Category: Cardiovascular Disease

Categories : Cardiovascular Disease Diseases, Syndromes and ConditionsTags :

Even Modest Drop in Kidney Function is Linked to Greater Health Risks

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A Canadian study of more than 8 million adults suggests that even a modest loss of kidney function is associated with increased health risks. The study, published in The BMJ, could lead to better approaches to prevent chronic kidney disease and related conditions, particularly in younger adults.

“The dogma is that healthy, young adults don’t need to worry about kidney function unless it drops to around 50% of the normal level, but our research suggests that even a more modest 20–30% drop may have consequences and we may want to have earlier conversations about prevention and monitoring,” explained senior author Dr Manish Sood at the University of Ottawa.

The research team used health records from 2008 to 2021 for every Ontario, Canada adult aged 18–65 who had at least one blood test for kidney function, but no history of kidney disease. They found that 18% of those in the 18–39 age group had kidney function that was modestly below normal levels, but not low enough to be diagnosed with chronic kidney disease. Individuals in this ‘grey zone’ faced a modestly increased risk of kidney failure, death and cardiovascular events.

For example, in young adults (age 18–39), a 20–30% loss in kidney function was associated with a 1.4-fold increase in death, 1.3-fold increase in a cardiac event and a 6-fold increase in the risk of kidney failure. The absolute risk of any of these events was still low at less than 2 per 1000.

“Thankfully, the absolute risk for any one individual with kidney function in this grey zone is low, but when we look at the whole population, the impact could be quite significant,” said co-senior author Dr Greg Knoll, senior scientist, nephrologist and Head of the Department of Medicine at The Ottawa Hospital and the University of Ottawa. “We need further research to confirm these findings and then see if we can reduce the risk through lifestyle modification.”

While the blood creatine test for kidney function is relatively inexpensive and readily available, the researchers are not suggesting routine testing for all individuals at this time. However, if an individual has had a kidney test that shows a modest reduction in function, it could prompt consulting health care provider. All individuals can also reduce their risk of kidney disease by eating a healthy diet with lower salt, exercising regularly and limiting alcohol intake.

Dr. Sood and his colleagues previously developed the Project BigLife Chronic Kidney Disease calculator to help individuals calculate their kidney disease risk and see the impact of lifestyle changes. The calculator will continue to be refined as new research arises.  

Source: EurekAlert!

Categories : Cardiovascular DiseaseTags :

Repurposed Cancer Drug Might Treat Cardiac Arrhythmias

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Ruxolitinib, a drug that is already approved by the U.S. Food and Drug Administration (FDA) for treating certain cancers and skin conditions, is effective at inhibiting CaMKII, a protein kinase linked to cardiac arrhythmias.

In a new study published in Science Translational Medicine, researchers invented a new reporting technique to monitor activity of CaMKII while screening the effects of nearly 5000 FDA-approved drugs on human cells that expressed the enzyme. The screen identified five previously unknown CaMKII inhibitors; ruxolitinib, which is used to treat cancers of the blood and bone marrow, along with skin conditions like atopic dermatitis and vitiligo, was the most effective.

CaMKII, or Calcium and calmodulin-dependent protein kinase II, is critical to cardiomyocytes, the muscle cells of the heart, where it maintains the balance of calcium. Activation of CaMKII helps facilitate rapid changes in heart activity, such as initiating a fight-or-flight response in the body. Overactivation can lead to impaired heart function and cell death, which can in turn lead to poor heart health outcomes like arrhythmia.

CaMKII is perhaps best known, however, for its role in the brain, where it is believed to play key roles in learning and memory. This has slowed the development of CaMKII inhibitors to treat arrythmia, for fear they could impact cognitive function.

“Finding an FDA approved drug means that millions of people have been taking CaMKII inhibitors, and in the case of ruxolitinib, there are no reported major problems with the brain,” said Mark Anderson, MD, PhD, a senior author of the paper. “That should give pharma and biotech companies confidence that they could carry out development of a CaMKII inhibitor program, because the biggest obstacle seems to be surmountable.”

The research began in Anderson’s lab at Johns Hopkins University Oscar Reyes Gaido, the study’s first author and an MD-PhD student in the lab, developed a new tool to measure activity of CaMKII in living cells. He started with a protein called green fluorescent protein (GFP), originally derived from jellyfish, that emits green light. He then engineered the GFP tag to detect CaMKII activation, making a new reporter called CaMKAR (CaMKII Activity Reporter). When this reporter was inserted into human heart cells, it helpfully glowed bright green whenever CaMKII became active, allowing researchers to monitor enzyme activity.

“This biosensor will be very useful for studying how CaMKII activity changes in both healthy and pathological contexts. Existing methods can measure CaMKII activity, but they lack the versatility and resolution to track in real time and with high sensitivity,” Reyes Gaido said. “This has been a real obstacle for studying enzyme biology in general, so this gives the field an important new tool.”

Using this tool, the researchers conducted a drug repurposing screen to test the effects of 4,475 approved compounds on cultured human cardiomyocytes. This identified five previously unknown CaMKII inhibitors: ruxolitinib, baricitinib, silmitasertib, crenolanib, and abemaciclib. Of the five, ruxolitinib was the most effective at inhibiting CaMKII activity in cell and mouse models of CaMKII-driven arrhythmias. A 10-minute application of the drug was enough to prevent catecholaminergic polymorphic ventricular tachycardia (CPVT), a congenital source of pediatric cardiac arrest, and rescue atrial fibrillation, the most common clinical arrhythmia. Crucially, the mice treated with ruxolitinib did not show any adverse cognitive effects when they were tested with memory and learning tasks.

Anderson said that new drugs based on ruxolitinib could be used in several ways to treat heart conditions. One would be what he called the “pill in a pocket” scenario. In the early stages of atrial fibrillation, people could take the medication occasionally as symptoms arise. Patients with CPVT are often resistant to standard treatments, and a ruxolitinib-based treatment could provide another option. Finally, there is evidence that inhibiting CaMKII during a heart attack can prevent heart muscle from dying, so emergency responders could potentially administer such a drug as part of standard practice.

“There’s been a long search for fundamental pathways that could be targets for therapeutics in arrhythmias,” Anderson said. “This could be a finding that will translate relatively rapidly into people now since it’s already been proven to be safe in humans.”

Source: University of Chicago

Categories : Cardiovascular DiseaseTags :

Restoring the Integrity of the Blood–Brain Barrier

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Source: CC0

A new paper published in Nature Communications describes a treatment that restores intercellular signalling and which could be instrumental in restoring the barrier’s normal function. Key to the process is ‘frizzled’, a key protein receptor implicated in blood-brain abnormalities.

When the blood-brain barrier isn’t working properly, a variety of conditions can crop up. Barrier-invading cancer cells can develop into tumours, and multiple sclerosis can occur when too many white blood cells slip pass the barrier, leading to an autoimmune attack on the protective layer of brain nerves, hindering their communication with the rest of the body.

“A leaky blood-brain barrier is a common pathway for a lot of brain diseases, so to be able to seal off the barrier has been a long sought-after goal in medicine,” said senior author Calvin Kuo, MD, PhD, professor of hematology.

Methods of repairing the blood-brain barrier remain understudied, according to Kuo. But the recent paper he and colleagues led describes a possible treatment.

“We have evaluated a new therapeutic class of molecules that can be used to treat a leaky blood-brain barrier; previously, there were no treatments directed at the blood-brain barrier specifically,” Kuo said.

The researchers started their quest by looking at WNT signalling, a communication pathway used by cells to promote tissue regeneration and wound healing. WNT signalling helps maintain the blood-brain barrier by promoting cell-to-cell communication that lines brain blood vessels.

“There’s a lot of historical data that indicated that the WNT signalling pathway would be important for maintaining the blood-brain barrier,” Kuo said. “The opportunity arose to test a novel WNT signalling pathway that would turn on signalling in the blood-brain barrier by binding very selectively to a receptor called frizzled.”

Scientists have been focusing on ‘frizzled’, a protein receptor that initiates the WNT pathway, for blood-brain barrier therapies since mouse mutations in the frizzled gene cause blood-brain barrier abnormalities.

How it’s made

Many different molecules bind to frizzled protein receptors, so to narrow their search for a potential therapeutic molecule, the researchers selected only those that specifically target cells that line the brain’s blood vessels.

Chris Garcia, PhD, a professor of molecular and cellular physiology as well as the Younger Family Professor, developed prototype therapeutic WNT pathway molecules in the lab, including a molecule that activates the frizzled receptor FZD4. Building off of the work of Garcia and Kuo, collaborators at a research company created L6-F4-2, a FZD4 binding molecule that activates WNT signalling 100 times more efficiently than other FZD4 binders.

When the team, including Jie Ding, a research scientist and the lead author of the paper, activated WNT signaling at a higher rate, they saw an increase in blood-brain barrier strength.

Keeping the barrier up

The researchers wanted to study what happens when the natural molecular key for frizzled is missing, and whether it can be replaced successfully with L6-F4-2. So they turned to Norrie disease, a genetic abnormality that results in a leaky blood-retinal barrier.

The blood-retinal barrier performs the same function for the eye as the blood-brain barrier does for the brain. In Norrie disease, the development of blood vessels of the retina is hindered, resulting in leaky blood vessel connections, improper development and blindness.

Norrie disease results from mutations in the NDP gene, which provides instructions for making a protein called Norrin, which is the key that fits the lock of the FZD4 receptor and turns it on. In the study’s mice, the gene is inactivated, and the key is missing causing a leaky barrier and blindness. The scientists replaced the missing Norrin protein with L6-F4-2, which they call a surrogate.

When L6-F4-2 replaced the missing Norrin protein, the blood-retinal layer was restored in the mice. Researchers knew this because they imaged the blood vessels and found them to be denser, and less leaky, than before treatment. Scientists also showed that, for the blood-brain barrier surrounding the mice cerebellum L6-F4-2 replaced Norrin and activated WNT signalling.

Next, the researchers wanted to study a more common human condition — ischemic stroke (in which blood vessels and the blood-brain barrier are damaged, and fluid, blood and inflammatory proteins involved in cellular communication can leak into the brain. They found that L6-F4-2 reduced the severity of stroke and improved survival of mice compared with mice that had untreated strokes. Importantly, L6-F4-2 reversed the leakiness of brain blood vessels after stroke. Mice treated with L6-F4-2 had increased stroke survival, compared to those that were not treated.

The finding shows that, in mice, the blood-brain barrier could be restored by drugs that activate FZD receptors and the WNT signalling pathway.

Because a variety of disorders have their origin in blood-brain barrier dysfunction, Kuo is excited about the treatment potential for a variety of other neurological diseases, such as Alzheimer’s, multiple sclerosis and brain tumours.

“We hope this will be a first step toward developing a new generation of drugs that can repair the blood-brain barrier, using a very different strategy and molecular target than current medications,” Kuo said.

Source: Stanford Medicine

Categories : Cardiovascular Disease GastrointestinalTags :

IBD Patients Have an Increased risk of Ischaemic Stroke

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Credit: American Heart Association

In a nationwide Swedish study of more than 85 000 patients with biopsy-confirmed inflammatory bowel disease (IBD), researchers saw an increased risk of stroke, especially ischaemic stroke, compared to the general population. The results are published in Neurology.

IBD is a chronic intestinal disease with a relapsing-remitting manner, including Crohn’s disease (CD), ulcerative colitis (UC), and IBD-unclassified. Prior studies have suggested that IBD patients have a greater risk of thromboembolic events, but evidence for long-term risk of stroke remains scarce. A recent postmarketing safety study on tofacitinib, a new drug approved for IBD treatment, found an increased stroke risk.

The researchers, from Karolinska Institutet and Örebro University (Sweden), conducted a cohort study by linking a nationwide histopathology cohort (the ESPRESSO study) to national healthcare registers in Sweden to explore whether patients with a biopsy-confirmed IBD had an increased long-term risk of stroke compared to their IBD-free siblings or the general population.

During an average follow-up of 12 years, 3720 of IBD sufferers had a stroke (32.6/10 000 person years), compared with 15 599 of the IBD-free people (27.7/10 000 person-years). When accounting for other factors, such as heart disease, hypertension and obesity, they found that people with IBD were 13% more likely to have a stroke than those without IBD. The risk stayed elevated even 25 years after IBD diagnosis, equating to one additional stroke case per 93 IBD patients. The excess risk was mainly driven by ischaemic stroke rather than haemorrhagic stroke.

The risk for ischaemic stroke was significantly increased across all IBD subtypes (ie, CD, UC, and IBD-U). Sibling comparison analyses confirmed the main findings, suggesting the excess risk of stroke may be independent of familial factors.

Clinical implications

“Due to the excess risk of stroke in IBD patients, screening and management of traditional stroke risk factors in IBD patients could be more urgent to prevent fatal CVD complications”, says first author Jiangwei Sun, postdoc at the Department of Medical Epidemiology and Biostatistics.

“These findings highlight the need for clinical vigilance about the long-term excess risk of cerebrovascular events in IBD patients”, adds last author Jonas F Ludvigsson, professor at Karolinska Institutet and pediatrician at Örebro University Hospital.

Source: Karolinska Institutet

Categories : Ageing Cardiovascular DiseaseTags :

Long-term Daily Aspirin Use in Older Adults Increases Anaemia Risk

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A new study analysing data from the landmark ASPREE trial has found that long-term daily aspirin use increases the risk of anaemia by 20% in people mostly aged 70 and over. The results, which are published in Annals of Internal Medicine, have prompted researchers to suggest considering regular monitoring for anaemia in older adults taking low-dose aspirin. In addition, they should discuss any concerns about their health or medications with their GP.

Anaemia is commonly experienced by older adults, potentially affecting overall function and increasing fatigue, disabilities, depressive symptoms and cognitive problems.

The Monash University-led study followed 18 153 initially healthy older adults in Australia and the USA and recorded incidents of anaemia over an average 4.7 years.

It was the largest study to investigate anaemia in older people as part of a randomised controlled trial, ASPREE (ASPirin in Reducing Events in the Elderly) – with half the participants taking a placebo and the other half a daily low dose (100mg) of aspirin.

The risk of developing anaemia was found to be 20% higher in the aspirin group compared to those in the placebo group.

In addition to a higher risk of anaemia, blood tests revealed a faster decline of haemoglobin and reduced ferritin (a protein that carries iron) levels in the aspirin group compared to the placebo group.

Lead author, Associate Professor Zoe McQuilten from Monash University, said that while bleeding was a known side-effect of aspirin, few previous studies had looked at the effect of prolonged aspirin use on the progressive development of anaemia in older adults.

“This study gives a clearer picture of the additional risk of becoming anaemic with aspirin use and the impact is likely to be greater in older adults with underlying diseases, such as kidney disease,” Associate Professor McQuilten said.

Associate Professor McQuilten said the new data gave doctors insight into the risk of anaemia from prolonged aspirin use by their older patients. “Older adults are more likely to become anaemic generally and now doctors can potentially identify patients at higher risk of developing anaemia,” she said.

Associate Professor McQuilten urged patients to follow the advice of their doctor about their daily use of aspirin. She cautioned that for some older adults, aspirin was recommended as a valuable therapy to prevent recurring heart attacks or stroke. “Patients should not change their aspirin regimen without speaking to their GP,” she said.

Source: Monash University

Categories : Cancer Cardiovascular DiseaseTags :

Some Antihypertensives might Boost the Effectiveness of Cancer Immunotherapy

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A study reported in the latest issue of Nature has shown that some molecules previously used to treat hypertension might also help the immune system to better target cancer cells. The researchers believe that these findings could eventually be applied to significantly improve the effectiveness and applicability of cancer immunotherapy.

“Immunotherapy today can effectively fight only 30% to 40% of cancers,” said Benoît Van den Eynde, at the Ludwig Institute for Cancer Research, co-director of the de Duve Institute and professor of Tumour Immunology at the University of Oxford. “Many cancers are resistant, largely because their T lymphocytes are not reactive enough. We discovered that drugs once used to treat hypertension could have a very interesting effect in combating these forms of immunotherapy-resistant cancers.”

T lymphocytes are active components in the immune system, recognising and destroying cells that appear foreign. Cancer cells, however, are not foreign and are therefore often not recognised and attacked by T lymphocytes. But about thirty years ago, Thierry Boon and his colleagues at the former Brussels Branch of the Ludwig Institute for Cancer Research at the de Duve Institute discovered specific markers on the surface of cancer cells – tumour antigens – that can be recognised by T cells that then destroy the cancerous cells.

This work paved the way for cancer immunotherapy, a treatment approach that helps T cells destroy cancerous cells. Thanks to T cells’ specificity and memory of tumour antigens, immunotherapy makes it possible to treat advanced cancers with some success. It is now used worldwide. However, such therapies are not equally effective in all patients or against all types of cancer.

In the current study, a team led by Jingjing Zhu in Van den Eynde’s laboratory shows that anti-hypertensive drug-molecules known as α2-adrenergic receptor (α2AR) agonists also influence the behaviour of macrophages. While doing that job, macrophages also alert T cells of any abnormalities they encounter, presenting suspicious antigens to the cells to trigger a possible immune response.

Zhu, Van den Eynde and colleagues discovered that alongside their known hypotensive and anaesthetic effects, α2AR agonists can also stimulate macrophages in their role as sentinels, making T cells more reactive and more effective at rejecting cancer cells. The effect extended, most notably, to cancer models that are resistant to standard immunotherapy. This suggests the new approach could boost the efficacy of clinical immunotherapy, even for the many types of cancer that are largely unresponsive to such interventions.

These findings also present a rationale for the development of new molecules that might be used in combination with immunotherapy to improve its efficacy.

“One could imagine using existing blood pressure-lowering drugs,” said Van den Eynde. “But that would be quite risky, owing to the undesired effects and the toxicity of these drugs at the necessary doses. Another approach would be to develop new molecules that would act in the same way on macrophages but would not have the unwanted toxic effects. We have already made significant progress in this direction.”

Source: Ludwig Cancer Research

Categories : Ageing Cardiovascular DiseaseTags :

Oestrogen Pills may Increase Hypertension Risk

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Women ages 45 years and older taking oral oestrogen pills were more likely to develop hypertension than those using transdermal or vaginal formulations, according to new research published in Hypertension.

Less oestrogen and progesterone is produced in a woman’s body after menopause, which may increase the risk for cardiovascular diseases including heart failure, according to the American Heart Association.

Hormone therapy may be prescribed to relieve symptoms of menopause, in gender-affirming care and in contraception. Previous studies have found that some hormone therapies may reduce cardiovascular disease risk in menopausal women under 60 years of age or for whom it has been fewer than 10 years since menopause. The authors of this study noted that while hypertension is a modifiable risk factor for cardiovascular disease, the potential effects of different types of hormone therapy on blood pressure in menopausal women remain uncertain. 

“We know oestrogens ingested orally are metabolised through the liver, and this is associated with an increase in factors that can lead to higher blood pressure,” said lead study author Cindy Kalenga, an MD/PhD-candidate at the University of Calgary. 

“We know that post-menopausal women have increased risk of high blood pressure when compared to pre-menopausal women, furthermore, previous studies have shown that specific types of hormone therapy have been associated with higher rates of heart disease,” Kalenga said. “We chose to dive deeper into factors associated with hormone therapy, such as the route of administration (oral vs non-oral) and type of oestrogen, and how they may affect blood pressure.”

This study involved a large group of over 112 000 women, ages 45 years and older, who filled at least two consecutive prescriptions (a six-month cycle) for oestrogen-only hormone therapy, as identified from health administrative data in Alberta, Canada between 2008 and 2019. The main outcome of high blood pressure (hypertension) was identified via health records.

First, researchers investigated the relationship between route of oestrogen-only hormone therapy administration and risk of developing high blood pressure at least one year after starting the treatment. The 3 different routes of hormone therapy administration were oral (by mouth), transdermal and vaginal application. Additionally, researchers evaluated the formulation of oestrogen used and the risk of developing high blood pressure. For this study, the researchers reviewed medical records of individuals taking oestrogen-only hormone therapy. The two most common forms of oestrogen used by study participants were oestradiol – a synthetic form of oestrogen closest to the naturally produced form – and conjugated equine oestrogen, an animal-derived form of oestrogen and the oldest type of oestrogen therapy.

The analysis found:

  • Women taking oral oestrogen therapy had a 14% higher risk of developing high blood pressure compared to those using transdermal oestrogen and a 19% higher risk of developing high blood pressure compared to those using vaginal oestrogen creams or suppositories. After accounting for age, a stronger association was seen among women younger than 70 years of age compared to women older than 70.
  • Compared to estradiol, conjugated equine estrogen was associated with an 8% increased risk of developing high blood pressure.

Taking oestrogen for a longer period of time or taking a higher dose was associated with greater risk of high blood pressure, the authors noted. According to Kalenga, the study’s findings suggest that if menopausal woman take hormone therapy, there are different types of oestrogen that may have lower cardiovascular risks.

“These may include low-dose, non-oral oestrogen – like oestradiol, in transdermal or vaginal forms – for the shortest possible time period, based on individual symptoms and the risk–benefit ratio, Kalenga said. “These may also be associated with the lowest risk of hypertension. Of course, this must be balanced with the important benefits of hormone therapy, which include treatment of common menopausal symptoms.”

The average age of natural menopause among women worldwide is about 50 years of age. Current evidence supports that initiating menopausal hormone therapy in the early stages may have cardiovascular benefits, though not in the late stages of menopause, according to the American Heart Association’s 2020 Statement on Menopause Transition and Cardiovascular Disease Risk: Implications for Timing of Early Prevention. Previous studies have found that menopausal hormone therapy may help relieve symptoms of menopause, including hot flashes, night sweats, mood changes or sleep disturbances.

Limitations included being based only on medical records, not including women younger than the age of 45 and not collecting data about hysterectomies or menopausal status (which was inferred by taking oestrogen after 45).

The authors will be conducting more research investigating combined oestrogen and progestin, as well as progestin-only formulations of hormone therapy and their impact on heart and kidney diseases.

Source: American Heart Association

Categories : Ageing Cardiovascular DiseaseTags :

Ischaemic Heart Disease in the Elderly Linked to Increased Dementia Risk

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Older people with ischaemic heart disease have an increased long-term risk of dementia and accelerated cognitive decline. Recent research in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association suggests that the heart, the brain, and cognitive function are all connected in the ageing process. Appropriate prevention and treatment of ischaemic heart disease in older people might reduce the burden of dementia, the researchers suggest.

The researchers regularly followed a cohort of 2568 older people aged 60 years or older, without dementia at baseline and living in Stockholm, from 2001–2004 through 2013–2016. Heart diseases at the study entry were ascertained via clinical examination and linkage to the Swedish National Inpatient Register. Dementia status and cognitive function during the follow-up period were diagnosed and assessed regularly following the standard approaches.

“We used statistical methods to link ischemic heart disease at the study entry to an increased risk of dementia and a faster decline in cognitive function during the follow-up period”, says Chengxuan Qiu, at the Department of Neurobiology, Care Sciences and Society, Division of Aging Research Center (ARC) and one of the authors of the study.

Explore cognitive trajectories

Future works should explore cognitive trajectory following the onset of ischemic heart disease and further investigate to what extent medical treatments of ischemic heart disease may affect cognitive decline and dementia onset.

The SNAC-K project on which this study is based is supported by the Swedish Ministry of Health and Social Affairs. This study is supported by additional grants from the Swedish Research Council (VR), FORTE and STINT.

Categories : Cardiovascular DiseaseTags :

A Super-cheap Smartphone Accessory for Blood Pressure Monitoring

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Photo by Ivan Samkov on Pexels

Engineers have developed a simple, low-cost clip that uses a smartphone’s camera and flash to monitor blood pressure at the user’s fingertip. The clip works with a custom smartphone app and currently costs about $0.80 to make. The researchers estimate that the cost could be as low as $0.10 apiece when manufactured at scale. The technology was described in the journal Scientific Reports.

Researchers say it could help make regular blood pressure monitoring easy, affordable and accessible to people in resource-poor communities. It could benefit older adults and pregnant women, for example, in managing conditions such as hypertension.

“We’ve created an inexpensive solution to lower the barrier to blood pressure monitoring,” said study first author Yinan (Tom) Xuan, an electrical and computer engineering PhD student at University of California San Diego.

“Because of their low cost, these clips could be handed out to anyone who needs them but cannot go to a clinic regularly,” said study senior author Edward Wang, a professor of electrical and computer engineering at UC San Diego and director of the Digital Health Lab. “A blood pressure monitoring clip could be given to you at your checkup, much like how you get a pack of floss and toothbrush at your dental visit.”

Another key advantage of the clip is that it does not need to be calibrated to a cuff.

“This is what distinguishes our device from other blood pressure monitors,” said Wang. Other cuffless systems being developed for smartwatches and smartphones, he explained, require obtaining a separate set of measurements with a cuff so that their models can be tuned to fit these measurements.

“Our is a calibration-free system, meaning you can just use our device without touching another blood pressure monitor to get a trustworthy blood pressure reading.”

To measure blood pressure, the user simply presses on the clip with a fingertip. A custom smartphone app guides the user on how hard and long to press during the measurement.

The clip is a 3D-printed plastic attachment that fits over a smartphone’s camera and flash. It features an optical design similar to that of a pinhole camera. When the user presses on the clip, the smartphone’s flash lights up the fingertip. That light is then projected through a pinhole-sized channel to the camera as an image of a red circle. A spring inside the clip allows the user to press with different levels of force. The harder the user presses, the bigger the red circle appears on the camera.

The smartphone app extracts two main pieces of information from the red circle. By looking at the size of the circle, the app can measure the amount of pressure that the user’s fingertip applies. And by looking at the brightness of the circle, the app can measure the volume of blood going in and out of the fingertip. An algorithm converts this information into systolic and diastolic blood pressure readings.

The researchers tested the clip on 24 volunteers from the UC San Diego Medical Center. Results were comparable to those taken by a blood pressure cuff.

“Using a standard blood pressure cuff can be awkward to put on correctly, and this solution has the potential to make it easier for older adults to self-monitor blood pressure,” said study co-author and medical collaborator Alison Moore, chief of the Division of Geriatrics in the Department of Medicine at UC San Diego School of Medicine.

While the team has only proven the solution on a single smartphone model, the clip’s current design theoretically should work on other phone models, said Xuan.

Next steps include making the technology more user friendly, especially for older adults; testing its accuracy across different skin tones; and creating a more universal design.

Source: University of California San Diego

Categories : Cardiovascular Disease ExerciseTags :

Strong Legs Reduce Risk of Heart Failure after Heart Attack

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People with strong legs are less likely to develop heart failure after a heart attack, according to new research. Myocardial infarction is the most common cause of heart failure, with around 6–9% of heart attack patients going on to develop the condition. Previous research has shown that having strong quadriceps is associated with a lower risk of death in patients with coronary artery disease.

Presented at Heart Failure 2023, a scientific congress of the European Society of Cardiology (ESC), this study tested the hypothesis that leg strength is associated with a lower risk of developing heart failure after acute myocardial infarction. The study included 932 patients hospitalised in 2007 to 2020 with acute myocardial infarction who did not have heart failure prior to the admission and did not develop heart failure complications during their hospital stay. The median age was 66 years and 753 participants (81%) were men.

Maximal quadriceps strength was measured as an indicator of leg strength. Patients sat on a chair and contracted the quadriceps muscles as hard as possible for five seconds. A handheld dynamometer attached to the ankle recorded the maximum value in kg. The measurement was performed on each leg and the researchers used the average of both values. Strength was expressed relative to body weight, meaning that quadriceps strength in kg was divided by body weight in kg and multiplied by 100 for a % body weight value. Patients were classified as ‘high’ or ‘low’ strength according to whether their value was above or below the median for their se

The median value for women was 33% body weight and the median value for men was 52% body weight. A total of 451 patients had low quadriceps strength and 481 had high strength. During an average follow-up of 4.5 years, 67 patients (7.2%) developed heart failure. The incidence of heart failure was 10.2 per 1000 person-years in patients with high quadriceps strength and 22.9 per 1000 person-years in those with low strength.

The researchers analysed the association between quadriceps strength (low vs. high) and the risk of developing heart failure. The analysis was adjusted for factors known to be associated with the development of heart failure after myocardial infarction including age, sex, body mass index, prior myocardial infarction or angina pectoris, diabetes, atrial fibrillation, chronic obstructive pulmonary disease, peripheral arterial disease and kidney function. Compared with low quadriceps strength, a high strength level was associated with a 41% lower risk of developing heart failure (hazard ratio [HR]: 0.59; 95% confidence interval [CI] 0.35–1.00; p=0.048).

The investigators also analysed the association between quadriceps strength as a continuous variable and the risk of developing heart failure. Each 5% body weight increment in quadriceps strength was associated with an 11% lower likelihood of heart failure (HR 0.89; 95% CI 0.81–0.98; p=0.014).

Study author Mr. Kensuke Ueno, a physical therapist at the Kitasato University Graduate School of Medical Sciences, Sagamihara, Japan said: “Quadriceps strength is easy and simple to measure accurately in clinical practice. Our study indicates that quadriceps strength could help to identify patients at a higher risk of developing heart failure after myocardial infarction who could then receive more intense surveillance. The findings need to be replicated in other studies, but they do suggest that strength training involving the quadriceps muscles should be recommended for patients who have experienced a heart attack to prevent heart failure.”

Source: European Society of Cardiology