The University of Manchester has pledged to match the funding awarded by the BHF, taking the total investment in cardiovascular disease research at the University to £8 million.

Researchers at the University welcomed the announcement. Professor Bernard Keavney, BHF Professor of Cardiovascular Medicine at the University of Manchester, said: “This is a landmark moment for cardiovascular research in Greater 91ֱ��. We’re thrilled that the progress we have made in our research at The University of Manchester in recent years has been recognised with this award, alongside other top-ranking institutions nationally.

“We will focus particularly on science that will meet the needs of those who suffer disproportionately from cardiovascular disease because they are disadvantaged – be that by socio-economic status, race or ethnicity, geography or genetics. We are determined that this award will lead to positive health changes for our local population in the North West – who suffer the worst rates of cardiovascular illness and death in England – as well as nationally and internationally.”

Prof Keavney , will lead the Centre of Excellence at the University, along with Professor Maciej Tomaszewski from the University of Manchester.

The funding will support the university to cultivate a world-class research environment that encourages collaboration, inclusion and innovation, and where visionary scientists can drive lifesaving breakthroughs.

The award from the BHF is part of a much needed £35 million boost to UK cardiovascular disease research from the British Heart Foundation. The funding comes from the charity’s highly competitive Research Excellence Awards funding scheme. The award to the University of Manchester will support researchers to:

• Discover the reasons why some babies are born with heart problems (congenital heart disease) and find ways in which these problems could be better predicted, potentially avoided, and treated when they occur in families.
• Better understand the genetic drivers of high blood pressure, kidney disease, diabetes and other chronic conditions.
• Provide new insights into the causes and consequences of heart failure and identify new potential treatment strategies.
• Uncover the links between inflammation and inflammatory diseases (such as certain types of arthritis) and the higher risk of cardiovascular disease and stroke these patients carry and find ways to break these links.
• Use Artificial Intelligence on largescale datasets to identify how we can better identify and prevent disease in patients with cardiovascular diseases, including those suffering from other conditions such as cancer.

Professor Bryan Williams, Chief Scientific and Medical Officer at the British Heart Foundation, said: “We’re delighted to continue to support research at the University of Manchester addressing the biggest challenges in cardiovascular disease. This funding recognises the incredible research already happening at the university and will help to cement its status as a global leader in the field.

“With generous donations from our supporters, this funding will attract the brightest talent, power cutting-edge science, and unlock lifesaving discoveries that can turn the tide on the devastation caused by heart and circulatory diseases.”

Research Excellence Awards offer researchers greater flexibility than traditional research funding, allowing scientists to quickly launch ambitious projects that can act as a springboard for larger, transformative funding applications.

The funding also aims to break down the silos that have traditionally existed in research, encouraging collaboration between experts from diverse fields. From clinicians to data scientists, biologists to engineers, the funding will support universities to attract the brightest minds, nurture new talent and foster collaboration to answer the biggest questions in heart and circulatory disease research.

The University of Manchester received a £1 million Accelerator Award from the BHF in 2019 to enable the university to develop its cardiovascular research programme. This funding has supported research that will lay the foundations for future breakthroughs, including:

• Development of a biodegradable gel that could help to . Researchers showed that the gel can be safely injected into the beating heart to act as a scaffold for cells to grow into new heart tissue. They hope that it could form a new generation of treatments to repair damage caused by a heart attack.
• Identifying how high blood pressure causes the small arteries in the brain to become constricted, reducing the blood flow through them and increasing the risk of developing vascular dementia. The mechanism could be the target of new drugs to prevent vascular dementia.
• Providing new biological insights into high blood pressure by studying the genes that influence differences in blood pressure in the kidney, the key organ controlling blood pressure. This work identified opportunities to repurpose drugs currently used for other conditions to better treat high blood pressure.

Its recent successful funding bid will now support the university to take the next steps towards internationally recognised excellence in cardiovascular disease research.

The news offers hope that doctors may one day be able to investigate suspected kidney pathologies without carrying out invasive procedures such as biopsies, raising the tantalising prospect of earlier and simpler disease detection.

The impact of late detection of kidney disease can be severe and can lead to serious - and sometimes life threatening - complications.

The team led by University of Manchester scientists measured the levels of approximately 20,000 genes in each cellular sediment sample of urine using a technique called transcriptomics.

The British Heart Foundation-funded study benefited from access to the world's largest collection of human kidney samples collected after surgery or kidney biopsy conducted before transplantation, known as the Human Kidney Tissue Resource, at The University of Manchester.

They extracted both DNA and RNA from each sample and connected information from their analysis, together with data from previous large-scale analyses of blood pressure (called genome-wide association studies), using sophisticated computational methods.

Transcriptomics allows scientists to understand which genes are turned on or off in different situations so they can understand how cells respond to changes in their environment.

Such molecular-level understanding enhances the precision and effectiveness of diagnostic approaches, potentially improving patient care and outcomes.

The study, published in Nature Communications today (19/03/24) also showed that low levels of a specific gene in the kidney is likely to be one of the causes of high blood pressure.

The gene, called ENPEP, is an important part of the hormonal system which is essential for regulation of blood pressure, by making an enzyme called aminopeptidase A.

It was one of 399 genes identified by the researchers whose levels in the kidney are also causally related to either increasing or decreasing in blood pressure.

The study was led by Chair of Cardiovascular Medicine at The University of Manchester and Honorary Consultant Physician at 91ֱ�� University NHS Foundation Trust.

He is also Integrative Cardiovascular Medicine Co-Theme Lead at the National Institute for Health and Care Research (NIHR) 91ֱ�� Biomedical Research Centre (BRC), which supported the research.

He said: “This study shows that using cutting-edge technology we are able to combine different unique datasets together using genetics as a connector.

“One of the most exciting findings of that is we discover how cells harvested from urine have the potential to provide a glimpse into the molecular operation of the human kidney.

“That gives us an exciting avenue of research for non-invasive diagnostic testing.”

He added: “Persistent high blood pressure—or hypertension—can increase the risk of a number of serious and potentially life-threatening health conditions, such as heart disease, heart attacks and strokes.

“Our results also show that the gene ENPEP in the kidney is a new promising target for development of new blood pressure lowering medications.

“There are several classes of effective antihypertensives available, though the last new medication approved for management of high blood pressure was over a decade and a half ago.

“While for some people, they are effective, side effects make it difficult for others to take over the long term. That is why we need more choice.”

Professor Bryan Williams, Chief Scientific and Medical Officer at the British Heart Foundation, said: “There is a well-known link between the heart and the kidneys in regulating blood pressure. This study uses cutting-edge scientific techniques to analyse genes present in kidney cells that are normally expelled in the urine. Analysing these cells could reveal which genes may be playing a key role in people with high blood pressure, and could potentially offer clinicians a new, non-invasive way to help diagnose those with kidney disease early on.

“High blood pressure is a major risk factor for heart disease and stroke, and this research has identified a gene called ENPEP that regulates important enzymes in the kidney that could be a promising target for blood pressure-lowering drugs. This study has demonstrated the power in using large sets of data and in doing so, shows how funding research like this can help us to improve treatment for people with high blood pressure.”

The paper Genetic imputation of kidney transcriptome, proteome and multi-omics illuminates  new blood pressure and hypertension targets  is available . The DOI for the paper is 10.1038/s41467-024-46132-y

The Atrial Fibrillation Ambassadors in the Community project was named Provider Collaboration of the Year in the Health Service Journal annual awards held last week (Thursday 18 November.)

"For me – the personal gain is just ONE person who is positive and is referred to their GP for investigation which will hopefully minimise the effect of AF on their lives," volunteer ambassador Wendy Westoby said. "It never ceases to amaze me how people generally aren’t aware of how to check their own pulse rate and rhythm." 

Wendy is currently volunteering as a patient representative on the Trial Steering Group of Professor Craig Smith’s CHOSEN trial- which is looking at oral health interventions in the early days after Stroke.

He  is a Professor of Stroke Medicine at The University of Manchester and a clinician at Salford Royal Foundation Trust, working  within the Division of Cardiovascular Sciences and the Geoffory Jefferson Brain Research Centre.

The AF Ambassador role was created by the Innovation Agency in partnership with the Stroke Association to prevent strokes – saving lives and avoiding life-changing disabilities. Using portable ECG devices to identify people who may have atrial fibrillation (AF) – an irregular heartbeat which can lead to a life-threatening stroke - volunteers were recruited to help spot friends, colleagues and relatives at particular risk.

It is estimated that in the North West Coast region there are over 20,000 people who have AF. The initiative is predicting to identify over 1,000 new cases of atrial fibrillation during the initial two year campaign which could prevent up to 34 strokes and save more than £750,000 in associated health care costs.

"This award is truly a team effort and I am really proud of our work and the AF ambassadors," Debbie Parkinson, public involvement lead for the Innovation Agency said: "Detecting AF, helping prevent stroke and saving lives is thanks enough, but this award will help us make more people aware and understand the importance of #knowyourpulse."

Dr Phil Jennings, chief executive of the Innovation Agency, said: "This is a fantastic achievement and richly deserved. It’s great to see this team who have worked relentlessly often in their own time to receive recognition - well done!"

The Innovation Agency-led work to proactively manage patients with asthma in Knowsley was also shortlisted in the Primary Care Innovation of the Year category which was won by a palliative care phone service operated in Cambridgeshire.

Comedian and presenter Sue Perkins, along with HSJ editor Alastair McLellan announced the winners of 23 categories at the culmination of a process that had involved two judging stages,136 judges and 1,008 entries.

“I’d like to offer my congratulations to the Innovation Agency," Alastair McLellan said. "It is always so inspirational to see projects adapting, developing and improving their services for the benefit of patients across the country."

Caption for image:  Sue Perkins with the Innovation Agency team at trhe HSJ awards

Results from a large clinical trial indicate that patients with rheumatoid arthritis are likely to experience the same level of cardiovascular benefits from statins as other individuals, without additional risks. The findings appear in , an official journal of The American College of Rheumatology.

The paper’s lead author is Professor George Kitas of Dudley Group NHS Foundation Trust, while co-senior authors are Professor Jill Belch of the University of Dundee and Professor Deborah Symmons of the University of Manchester.

Patients with rheumatoid arthritis have an approximately 50 percent higher risk of experiencing cardiovascular events such as heart attack and stroke compared with the general population. By lowering LDL cholesterol, statins are known to help prevent cardiovascular events in certain high-risk individuals, but it’s unclear whether they are safe and effective for patients with inflammatory conditions such as rheumatoid arthritis.

To investigate the potential risks and benefits of statins in moderate risk patients with rheumatoid arthritis, researchers designed the Trial of Atorvastatin for the Primary Prevention of Cardiovascular Events in Patients with Rheumatoid Arthritis (TRACE RA), a multi-center, randomized, double-blind trial comparing the statin atorvastatin with placebo.

The trial included 3,002 patients with rheumatoid arthritis who were over aged 50 years or had rheumatoid arthritis for more than 10 years, without clinical atherosclerosis, diabetes, or myopathy. Patients were randomized to receive atorvastatin 40mg daily or placebo.

During a median follow-up of 2.5 years, 1.6 percent of patients who received atorvastatin and 2.4 percent of patients receiving placebo experienced cardiovascular death, heart attack, stroke, transient ischemic attack, or any arterial revascularization. After adjustments, there was a 40 percent lower risk of cardiovascular events for patients taking atorvastatin, although the difference was not statistically significant. This was because the overall rate of events was low.

At the end of the trial, patients taking atorvastatin had significantly lower LDL cholesterol as well as significantly lower levels of C-reactive protein, a marker of inflammation, compared with patients taking placebo. Adverse events in the atorvastatin and placebo groups were similar.

The paper’s lead author is Professor George Kitas of Dudley Group NHS Foundation Trust, while co-senior authors are Professor Jill Belch of the University of Dundee and Professor Deborah Symmons of the University of Manchester.

“The trial found that the statin reduced levels of cholesterol by similar amounts as has been seen in other populations studied. The results also show that it is as safe for patients with rheumatoid arthritis to take statins as for the general population,” said Prof. Symmons. “In addition, because of the low overall rate of cardiovascular events in the trial population, there is no indication for all patients with rheumatoid arthritis to be prescribed a statin. This is unlike diabetes where the great majority of patients are recommended to take a statin.”

The study authors recommend that patients with rheumatoid arthritis be prescribed statins according to national or local guidelines for managing cardiovascular risk in the general population.

An accompanying editorial notes that the study provides information that will be useful for researchers and clinicians who focus on rheumatoid arthritis, and the results may be helpful when considering cardiovascular risk across other rheumatic diseases.

“Trial of Atorvastatin for the Primary Prevention of Cardiovascular Events in Patients with Rheumatoid Arthritis (Trace Ra): A Multicenter, Randomized, Placebo Controlled Trial.” George D. Kitas, Peter Nightingale, Jane Armitage, Naveed Sattar, Jill J.F. Belch, and Deborah P.M. Symmons, on behalf of the TRACE RA consortium. Arthritis & Rheumatology; Published Online: April 15, 2019 (DOI: 10.1002/art.40892) is published .

A study by scientists at The University of Manchester and the Karolinska Institute in Sweden has found a link between the humble beetroot and blood pressure regulation in pregnant women.

Twenty women at Saint Mary’s hospital, 91ֱ��, with moderately high blood pressure were given a daily 70ml beetroot juice shot - which is naturally rich in nitrate - over 8 days.

Most of the women experienced increases in their blood nitrate and nitrite levels, two to three hours after taking the drink.

A second group of 20 women taking a placebo beetroot drink, which had the nitrate removed, did not experience any changes in blood nitrate or nitrite levels.

The study, published in the journal , was funded by Tommy’s, the British Heart Foundation and the NIHR.

Overall, there was no significant difference in blood pressure change between the nitrate and placebo groups.

However, in the women drinking the nitrate-rich beetroot juice there was a significant relationship between the change in plasma nitrite and the change in diastolic blood pressure - the pressure when your heart is resting between beats - 2-3 hours after drinking the juice shot.

Nitrate obtained from the diet is transformed in the body to nitrite and ultimately nitric oxide, which is linked to healthy blood vessels.

Lead author said: “Research already shows that the likely primary functional component in beetroot is inorganic nitrate, and that supplementation in non-pregnant adults with dietary nitrate can reduce blood pressure.

“It is definitely too early to say whether nitrate supplementation in the form of beetroot juice could be a potential solution to blood pressure control in pregnant women.

“But we did find differences between women in blood nitrite levels in response to nitrate-rich beetroot juice, which are likely related to the activities of bacteria in the mouth that turn nitrate into nitrite.

“Research from a number of other groups has shown that bacteria in the mouth play a key part in the transformation of nitrate to nitrite, and may determine whether an individual could benefit from dietary nitrate supplementation to lower blood pressure.

“Understanding this biology better could have important implications in our hunt for sustainable ways to intervene in the cycle which regulates blood pressure.

“Our next step will be to investigate the role of the bacteria that live in the mouth in determining blood pressure regulation in pregnancy, and how that links to the ability of nitrate supplementation to lower blood pressure.”

Consultant obstetrician Dr Jenny Myers, from The University of Manchester and Saint Mary’s Hospital said: “Women with increased blood pressure are at increased risk of developing pre-eclampsia, and all the associated dangers of this such as poor growth of the baby in the womb, preterm delivery and maternal seizures.

“So if there are indeed benefits of having nitrate in their diet, it might have implications on the development of treatments for pregnant women with high blood pressure.”

Scientists from The University of Manchester have discovered how the severity of trauma to arterial blood vessels governs how the body repairs itself.

says the discovery could have major implications on how complications from vascular surgeries are prevented and treated.

Their discovery, published in , shows how with minor surgical trauma caused by procedures such as angiography, stenting, arterial lines and minor surgery, vessels heal by the rapid division of smooth muscle cells – the most important layer in the blood vessel wall, which controls and regulates blood flow.

With more invasive surgical trauma such as aortic aneurysm repair, bypass grafting, transplantation, and reconstructive microsurgery, it is the fibrous outer layer of adventitial cells which take on the role of healing the vessel.

Using the pioneering gene editing technique CRISPR, the team also discovered the gene called ‘Mcam’ which makes smooth muscle cells more immature.

“The fact that vessels have a completely different response according to whether the trauma is severe or minor, has important implications to the way we may think about vascular surgery, “said Dr Roostalu.

Co-author and Reconstructive Plastic Surgeon, Dr Jason Wong said: “This research provides us with a fundamental understanding of how our surgical repair influences the cells that contribute to healing, and perhaps needs us to rethink how we repair blood vessels.

“If we can derive new techniques or develop new strategies that are less traumatic to arteries, or develop drugs and compounds that promote specific cell recruitment, we may be able to influence healing and hence clinical outcomes – this could have major implications on how we ensure safer and more successful surgical procedures.”

According to the scientists, in minor trauma the smooth muscle cells divide rapidly and create a thick wall which may occlude the artery, prompting the need for more surgery to prevent occlusion or thrombosis.

In major trauma, however, the smooth muscles die, leaving behind collagen rich vascular wall that is recolonized by immature adventitial cells.

The team have also discovered the origin of smooth muscles that make up the large arteries. These cells arise by primitive cells that colonize the blood vessel walls in early embryonic development and within two to three days divide extensively to generate the ancestors of all the smooth muscle cells that exist in the mature blood vessel.

The team noticed a small number of original immature cells remaining at points in arterial vessels where they branch.

Dr Roostalu said: “Using special genetically engineered mice we have pioneered an approach to study the origin and maturation of arterial smooth muscle. In these transgenic mice, primitive and immature smooth muscle is brightly lit by red and green fluorescent marker proteins. When the cells in blood vessels mature the red marker is turned off, leaving mice with brightly green fluorescent aorta.

“So when we noticed ‘red’ cells remaining at the parts where aorta branches, we were surprised and intrigued. These branching points are often subject to cardiovascular disease. The discovery of a unique cell population here might lead to a better understanding of what makes vascular branching points susceptible to diseases and how this can be prevented.”