to interpret these findings.  But I will do marijuana after my next stroke.

My 13 reasons for marijuana use post-stroke. 

Consuming Cannabis Could Slash Your Chances Of Blood Clots, Stroke: Study

Consuming cannabis can significantly cut your chances of having a stroke, according to a new study published in the journal, ‘Neuropsychopharmacology.’
Researchers from the University of Texas at Dallas found that cannabis improves blood and oxygen flow, consequently slashing the risk of blood clots and stroke.
Head researcher Dr. Francesca Filbey said the "primary psychoactive ingredient present in cannabis —tetrahydrocannabinol (THC) — relaxes arterial walls resulting in lower blood pressure and increased blood flow to tissues.”
“Past marijuana research has shown changes in cognitive functions such as memory and executive functioning,” added Filbey in a press statement.

“Our study seeks to understand the possible neurophysiological mechanisms that may drive these cognitive changes.”

The research team analyzed 175 volunteers – 74 drug users and 101 non-users – for 60 days, although all participants refrained from taking drugs 72 hours prior to the examination. All the drug users selected for the study had consumed cannabis at least 5,000 times in their lifetime.
Throughout the study, researchers administered MRIs to the volunteers, as well as analyzed their THC metabolite levels using urinalysis. It was revealed that those who regularly consumed cannabis had greater global oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen (CMRO2) than the non-consumers.
Researchers also found that the cerebral blood flow (CBF) in the putamen – located at the base of the forebrain and associated with learning – was greater in cannabis users than non-users.
“Currently, cannabis is the most widely used illicit drug [in the U.S.],” said Filbey. “As it becomes more widely legalized, understanding neurophysiological alterations and its effects on the brain's health and performance are becoming increasingly relevant.”

Healthy glucose levels the key to a healthy ageing brain

Totally useless information. No amounts per body size and sex. Protocols people, we need protocols.  No information on how to measure.
http://www.anu.edu.au/news/all-news/healthy-glucose-levels-the-key-to-a-healthy-ageing-brain

New research has found blood glucose levels even at the normal range can have a significant impact on brain atrophy in ageing.
Dr Erin Walsh, lead author and post-doctoral research fellow at ANU, said the impacts of blood glucose on the brain is not limited to people with type 2 diabetes.
"People without diabetes can still have high enough blood glucose levels to have a negative health impact," said Dr Walsh from the Centre for Research on Ageing, Health and Wellbeing (CRAHW) at ANU.
"People with diabetes can have lower blood glucose levels than you might expect due to successful glycaemic management with medication, diet and exercise.
"The research suggests that maintaining healthy blood glucose levels can help promote healthy brain ageing. If you don't have diabetes it's not too early and if you do have diabetes it's not too late."
Dr Walsh said people should consider adopting healthy lifestyle habits, such as regular exercise and healthy diets.
"Having a healthy lifestyle contributes to good glycaemic control without needing a diabetes diagnosis to spur them into adopting these good habits," she said.
"It helps to keep unhealthy highly processed and sugary foods to a minimum. Also, regular physical activity every day can help, even if it is just a going for walk."
The research is part of the "Too sweet for our own good: An investigation of the effects of higher plasma glucose on cerebral health" project led by Associate Professor Nicolas Cherbuin, which is part of the longitudinal PATH through life study led by Professor Kaarin Anstey at ANU.
"The work would not be possible without being able to longitudinally explore blood glucose in members of the general public," said Dr Walsh. 
The research has been published in the journal Diabetes and Metabolism.

High level of heart disease pipeline innovation could bridge unmet need in treating CVD

Nothing about stroke probably because 'Stroke is Treatable'. Tell that to the 10 million yearly stroke survivors.

High level of heart disease pipeline innovation could bridge unmet need in treating CVD

• Download PDF Copy

August 24, 2017

With over 1,400 products in active development, the innovation pipeline for cardiovascular disease (CVD) is extensive, with four key CVD indications – hypertension, heart failure, dyslipidemia and thrombosis – now accounting for around half of all pipeline innovation, according to GBI Research, a recognized leader in providing business information and analytics.
The company’s latest report on cardiovascular disease looks at the current clinical and commercial landscape and highlights the particularly high level of heart failure pipeline innovation. This reflects efforts by the pharmaceutical industry to remedy the unmet need in treating this disease, which is associated with a five-year mortality rate of 50%.
Currently, CVD therapeutics focus on managing risk factors such as high cholesterol and high blood pressure, and slowing disease progression. However, current treatments are ineffective at reversing damage, which typically relies upon surgical procedure. Anti-dyslipidemic drugs are unable to reverse the build-up of atherosclerotic plaque, and anti-thrombotic drugs only focus on preventing new thrombus from forming rather than dissolving current clots. The current pipeline shows evidence of addressing this challenge with potentially more damage reversal treatments on the horizon.
Heart failure and pulmonary hypertension remain poorly treated, and are associated with poor prognosis. The large pipeline for heart failure includes a high proportion (23%) of first-in-class products relative to other CVD indications, and possesses the potential for breakthroughs in the treatment of this condition.
Tom Jarratt, Associate Analyst for GBI Research, commented:

In this landscape, adopting a strong focus on innovation as a means of adding product value and creating differentiation remains a vitally important component of company strategy. There are 320 first-in-class products in the CVD market that act on a novel molecular target that is not present in an approved product across any indication in the pharmaceutical industry. However, they remain a key product development strategy with the potential to provide the greatest degree of differentiation, extending to a first-mover advantage, and potentially a significant market share.

The clinical and commercial landscape across the pharmaceutical industry is set for significant change over the coming decade and beyond, driven by a number of factors including low R&D productivity and stubbornly high clinical attrition rates.
Jarratt continued:

The net effect is an increasingly challenging, complex and often unpredictable commercial environment which we explore in the report.

Related Stories

• Research on electrical nerve-block implant aims at treating asthma and heart failure
• Slow walkers could be at higher risk of heart disease, say researchers
• Drug combination superior in preventing further heart complications in people with vascular disease

GBI Research analysis also indicates that companies across the pharmaceutical spectrum pursue a first-in-class product development strategy, ranging from major pharmaceutical players to start-up biotech firms, despite the typically higher attrition risk of these products. The proportion of first-in-class products in the pipeline for the top 20 major pharmaceutical companies ranges from 20% (for Novo Nordisk) to 60% (for Amgen), indicating a significant focus on breakthrough innovation. Moreover, 41% of start-up biotech companies with no marketed products and up to five pipeline products have at least one first-in-class product in their R&D portfolio.
Jarratt added:

The data indicates that, despite challenging market conditions, there are reasons for sustained optimism that a stream of clinically and commercially successful first-in-class products will reach the market over the coming decade and beyond.

An analysis of strategic consolidations also revealed a modest level of deal activity in recent years, and a large number of first-in-class products not yet involved in any deals.

Source:

http://gbiresearch.com/

PinnacleHealth’s new technology helps protect patients from risk of stroke during TAVR

63% reduction and 99% capture rate is still not good enough, better than nothing but send them back to the drawing board. We let the known failure rate of tPA being 88% last for decades without being challenged. Demand better, your doctors probably won't, it is not their problem if you get a stroke..
https://www.news-medical.net/news/20170824/PinnacleHealthe28099s-new-technology-helps-protect-patients-from-risk-of-stroke-during-TAVR.aspx

• Download PDF Copy

August 24, 2017

PinnacleHealth is the first hospital in Pennsylvania and one of the first 10 in the country to introduce new technology shown to help protect patients from the risk of stroke during transcatheter aortic valve replacement (TAVR).
Minimally invasive TAVR is proven effective in treating aortic stenosis without open heart surgery for patients at too high of a risk for surgery. However, during TAVR, calcium deposits from the heart valve or tissue can be dislodged and may travel to the brain, which can create a stroke risk. Based on clinical trial results and major TAVR registry data, the reported risk of stroke for TAVR patients varies between 1-5 percent.

Related Stories

• Research on electrical nerve-block implant aims at treating asthma and heart failure
• Study: Left atrial appendage closure during open heart surgery protects against brain infarctions
• Researchers explore freshwater turtles to understand mechanisms that protect from heart damage

PinnacleHealth is implementing the Sentinel Cerebral Protection System, the first FDA-cleared device available in the U.S., to capture and remove this debris before it reaches the brain. The device has been shown to reduce strokes by 63 percent during the procedure and in the first 72 hours post-procedure, when most strokes occur.
In the U.S. clinical trial of the technology, the device captured debris in 99 percent of TAVR cases,⁶ with no added risk for the overall procedure. The Sentinel device is inserted through the catheter before the TAVR device and comes out after the valve is deployed. It is shaped like a butterfly net, collapsing around the debris and allows the debris to be removed from the body after the procedure.
"Any stroke is one stroke too many," says Hemal Gada, MD, MBA, medical director of structural heart at PinnacleHealth CardioVascular Institute.
"We are proud to be on the vanguard of offering the most advanced medical technology to keep our patients safe and value the added layer of protection this device brings to our patients," says Mubashir Mumtaz, MD, FACS, FACC, chief of cardiothoracic surgery and surgical director of structural heart at PinnacleHealth CardioVascular Institute.
More than 3,500 patients worldwide have been protected with the innovative technology to-date.

Source:

http://www.pinnaclehealth.org/our-health-system/news-and-announcements/article/new-technology-helps-protect-pinnaclehealth-patients-from-risk-of-stroke-during-heart-valve-replacement

Simple breath test can detect cancer and 16 other diseases - Crohn's disease, Parkinson's disease, pulmonary hypertension

Now there will be no excuse for your doctor not identifying your Parkinsons.

Parkinson’s Disease May Have Link to Stroke

Simple breath test can detect cancer and 16 other diseases - Crohn's disease, Parkinson's disease, pulmonary hypertension

Steve Dent, @stevetdent

12.29.16 in Medicine

 

Ancient Greek physicians figured that our breath was a strong health indicator, but researchers from the Israel Institute of Technology have proven just how true that is. They developed a device that uses nanoparticles to identify 17 different diseases, including lung cancer and Parkinson's disease, from just a single breath. While the machine isn't accurate enough yet for real-life clinical diagnoses, it shows high promise as a quick, non-invasive test that could catch diseases in their early stages

The team tested breath samples from more than 1,400 patients and identified 13 chemicals found in eight types of cancers, Crohn's disease, Parkinson's disease, pulmonary hypertension and other diseases. Each of those volatile organic compounds is present in varying amounts, forming a distinctive "fingerprint" for each ailment. "These odor signatures are what enables us to identify the diseases using the technology that we developed," says research lead Prof. Hossam Haick.
To pick up the presence and ratio of the chemicals, the team built an "artificially intelligent nanoarray" called the Na-Nose. It uses specific sensors, like one made from gold nanoparticles and another that uses a network of carbon nanotubes, to sense the different compounds. The data is then analyzed by an artificial intelligence system, which takes into account age, gender and other factors, picking out the right affliction 86 percent of the time.
That's not enough accuracy for clinical diagnosis, but it could eventually be used as a routine test to catch diseases in their early phases when they're much more treatable. "For example, in the case of lung cancer we can increase the survival rate from 10 to 70 percent by early diagnosis," Haick said in a video (above). It could even be used to identify people who aren't sick yet, but have a higher risk than others for certain conditions. Moreover, Haick adds, "it is available without the need for invasive and unpleasant procedures, it's not dangerous, and you can sample it again and again if necessary."

Via: Quartz

Source: ACS Nano

In this article: AI, Breathalizer, BreathTest, Cancer, Disease, medicine, Nanoparticles, science, VolatileCompounds

 

Stroke inertia

No, not the amount of time it takes after standing up before you take a step. Which your therapist should have a protocol to solve.  The frozen in time and place inertia of our stroke medical professionals and fucking failures of stroke associations doing nothing to solve ANY of the problems in stroke.  Proven by not acknowledging the 88% failure rate of tPA for full recovery yet continuing to push tPA as the complete solution. I don't know how to get thru to them. Screaming on this blog is not doing one damn bit of good except to make me feel better.  With 10 million survivors a year screaming at their doctors for solutions that could easily cause some movement. But YOU have to scream at your doctor, don't accept their dumbed down recovery goals. 100% recovery is the only goal.

Altered bacterial communities in the gut could be an indicator for Parkinson’s disease

You better hope your doctor has the skills to diagnose this early enough and has the protocols to prevent Parkinsons.

Parkinson’s Disease May Have Link to Stroke

Altered bacterial communities in the gut could be an indicator for Parkinson’s disease

29 August 2017 Université du Luxembourg

Parkinson’s disease is an insidious disease: by the time it manifests as the typical motor dysfunctions such as tremors or muscle rigidity, portions of the brain have already been irreversibly destroyed. By this stage, the disease will have often begun already decades earlier. In search of an early portent of the disease, researchers led by Prof. Paul Wilmes, head of the Eco-Systems Biology Group at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg, may now have found one in the gut: they have shown that the bacterial community in the gut of Parkinson’s patients differs from that of healthy people even at a very early stage of the disease. The researchers present their results in the scientific journal “Movement Disorders”.
Experts have long been discussing the notion that Parkinson’s disease originates far outside the brain. According to the “dual hit” hypothesis, a hitherto unknown pathogen intrudes into the body through two ports of entry: the nose or the gastrointestinal tract. Once there, it sets a pathological process in motion, above all the misfolding of the protein alpha-synuclein. This is a protein whose exact function remains unknown. Among other things, it is presumed to be involved in the excretion of messengers such as dopamine. The misfolding of this protein could propagate through the nerve pathways, where – decades later – it produces the typical clumping in the dopaminergic cells, known as Lewy bodies, that are characteristic of Parkinson’s. Ultimately, nerve cells start to die off and the typical symptoms of Parkinson’s disease appear.
The researchers led by Wilmes, together with physicians Prof. Brit Mollenhauer and Prof. Wolfgang Oertel and their teams in Göttingen, Kassel and Marburg, explored the question of whether the early events in the course of the disease also change the bacterial community, the microbiome, at the two possible ports of entry. They took samples from the nose and gut of 76 Parkinson’s patients and 78 healthy control people who are taking part in a long-term study. They also examined the microbiome of 21 subjects diagnosed with iRBD, Idiopathic Rapid-Eye-Movement Sleep Behaviour Disorder. People with this sleep disorder have a greatly elevated risk of developing Parkinson’s disease later in life.
It turned out that the bacterial community of the gut differed considerably between all three groups. “Parkinson’s patients could be differentiated from healthy controls by their respective gut bacteria,” explains the first author Dr. Anna Heintz-Buschart from the Eco-Systems Biology Group. And the majority of the differential bacteria showed similar trends in the iRBD group. For example, certain germs were more prevalent in one group while the count was lower in others. In the samples from the subjects’ nasal cavities, however, the researchers found no such differences. The study also revealed that certain gut microbes are associated with non-motor Parkinson’s symptoms, for example depression.
“We hope that, by comparing the groups, we will learn to better understand the role of the microbiome in the process of the disease and to find out what changes occur and when,” Paul Wilmes explains. “This might deliver new starting points for early treatment of the disease. It would also be essential knowledge for one day being able to use the absence or presence of certain bacteria as a biomarker for early detection of the disease.”
Apart from the LCSB researchers, scientists from the Paracelsus-Elena-Klinik in Kassel, the Department of Neurology of Philipps Universität in Marburg, and the Departments of Neurology and Neuropathology of the University Medical Center Göttingen were involved in the study. The work was supported by the Luxembourg Rotary Club under its “Espoir en tête” programme, by the Luxembourg National Research Fund (FNR) and the German Research Foundation (DFG).

• Full bibliographic informationAnna Heintz-Buschart, Paul Wilmes et al. The nasal and gut microbiome in Parkinson's disease and idiopathic rapid eye movement sleep behaviour disorder; in: Movement disorders : official journal of the Movement Disorder Society; DOI: 10.1002/mds.27105

Large scale study shows slow walking pace is good predictor of heart-related deaths

What is your doctors protocol to get you walking at a brisk pace? I can do it but using the Trendelenburg gait and popping of the left knee.  That took years to accomplish and a few falls.  Hopefully those years of slow walking didn't leave me with a heightened risk of dying from heart problems.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=178448&CultureCode=en

29 August 2017 Leicester, University of

A team of researchers at the NIHR Leicester Biomedical Research Centre, UK - a partnership between Leicester’s Hospitals, the University of Leicester and Loughborough University - has concluded that middle-aged people who report that they are slow walkers could be at higher risk of heart disease compared to the general population.
The data analysed was collected between 2006 and 2010 by the UK Biobank from nearly half a million middle-aged people across the UK. 420,727 people were included in the research because they were free from cancer and heart disease at the time of collecting their information.
The study is published in the European Heart Journal.
In the following 6.3 years after the data was collected there were 8598 deaths with the sample population being studied: 1654 from cardiovascular disease and 4850 from cancer.
Professor Tom Yates, a Reader in Physical Activity, Sedentary Behaviour and Health at the University of Leicester and Principal Investigator for the study, said: “Our study was interested in the links between whether someone said they walked at a slow, steady or brisk pace and whether that could predict their risk of dying from heart disease or cancer in the future.
“Slow walkers were around twice as likely to have a heart-related death compared to brisk walkers. This finding was seen in both men and women and was not explained by related risk factors such as smoking, body mass index, diet or how much television the participants in the sample watched. This suggests habitual walking pace is an independent predictor of heart-related death.
“We also found that self-reported walking pace was strongly linked to an individual’s objectively measured exercise tolerance, further suggesting walking pace is a good measure of overall physical fitness. Therefore, self-reported walking pace could be used to identify individuals who have low physical fitness and high mortality risk that would benefit from targeted physical exercise interventions.”
The research team also analysed actual handgrip strength as measured by a dynamometer to see if it was a good predictor of cancer or heart-related deaths. Handgrip strength appeared to be only a weak predictor of heart-related deaths in men and could not be generalised across the population as a whole.
Associations between self-reported walking pace and handgrip strength and cancer-related deaths were not consistent.
The paper, ‘Association of walking pace and handgrip strength with all-cause, cardiovascular, and cancer mortality: a UK Biobank observational study’ was published on 21 August 2017 in the European Heart Journal.

Magnetic stimulation of the brain improved awareness of subject's own cognitive abilities

Usefulness in stroke? We'll never know since we have NO strategy to update and NO leadership to execute that strategy. You're screwed along with your children and grandchildren.
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29 August 2017 Aalto University

Researchers at Aalto University and the University of Helsinki have succeeded for the first time ever in affecting metacognition of a tactile working memory task by combining neural pathway imaging and magnetic stimulation of the brain. Understanding brain function might help in the development of new treatments for neuropsychiatric illnesses in the future.
By combining different brain research methods in a versatile manner the researchers showed for the first time that transcranial magnetic stimulation of the brain targeting the prefrontal cortex can improve a test subject's ability to evaluate his or her performance in a tactile working memory task. The ability of human subjects to monitor and control their own cognitive processes is called metacognition.
Metacognition is important for people and in many neuropsychiatric illnesses, it is possible to recognize that it has weakened.
‘The patient's reduced sense of being ill is familiar from conditions such as Alzheimer's disease, schizophrenia, and traumatic brain injury. Understanding the brain function of healthy test subjects could help in the development of new treatment methods for neuropsychiatric illnesses in the future,’ says Doctoral Candidate Juha Gogulski.
Safe method
Transcranial magnetic stimulation refers to a method in which the nerve cells of the brain are activated from outside the skull with the help of a magnetic field. When used correctly the method is safe, and it is utilized in procedures such as pinpointing the location of the primary motor cortex or the speech area before brain surgery, and in the treatment of depression.
Taking part in the study as test subjects were 14 healthy volunteers. They first underwent structural magnetic resonance imaging (MRI) of the brain as well as a diffusion MRI that is sensitive to the movement of water molecules in the brain, making it possible to identify the direction of neural pathways. After the MRI, the neural pathway connections between the primary somatosensory cortex and the prefrontal cortex were determined for each individual.
In the last part of the study the test subjects completed working memory tasks in which they were asked to keep in mind the characteristics of touch sensations from the fingertip and to evaluate whether or not the touch stimulation that was just given was similar to or different from the previous stimulus. During the test they were given magnetic pulses to prefrontal cortex areas that had a neural pathway connection to the part of the somatosensory cortex representing the index finger. The test subjects also evaluated how certain they were about their answers, on which basis calculations were made on how well a person's own evaluation corresponded to the actual performance level.
Magnetic stimulation of the prefrontal cortex improved the test subjects’ evaluation of their performance, as they were able to assess more accurately if their answers had been correct or incorrect.
The study was a collaboration between the Department of Neuroscience and Biomedical Engineering at Aalto University, and Department of Physiology in the Faculty of Medicine, University of Helsinki. The original article was published in the prestigious international science journal Cerebral Cortex.
Article: https://academic.oup.com/cercor/article/4096366/Neural-Substrate-for-Metacognitive-Accuracy-of
http://www.aalto.fi/en/current/news/2017-08-29-004/

• Full bibliographic informationNeural Substrate for Metacognitive Accuracy of Tactile Working Memory
  Juha Gogulski, Rasmus Zetter, Mikko Nyrhinen, Antti Pertovaara, Synnöve Carlson
  Cerebral Cortex, https://doi.org/10.1093/cercor/bhx219
  Published: 28 August 2017

Why a Diabetes Drug Could Help in Parkinson’s Disease

You may need this, but you probably have to educate your doctor on this. What is your doctors protocol on preventing Parkinsons? No protocol, call the hospital president and ask why such incompetency exists in their hospital.

Parkinson’s Disease May Have Link to Stroke

http://www.alphagalileo.org/ViewItem.aspx?ItemId=178436&CultureCode=en

29 August 2017 Universitaet Tübingen

A diabetes drug might help in certain types of Parkinson’s disease, reports a team of German brain researchers headed by Dr. Julia Fitzgerald at the Hertie Institute for Clinical Brain Research, the University of Tübingen and the German Center for Neurodegenerative Diseases in Tübingen. The neuroscientists identified a protein that plays an important role in the energy balance of cells. If the protein is missing, the energy balance is disturbed leading possibly to cell death and ultimately to the onset of the disease. In Parkinson’s disease, nerve cells die off in a brain area responsible for movement control. Using cell cultures, the research team has now shown that the diabetes drug metformin acts on the energy budget, thereby protecting the cells. The study has been published in the current issue of the journal Brain.
“When studying cells from a patient suffering from Parkinson’s disease we saw that they lack an important protein which regulates the energy production,” explains Fitzgerald. As a result, the cells keep on producing energy in their mitochondria — the cells’ powerhouses — unchecked and less regulated. Energy production comes at the cost of the generation of free oxygen radicals. The radicals damage the cell and lead to aging and, in the long term, sometimes to cell death. “The diabetes drug acts like a brake in this process. It slows down the uncontrolled generation of energy, thereby protecting the cells from the negative effects,” the researcher reports.
The study by the Tübingen neuroscientists provides another indication that diabetes drugs might have a positive influence on certain types of Parkinson’s disease. “Only recently, an Anglo-American research collaboration showed that another diabetes drug can reduce movement disorder symptoms in patients with Parkinson’s disease,” says Fitzgerald. The new findings of Fitzgerald and her colleagues contribute to the development of personalized medicine which aims at treating the disease with interventions tailored to the underlying individual trigger factor in each patient. In Parkinson’s disease, both hereditary predisposition and environmental influences play a role in the development of the disease. “Ultimately, the cause varies from person to person,” explains Fitzgerald. “In the long term, our study will be beneficial to patients suffering from faulty energy production in cells.” At present, there are no drugs available that may stop or slow down Parkinson’s disease, physicians may only treat symptoms. Worldwide, there are about 10 million people affected by the disease.

Attached files

• Cells imaged in an electron microscope. A mitochondrion of one cell is highlighted in red. Copyright: Hartwig Wolburg / Universität Tübingen
  

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• Full bibliographic informationFitzgerald et al. (2017): Metformin reverses TRAP1 mutation-associated alterations in mitochondrial function in Parkinson’s disease. Brain 140(9), pp 2444–2459. doi: 10.1093/brain/awx202

Researchers identify a common genetic variant linked to muscle pains in statin users

In case you get muscle pain from statins. Of course no real solution is provided, just switch to something else.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=178364&CultureCode=en

28 August 2017 European Society of Cardiology (ESC)

• Under embargo until 29 August 2017 23:05 GMT

People who have been prescribed statins to lower their cholesterol levels sometimes complain of muscle aches and pains and therefore stop taking their medication in the belief that it is causing their symptoms. This puts them at higher risk of developing diseases of the heart and blood vessels which the statins had been prescribed to prevent.
Now, researchers have found that there is a common variant in a gene that predisposes people to developing muscle aches, regardless of whether they are taking statins. However, they also found that there is a genetic sub-group of people who have a higher risk of statins-induced muscle aches.
The findings, which are published today (Wednesday) in the European Heart Journal [1], open the possibility of screening people for this and other genetic variations to identify those who are most likely to have an adverse reaction to statins and who could be prescribed an alternative drug. Those genetically predisposed to muscle aches could be forewarned about the possibility of developing symptoms and be closely monitored.
Previous research had found that a genetic variant of the LILRB5 (leukocyte immunoglobulin-like receptor subfamily-B member 5) gene was associated with lower levels of enzymes called creatine phosphokinase (CK) and lactate dehydrogenase (LDH). These enzymes are released from injured muscle tissue. Raised CK levels are often taken as clinical confirmation of adverse muscle-based reactions to statin therapy. This suggested to the researchers that the LILRB5 variant could be involved in muscle-related symptoms; they hypothesised that the variant would reduce the risk of muscle-based symptoms, while the more common form of the gene, seen in 60% of the Caucasian population, might increase risk.
In this current study, an international team led by researchers at the University of Dundee’s Ninewells Hospital and Medical School (Dundee, UK) looked at the association between the LILRB5 variant and statin intolerance. They selected statin users who had not been adherent to their therapy and then divided them into two groups: the first in which patients had raised CK levels (general statin intolerance), and the second in which patients were intolerant to the lowest approved dose of a statin before switching or discontinuing therapy (low dose intolerance). This was done because some patients do not necessarily show the expected raised CK levels, but do experience muscle aches.
Among 11,912 Scottish statin users taking part in the Genetics of Diabetes Audit and Research, Tayside Scotland (GoDARTS) study, the researchers found that the likelihood of statin intolerance was increased in patients who carried two identical copies of the common form of the LILRB5 gene; there was a two-fold increased risk of general statin intolerance and a 1.4-fold increased risk of low dose intolerance after taking into account important factors that could affect the results, such as the patients’ use of other medications, type of statin and its dosage, diabetes status, age and sex.
These results were replicated when the researchers examined two other studies, one of a more severe type of intolerance, statin-induced myopathy (or muscle disease), in 661 patients (229 cases and 432 controls) from centres in Sweden and the UK; and the other was an international clinical trial to evaluate the efficacy of a statin called rosuvastatin in 8,749 patients from 26 countries who developed muscle aches. A meta-analysis of these studies and of a third one, in which no significant effect could be seen, showed that patients with two copies of the common form of the gene had 1.3-fold increased risk of suffering adverse effects associated with statin intolerance compared to those without identical copies.
In the international clinical trial, the researchers could determine how many patients receiving statin therapy developed muscle aches, as opposed to those who were given placebo. Statins were not associated with an increased risk, while the common form of the LILRB5 gene was clearly associated with an overall increased risk of muscle aches. However, true statin-specific muscle aches could only be observed in patients who had one or both copies of the variant form of the gene, which would normally have protected them from muscle aches that were not caused by statins.
The leader of the research team, Professor Colin Palmer from the University of Dundee, said: “We found that there are people in the general population who carry a genetic factor that predisposes them to muscle aches. If these people are put on statins, they might discontinue their medication in the erroneous belief that it is the statin that is making their muscles ache. At the same time, we observed that there is a genetic sub-group of patients who are susceptible to statin-specific muscle ache, although at this stage we don’t understand the mechanism responsible for this effect.
“This means that it would be possible to test prospective statin users for key genetic variants, including LILRB5, to prevent people being put on statins if they are likely to have an adverse reaction to them. Adverse reactions are the driving reason for therapy cessation, which puts the patient at an increased risk of a cardiovascular event. This is the first time a genetic variant thought to be involved in the repair and regeneration of muscles has been found to be associated with this side effect.”
The researchers say further work needs to be done to confirm exactly how the genetic variant is involved in the repair of muscles. “All we know as facts are that the immune system is involved in the repair and regeneration of muscles, that our gene (LILRB5) is involved in the immune system, and, more specifically, that people with two identical copies of the genetic variant have lower expression of a key factor, called Foxp3, that enables the mechanism by which the immune system repairs muscle cells. So, we have a strong hypothesis for the involvement of our gene in the process of muscle repair and recovery,” said Dr Moneeza Siddiqui, the first author of the study.
Statins are the first choice for doctors who need to lower cholesterol in patients to prevent or treat heart and blood vessel diseases. However, between approximately 7-29% of users complain of muscle aches. For people who cannot tolerate statins, alternative treatments include ezetimibe and a new class of drugs called PCSK9-inhibitors.

• Full bibliographic information[1] “A common missense variant of LILRB5 is associated with statin intolerance and myalgia”, by Moneeza K. Siddiqui et al.
  European Heart Journal. doi:10.1093/eurheartj/ehx324

Poor sleep is associated with ischaemic heart disease and stroke

What is your doctors' sleep protocol?  Does taking sleeping pills count as good sleep?  Hospital nurses were handing them out every night for stroke survivors. 
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26 August 2017 European Society of Cardiology (ESC)

• Under embargo until 29 August 2017 12:00 GMT

Poor sleep is associated with ischaemic heart disease and stroke, according to research presented today at ESC Congress.1 The observational study in nearly 13 000 people revealed different patterns of sleep disturbance between the two conditions, with ischaemic heart disease being linked to shorter sleep and brief moments of waking up.
“Poor sleep is associated with cardiovascular diseases such as ischaemic heart disease and stroke but the kind of sleep disturbances that are most risky is not well documented,” said lead researcher Dr Nobuo Sasaki, of the Hiroshima Atomic Bomb Casualty Council, Japan.2,3 “‘Poor sleep’ includes too short or too long sleep, difficulty falling asleep, and difficulty maintaining sleep.”
This study investigated the association between sleep disturbances and cardiovascular disease. It also aimed to clarify possible differences in sleep disturbances between ischaemic heart disease and stroke.
The study included 12 876 residents of Hiroshima, Japan (6 762 men and 6 114 women, average age 68 years) who were registered for an annual health check. Of those, 773 patients had a history of ischaemic heart disease (myocardial infarction and/or angina), 560 patients had a history of stroke (intracranial haemorrhagic and/or cerebral infarction), and 11 543 had no cardiovascular disease. Patients with both ischaemic heart disease and stroke, or another type of cardiovascular disease, were excluded from the study.
Sleep habits were assessed with the Pittsburgh Sleep Quality Index (PSQI), a 19-item self-reporting questionnaire which yields seven component scores. C1 assesses subjective poor sleep quality, C2 long sleep latency, C3 short sleep duration, C4 low sleep efficiency, C5 difficulty in maintaining sleep, C6 use of sleeping pills, and C7 daytime dysfunction. Each component is ranked 0, 1, 2, or 3, with a score ≥ 2 defining sleep disturbance (except C6 score ≥ 1).
A sum of the seven scores was used to calculate the global PSQI score which ranged from 0 to 21. Higher scores indicated poorer sleep quality, and ‘poor sleep’ was defined as a global PSQI score ≥ 6.
Rates of ‘poor sleep’ and component sleep disturbances are shown in figures A and B. Poor sleep occurred in 52%, 48%, and 37% of patients with ischaemic heart disease, stroke, and no cardiovascular disease, respectively.
After adjusting for confounding factors (table) ‘poor sleep’ was significantly associated with ischaemic heart disease (odds ratio [OR], 1.71; p <0.0001) and stroke (OR, 1.45; p <0.0001). Component analysis revealed that subjective poor sleep quality (C1), long sleep latency (C2), low sleep efficiency (C4), and use of sleeping pills (C6) were significantly associated with both ischaemic heart disease and stroke. Difficulty maintaining sleep (C5), short sleep duration (C3), and daytime dysfunction (C7) were associated only with ischaemic heart disease (table).
Dr Sasaki said: “The proportion of people suffering from sleep disturbances is around 1.5-fold higher among patients with previous ischaemic heart disease or stroke compared to those with no history of cardiovascular disease.”
“Interestingly only patients with ischaemic heart disease reported difficulty maintaining sleep and short sleep duration,” he continued. “Difficulty maintaining sleep reflects an increase in sleep fragmentation, which refers to brief moments of waking up and causes overactivity of the sympathetic nervous system and adrenocortical axis.”4
Dr Sasaki concluded: “Our results support the hypothesis that sleep deterioration may lead to cardiovascular disease. Poor sleep in patients with ischaemic heart disease may be characterised by shorter sleep and brief moments of waking up.”
https://www.escardio.org/The-ESC/Press-Office/Press-releases?hit=wireag

Attached files

• Figure A: Poor sleep Proportion of poor sleep in ischaemic heart disease (IHD), stroke, and non-cardiovascular disease (CVD) populations. Poor sleep was defined as a global Pittsburgh Sleep Quality Index score of 6 or more.
  

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• Figure B: Sleep components Proportions of subjective sleep quality (C1), long sleep latency (C2), short sleep duration (C3), low sleep efficiency (C4), difficulty maintaining sleep (C5), use of sleeping pills (C6), and daytime dysfunction (C7) in ischaemic heart disease (IHD), stroke, and non-cardiovascular disease (CVD) populations. Each type of disturbed sleep was defined as a score ≥ 2 (except C6 score ≥ 1).
  

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• Table. Multiple logistic regression analysis for IHD or stroke Data adjusted for age, gender, body mass index, smoking, alcohol intake, and presence of hypertension, diabetes, and dyslipidaemia.
  

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• Full bibliographic information1The abstract “Poor sleep and cardiovascular disease: different pattern of sleep disturbance in ischemic heart disease and stroke” will be presented during ESC Congress 2017:
  • The press conference Living longer: tips and tricks on Sunday 27 August from 9:00 to 10:00.
  • Poster session 7: Prevention general on Tuesday 29 August from 14:00 to 18:00 in the Poster Area.
  
  2Cappuccio FP, et al. Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies. Eur Heart J. 2011;32:1484–1492.
  
  3Sivertsen B, et al. Insomnia as a risk factor for ill health: results from the large population-based prospective HUNT Study in Norway. J Sleep Res. 2014;23:124–132.
  
  4Chouchou F, et al. Sympathetic overactivity due to sleep fragmentation is associated with elevated diurnal systolic blood pressure in healthy elderly subjects: the PROOF-SYNAPSE study. Eur Heart J. 2013; 34:2122–2131.