Category: Cardiovascular Disease

Categories : Cardiovascular DiseaseTags : Leave a comment

Study Identifies Oestrogen Receptor as Key Protector of the Right Heart in Pulmonary Hypertension

On By ModernMedia
Human heart. Credit: Scientific Animations CC4.0

Researchers at National Jewish Health have identified a key way oestrogen receptor alpha (ERα) helps protect the right side of the heart in pulmonary hypertension. The preclinical findings reveal that ERα preserves the survival and movement of endothelial cells, which line blood vessels, allowing the stressed heart to maintain the small vessels it needs to function.

The study, published online Sept. 10 in Arteriosclerosis, Thrombosis, and Vascular Biology, may help explain an important difference between women and men with pulmonary hypertension and points to a potential path for developing therapies tailored to the right ventricle, the chamber that pumps blood through the lungs.

Pulmonary hypertension causes abnormally high pressure in the blood vessels of the lungs. That pressure forces the right ventricle to work harder, and a patient’s outlook depends heavily on how well the chamber adapts. Although women are more likely to develop certain forms of pulmonary hypertension, their right ventricles often function better than those of men. Researchers have been working to understand the biology behind that apparent paradox.

“We know that the right ventricle is a major driver of survival in pulmonary hypertension, but we still have very few treatments designed specifically to protect it,” said pulmonologist Tim Lahm, MD, senior author of the study and a researcher at National Jewish Health. “These findings show that oestrogen receptor alpha is doing important work inside the blood vessels of the right heart, particularly in females, by helping endothelial cells survive, move and build the vascular network the heart needs under stress.”

Using preclinical models of pulmonary hypertension and right ventricular pressure overload, researchers examined how ERα affects the endothelial cells that line blood vessels in the right side of the heart. When normal ERα function was disrupted, these cells were less able to migrate, form vessel-like networks and maintain the capillaries needed to support the heart under increased pressure. The effects were more pronounced in females and included increased endothelial cell death, greater enlargement of the right ventricle and reduced capillary density.

Single-nucleus RNA sequencing provided additional insight into the underlying mechanisms. In females with impaired ERα function, endothelial cells showed reduced activity in pathways involved in cell movement and increased activity in pathways associated with cell death. These changes were not observed to the same degree in males, further supporting a sex-specific role for the receptor.

“A healthy network of capillaries is essential when the right ventricle is working against increased pressure,” Dr Lahm said. “By showing how ERα supports that network, this work gives us a more precise biological target to investigate.”

The findings do not establish oestrogen or ERα-targeted therapy as a treatment for patients yet, but are an important first step. Additional research is needed to confirm the mechanism in people and determine whether it can be translated into a safe and effective therapy.

Source: National Jewish Health

Categories : Cardiovascular Disease ExerciseTags :

Cardiac Rehabilitation Cuts Hospital Admissions and Heart Attack Risk

On By ModernMedia

A new Cochrane review of 107 trials shows that exercise-based cardiac rehabilitation is associated with numerous benefits and helps people return to healthier, more active lives

Photo by Barbara Olsen on Pexels

Exercise-based cardiac rehabilitation reduces hospital admissions by a third and heart attack risk by more than a quarter, as well as remaining beneficial in the long term, a new Cochrane review finds. 

The evidence also suggests that newer home-based and digitally supported cardiac rehabilitation programmes can be just as effective as traditional centre-based services. 

Coronary heart disease is the single most common cause of death globally. It can lead to chest pain, heart attacks, or stroke. Cardiac rehabilitation programmes are widely recommended following a cardiac event, with exercise recognised as a core component.  

Effective and inexpensive intervention 

The researchers, led by the University of Glasgow, analysed 107 randomised controlled trials involving 26 886 people with coronary heart disease. Most participants had experienced a heart attack, undergone heart procedures, or experienced some sort of chest pain. Women were underrepresented, making up only 17% of participants despite being included in most studies.  

The overall results show that, compared with no programme, exercise-based cardiac rehabilitation reduces heart attacks by 28%, reduces all-cause hospital admissions by 35%, and probably reduces deaths. 

Participants also reported better physical functioning, general health, vitality, social functioning, and mental wellbeing. These benefits were seen across several validated quality-of-life measures.  

“Our review shows that exercise-based cardiac rehabilitation can reduce the risk of heart attack and hospital admission while helping people return to healthier, more active lives,” says Dr Grace Dibben, lead author from the University of Glasgow.  

“Many people lose confidence after a heart attack or cardiac procedure and worry that physical activity could be dangerous,” Dr Dibben adds. “Appropriately prescribed exercise is not only safe for most patients, but can play a vital role in recovery and long-term heart health.” 

Growing evidence for modern rehabilitation models

This new update included 22 new trials featuring just under 3500 participants, incorporating more recent data into the final results. The more recent studies included participants based in low- and middle-income countries (LMICs) and tested home-based and digital cardiac rehabilitation programmes.  

“This review confirms that exercise is a great tool for improving the overall health of people with coronary heart disease,” says Professor Rod Taylor, senior author from the University of Glasgow. “By adding newer studies to this update, we’re able to see that digital programmes work as well as in-person programmes, which really changes the game here. These approaches may help us reach people who cannot attend traditional centre-based services.” 

Several studies in this update were conducted in LMICs, examining different types of exercise in different countries; for example, yoga in India and tai chi in China. The authors suggest this not only improves the relevance of the evidence base, but that some populations may find rehabilitation built around traditional and cultural forms of exercise more appealing than conventional, machine-based rehab. 

Low uptake despite evidence-backed benefits 

Despite strong evidence supporting cardiac rehabilitation, uptake remains a challenge in many healthcare systems. Various guidelines, including NICE in the UK, recognise cardiac rehabilitation as a key component following a cardiac event. However, cardiac rehabilitation continues to be widely underused with generally low participation rates. According to the 2025 National Audit of Cardiac Rehabilitation (NACR) report, the uptake of cardiac rehabilitation for patients with acute coronary syndrome was 44.5% in England and 71.3% in Wales.

The authors explain that many patients face barriers to attending traditional hospital-based programmes, including work commitments, transport challenges, and caring responsibilities. This can disproportionately impact groups like women, older adults, and deprived communities the hardest.  
 

Exercise-based cardiac rehabilitation is an inexpensive and cost-effective intervention, but right now it’s underfunded and unprioritised.

We want this option to be available to everyone. This new research shows you don’t even have to go into a rehab centre to benefit – you can participate from home and still see the benefits.

– Dr Grace Dibben, University of Glasgow.  

Categories : Cardiovascular Disease Ethics and LawTags :

Eminent Cardiologist Involved in Treatment Guidelines Received £50m from Drug Research Contracts

On By ModernMedia

Eminent cardiologist involved in treatment guidelines received £50m from drug research contracts
Case shows what’s at stake in the debate around transparency of doctor-industry relations

Source: CC0

A British cardiologist and former president of the European Society of Cardiology (ESC) has been judged by the ESC to have committed severe misconduct after a Danish TV documentary reported that he had been involved in drawing up guidelines for the use of the heart drug ivabradine (Corlanor, Procoralan) while profiting from lucrative contracts with the drug’s maker.

An investigation published by The BMJ describes how between 2006 and 2015, Kim Fox, emeritus professor of clinical cardiology at the National Heart and Lung Institute, Imperial College London, who reportedly served as cardiologist to the late Queen Elizabeth II, and his wife Karen Summers, a former drug industry executive, received more than £50m as co-directors of the UK based contract research organisation Heart Research.

This company was involved in running at least three clinical trials of ivabradine, made by French drug company Servier, that were published in the same period, reports freelance journalist, Laura Spinney.

In 2006, when Fox became president of the ESC, he chaired an ESC taskforce that published a guideline recommending ivabradine as an alternative treatment for angina in patients who couldn’t tolerate beta blockers. Authors were asked to disclose conflicts of interests, but the guideline did not publicly identify what Fox had disclosed.

As outgoing ESC president in 2008, Fox championed the drug publicly though it had failed to meet the primary endpoint in the first of the three trials Heart Research was involved in.

Ivabradine remains approved for angina and heart failure in Europe, and for heart failure in the US, but persistent doubts have been expressed over its efficacy.

It’s rare for alleged conflicts of interest to involve such large sums of money. The case remains unreported in most of Europe and beyond, even though the ESC’s guidelines are influential worldwide.

The Danish documentary, which aired in September 2024, triggered an internal review by the ESC which found that the 2006 guideline recommendations were “appropriate” and reported “no evidence to suggest a bias towards ivabradine.”

But in March 2025, the ESC ethics committee found that Fox “had failed to meet his ethical obligations and considered his behaviour as a severe misconduct.”

Pulmonologist Irène Frachon, described the sums involved in the case as “monstrous” while Rita Redberg, a cardiologist and former editor in chief of JAMA Internal Medicine, said: “It totally goes against the grain of the profession.”

Fox rejected the ethics committee’s findings and resigned his ESC membership, claiming that he had always declared any conflicts of interest and that “he was not prepared to be judged on the basis of rules and regulations described in 2024 retrospectively for activities in 2006 to 2008.”

The ESC admitted to The BMJ that its declarations process was relatively lax in the early 2000s and said that it had been substantially strengthened since. Meanwhile, Servier said that it “strictly complies” with transparency guidelines established by the European Federation of Pharmaceutical Industries and Associations, a trade body.

The Fox story has emerged at a time when some in Europe are pushing for reforms that would end voluntary declaration of conflicts of interest and enshrine greater transparency in law.

For former ESC vice president John Martin, the ESC has not done enough to restore public trust, and the recent revelations risk damaging the doctor-patient relationship while also leaving the volunteers who run the society feeling betrayed. He urged further action. “The ESC board might be seen as tacitly complicit unless there is a thorough public investigation,” he said. “Many questions remain.”

Source: The BMJ Group

Categories : Cardiovascular DiseaseTags :

Too Much Nighttime Light Alters Cardiac Structure and Function

On By ModernMedia
Photo by Cottonbro on Pexels

Exposure to light during the nighttime is linked to important and potentially harmful changes to the structure and function of the heart, according to a study of more than 11 000 people published in the European Heart Journal today (Thursday).

The research was led by Professor Lu Qi from Tulane University, New Orleans, USA. He said: “Previous observational studies have linked nighttime light exposure with a higher risk of cardiovascular disease, but little is known about the related cardiac structure and functional changes. We carried out this research to find out what happens to the heart over time when people are exposed to too much light at nighttime.”

The research included 11 071 people who are part of the UK Biobank study. All participants wore a light sensor on their wrists for seven days to measure light levels over night. Three years later, participants were given a cardiac MRI scan to carefully examine the structures and functions of the heart.

Researchers compared people who were exposed to light levels of more than three lux with people exposed to almost no light at night.

This showed that people with high exposure to nighttime light had thickening of the wall of the left ventricle (one of the chambers of the heart), reducing the space inside of the chamber. There were signs that the heart muscle’s ability to flex during a heartbeat was reduced. This is an early indicator of heart dysfunction. Researchers also found changes in the right ventricles and left atria (two other chambers of the heart).

Professor Qi said: “This is the first study of its kind, and it shows that exposure to higher levels of light at nighttime is linked to cardiac remodelling. This is where the structure and function of the heart changes and we typically see it in response to chronic stress or injury to the heart. It’s our body’s way of adapting to that stress, but ultimately it weakens the heart and can lead to heart failure.

“Light pollution has emerged as a new risk factor for cardiovascular disease. Our findings, together with evidence from other studies, suggest that reduction of nighttime light exposure should be considered as one of the potential strategies for preventing heart disease by clinicians and policy makers.”

In an accompanying editorial Professor Thomas Münzel from University Medical Center Mainz, Germany and colleagues said: “It is time for clinicians, particularly those managing patients with heart failure or atrial fibrillation, to start asking about the sleep environment: how dark the bedroom is, whether the patient works night shifts, and how much screen use occurs after sunset. The advice is simple and inexpensive: blackout curtains, warm-coloured bedside lighting, and covering the small standby LEDs on household electronics. From a public health perspective, the implications are larger still. Light pollution is one of the few environmental hazards that cities can control directly and affordably. Shielded fixtures, warm-spectrum bulbs, and dimming or motion-activated streetlights are already available, energy-efficient, and climate-friendly.

“Ultimately, this study is more than an interesting observation. It provides a crucial link between what satellites already show us, i.e. a planet glowing ever brighter at night, and the clinical reality unfolding inside our chests: hearts that are becoming stiffer, weaker, and less efficient. The relationship is biologically coherent, the effect sizes are clinically meaningful, and the dose–response is unambiguous: more light, worse outcomes. The takeaway is clear, darkness deserves recognition as a vital sign, as essential to cardiovascular health as blood pressure control and clean air.”

Source: European Society of Cardiology

Categories : Cancer Cardiovascular DiseaseTags :

Cancer Drug Reduces Atherosclerosis Inflammation and Plaque

On By ModernMedia
Source: Wikimedia CC0

A new Yale study has identified a promising therapeutic avenue for atherosclerosis, a condition caused by inflammation and plaque buildup in arteries.

Martin Schwartz, PhD, Robert W. Berliner Professor of Medicine (Cardiology) and the study’s principal investigator, investigates how the mechanical forces from blood flow and pressure affect the cells lining the arteries and how cell responses to forces contribute to cardiovascular disease. Atherosclerosis predominantly impacts regions of the arteries that bend or branch, creating disturbances in blood flow dynamics that activate cells’ inflammatory pathways and eventually lead to plaque buildup.

In a study published August 31 in Proceedings of the National Academy of Sciences, Schwartz’s team, led by associate research scientist Divyesh Joshi, PhD, has now found that a protein complex called Polycomb Repressive Complex 2 (PRC2) is associated with disturbed blood flow, and that it inhibits anti-inflammatory mechanisms in the arteries that mitigate atherosclerosis.

By blocking PRC2, the team successfully reduced harmful plaque in animal models of the disease.

“By inhibiting PRC2, we boost protective pathways that reduce inflammation and could protect people from plaque rupture in atherosclerosis,” Schwartz says.

What causes atherosclerosis?

Atherosclerotic plaques are present in nearly all adults in developed countries. They are usually asymptomatic because a protective fibrous cap forms over the plaques. But if the cap weakens and ruptures, it triggers the formation of a blood clot that can lead to a heart attack or stroke. Plaques vulnerable to rupture tend to have a thinner cap or exhibit heightened inflammation.

Scientists believe there are three types of factors driving atherosclerosis. The first are metabolic risk factors, including elevated cholesterol and blood sugar. Inflammation is another – individuals with autoimmune or other inflammatory diseases are at a higher risk for the disease.

An important but overlooked third factor, Schwartz says, is the biomechanics of blood flow through the arteries. In places where the arteries are straight tubes, the blood flow activates protective, anti-inflammatory genes. Where arteries curve sharply, disturbing blood flow, there are fewer of these protective factors and increased inflammation.

Protein complex suppresses protective genes

The cells lining the arteries, called vascular endothelial cells, have receptors that detect blood flow. Previous research in Schwartz’s laboratory has shown that blocking those receptors can inhibit inflammatory processes and enhance protective ones. In the new study, the researchers investigated the underlying mechanisms of the inflammation associated with disturbed blood flow.

First, they used previously published datasets to investigate genes that interact with anti-inflammatory genes in endothelial cells, and then identified those that promote disease. These analyses revealed that genes associated with PRC2, a protein complex that inhibits gene expression, were strongly associated with suppression of certain anti-inflammatory genes.

“PCR2 is understood to be pro-inflammatory in vascular endothelial cells,” Joshi says.

The researchers also studied gene expression in human endothelial cells exposed to normal and disturbed blood flow. These experiments confirmed that genes associated with PRC2 are upregulated during disturbed blood flow where inflammation tends to be higher.

However, when the researchers treated endothelial cells with tazemetostat, a drug that inhibits PRC2 and was previously used to treat cancer, they found that inflammatory signals were reduced. The findings suggest targeting PRC2 could be a treatment for atherosclerosis.

A new avenue for treating atherosclerosis

To explore PRC2 inhibition as a therapeutic avenue, the researchers developed animal models of the disease and tested the effects of tazemetostat. They found that the drug slowed plaque growth and reduced the amount of vulnerable plaque.

“It takes an unstable plaque and turns it into a more stable form that is no longer at risk of rupture,” Schwartz says.

Since conducting the study, the manufacturers of tazemetostat have withdrawn it from the market due to emerging evidence that patients who take the drug have a slightly increased risk of secondary cancers. But there are other PRC2-inhibiting drugs that may be similarly useful for treating atherosclerosis, the researchers note.

“This is a potential path forward to treating patients,” Schwartz says.

By Isabella Backman

Source: Yale School of Medicine

Categories : Cancer Cardiovascular DiseaseTags :

Survivors of HER2+ Breast Cancer Could Avoid Lifelong Heart Medication

On By ModernMedia
Photo by Danilo Alvesd on Unsplash

Many breast cancer survivors whose treatment caused problems with their heart function can safely stop medication after their heart recovers, finds a new study led by researchers at University College London.

The trial, which was funded by the British Heart Foundation, involved 90 women who had recovered from heart problems caused by a specific type of breast cancer treatment. Most were in their 40s and 50s and would previously have been advised to stay on heart medication for life, due to fears their heart function would decline once the drugs were stopped. 

Researchers found that 98% of the group who stopped taking their heart medication had no change in their heart function after one year, with only one woman experiencing a decline in her heart’s pumping ability.

Women who came off their medication also reported a slightly better quality of life at 12 months than those who continued, based on their scores on questionnaires designed to measure quality of life in people with heart failure. The study is published in the European Heart Journal and was presented at the European Society of Cardiology Congress in Munich.

The women in the trial will continue to be followed up over the next five years to monitor their heart health. But the researchers suggest their findings can start important conversations between survivors and their doctors about whether they need to continue treatment long-term.

Professor Charlotte Manisty (UCL Institute of Cardiovascular Science), who is also a consultant cardiologist at Barts Heart Centre and UCLH, said: “Modern breast cancer treatment is a remarkable success story. But the damaging effects of these drugs on the heart leave survivors and their doctors with difficult questions about ongoing treatment to maintain their heart health. 

“Our study provides the first evidence that heart failure therapies can be safely stopped in survivors whose hearts have recovered, with the support of ongoing close monitoring. We hope these findings will be encouraging for survivors and their doctors, giving hope for a future free from treatment.” 

These patients are usually offered targeted biological treatments such as Trastuzumab (better known as Herceptin), which attach to HER2 receptors to help block the growth and spread of cancer. But in around 10% of patients, this treatment causes problems with heart function, leaving them in need of treatment with multiple medications – such as beta-blockers and ACE inhibitors – to help recovery. Survivors are currently advised to stay on these drugs for life, even after their cancer treatment ends and their heart recovers. 

The trial involved 90 breast cancer survivors at four hospitals in the UK who started taking heart failure medication after a diagnosis of HER2-targeted therapy-related cardiac dysfunction, but whose hearts later recovered following treatment. All study volunteers were women, with an average age of 50.

Everyone in the study was randomly assigned to either gradually withdraw from their heart failure medication (46 women) or to continue taking it (44 women). They were followed closely for one year with blood tests, quality-of-life questionnaires and cardiac MRI scans to check whether their heart function had worsened.

One woman in the group that stopped their medication experienced a decline in her left ventricular ejection fraction (a measure of the heart’s pumping ability). She didn’t report any symptoms, but the decrease was picked up on an MRI scan at 12 months. Her heart function improved when she started taking their heart failure medication again. 

None of the group that continued to take their heart failure treatment saw a decline in their heart function. 

Overall, left ventricular ejection fraction remained stable in both groups (minus one per cent in the withdrawal group and minus 0.2% in the continuation group) with no significant differences between the two groups after one year (withdrawal group 55.2 per cent compared to 55.6% in continuation group). 

None of the women in the trial reported any heart failure symptoms, required hospital treatment or experienced any other heart problems during the trial.

Dr Sonya Babu-Narayan, clinical director at the British Heart Foundation and consultant cardiologist, said: “These findings will be hugely encouraging for the thousands of breast cancer survivors whose heart health has been affected by lifesaving cancer treatment. 

“The study results give hope that many women will be able to safely stop medicines once their heart has recovered. The importance of ongoing monitoring is highlighted by the one study participant whose heart scan showed her heart function deteriorated but then bounced back when her heart treatment was restarted. More research is needed and the women will be followed up for longer, but in the meantime the good news for this group of breast cancer survivors is lifelong medications after heart complications need not be the default.”

Source: University College London

Categories : Cardiovascular DiseaseTags :

Monitoring After Syncope Identifies Cardiovascular Conditions

On By ModernMedia
Source: CC0

Fitting a wearable heart monitor for 14 days when patients go to A&E (accident & emergency) with unexplained fainting improves the detection of life-threatening heart problems, a study shows.

Using the two-week monitor more than doubled the detection rate of heart rhythm problems. After one year, heart rhythm problems were identified in 22% of the monitor group compared with 9% of those who received standard care.  

The death rate after one year in the two-week monitoring group, at 1.5%, was almost half that of the standard care group, at 2.9%. 

The reduction in death rate is strong evidence that the new strategy can save lives, experts say. 

Difficult diagnosis 

Around 650 000 people visit A&E with unexplained fainting each year in the UK. Although the cause is often harmless, fainting episodes can be a sign of abnormal heart rhythms – known as arrhythmias – which can be dangerous. 

Arrhythmias in these patients are hard to diagnose. People who have fainted have usually recovered by the time they reach A&E, meaning their heart rhythm has likely returned to normal, and tests won’t show any abnormalities. 

Currently, patients with unexplained fainting are referred for tests such as a Holter monitor – a small wearable device that records the heart’s rhythm. However, a Holter monitor is usually only worn for 48 hours, so can only identify an arrhythmia in this small window.  

Patients must also attend an outpatient cardiology clinic first, meaning that monitoring is done at any point from six weeks to two years after they attend A&E.   

Earlier monitoring 

The new heart monitor is smaller – about the size of a car key fob – and is worn in the middle of the chest. It can be worn continuously for the two-week period.  

The University of Edinburgh-led research team studied 2234 people who attended UK A&E departments with unexplained fainting. Half of the study volunteers were fitted with the new monitor, while the other half received the current standard monitoring. 

Data from the monitors were sent to clinicians after the two-week monitoring period, who then determined whether their recordings showed signs of an arrhythmia and if treatment was needed. If the monitor picked up a serious arrythmia, the patient’s clinician was alerted within 24 working hours.

We were able to begin patient monitoring within 72 hours of people arriving at A&E, which is much faster than the current standard. Continuous data on a patient’s heart rhythm for two weeks is invaluable to cardiologists when they are trying to diagnose an arrhythmia. As the results show, more patients with hidden heart rhythm problems were identified, and their treatment could be sped up. 

We believe that the lower death rate seen for this group is strong evidence that this new strategy can save lives. Hopefully it will be adopted by hospitals across the country, so that fewer people with a potentially life-threatening condition slip through the net. 

 Professor Matthew ReedStudy lead and Honorary Professor of Emergency Medicine at the Usher Institute

Faster treatment 

Arrhythmias were identified in an average of 22 days in those with chest-worn monitors, compared to 54.5 days with standard care. This included life-threatening arrhythmias like complete heart block and a pause in the heartbeat of over six seconds.  

As a result of increased and quicker detection, more people who used the chest-worn monitor started treatment for their arrhythmia.  

For the monitoring group, 10.8 per cent were given anti-arrhythmic medication and 6.8 per cent had a pacemaker implanted, versus 7.3 per cent and 4.6 per cent respectively for the standard care group. 

Experts hope that the strategy will become standard practice in the NHS now it has been shown to help doctors treat dangerous heart problems and reduce death rates.

This large trial is a good example of how BHF investment in research can drive life-changing innovations in healthcare. The study shows that monitoring the heart with simple new technology after a patient has had a sudden collapse can identify potentially life-threatening disturbances in heart rhythm that can be treated to reduce risk of death. 

The results of this trial should certainly help inform future clinical practice when treating patients with sudden unexplained collapse in the future. 

 Professor Bryan WilliamsChief Scientific and Medical Officer at the British Heart Foundation

The study, funded by the British Heart Foundation, is published in the New England Journal of Medicine and being presented at the European Society of Cardiology Congress in Munich. 

Read the study in the New England Journal of Medicine 

Source: The University of Edinburgh

Categories : Cardiovascular DiseaseTags :

Research Uncovers How SGLT2 Inhibitors Restore Power in Heart Failure

On By ModernMedia

A study identifies PANK1 as a previously unknown target of SGLT2 inhibitors, revealing how the medications boost energy production and improve heart function.

Top: ribbon model of PANK1 dimer. Bottom left: zoom-in of pantothenate binding to PANK1. Bottom right: super-imposed binding of AcCoA, showing extension into the PANK1 enzymatic pocket. Credit: University of Pennsylvania

Researchers have discovered that SGLT2 inhibitors, a class of drugs originally developed to treat diabetes and now widely used for heart failure, work by activating a key enzyme that helps heart cells produce and use energy more efficiently. The study, published in Science, potentially solves a longstanding gap in knowledge about these drugs and opening the door to potential new treatments for heart failure.

The study, led by researchers in the Perelman School of Medicine at the University of Pennsylvania, found that SGLT2 inhibitors directly activate an enzyme called PANK1 in heart cells. This activation boosts production of coenzyme A (CoA), a molecule essential for converting nutrients into energy. Researchers found that increasing CoA production improved the ability of human heart cells to contract and relax, two critical functions that are impaired in heart failure.

“Our findings suggest these drugs are helping the failing heart restore its energy-producing capacity,” said senior author Zoltan Arany, MD, PhD, the Samuel Bellet Professor of Cardiology and chair of Physiology at Penn Medicine. “We identified PANK1 as a direct target of these medications and found that activating this pathway makes heart cells work better. This may explain many of the remarkable benefits patients experience with these drugs.”

Figuring out why it works

For years, physicians have known that SGLT2 inhibitors significantly reduce hospitalisations and deaths among heart failure patients, but have struggled to explain exactly why, because the drugs were designed to target the SGLT2 protein which is found in the kidneys, not the heart.

Using human heart tissue from transplant recipients and donors, the researchers found that SGLT2 inhibitors increased the heart’s ability to use multiple fuel sources, including sugars, fats, amino acids, and ketones. The drugs also increased levels of CoA, which plays a central role in cellular energy production. To identify how that happened, the team traced the effect back to PANK1, an enzyme that regulates the first and most important step in CoA production. The researchers demonstrated that the drugs physically bind to PANK1 and activate it.

“The evidence was especially compelling when we found that activating PANK1 alone reproduced many of the benefits of the drugs, while blocking the pathway largely eliminated those benefits,” said Nicholas Forelli, MD, an internal medicine resident in the Arany lab and co-author of the study. “We cannot completely rule out other contributing mechanisms, but the data strongly support PANK1 as a major driver.”

The discovery may also help explain why SGLT2 inhibitors often begin benefiting heart failure patients within days of starting treatment.

Exciting possibilities ahead

Despite years of research into these medications, the role of PANK1 had gone unnoticed. “Honestly, no one thought to look,” Arany said. “Researchers knew these drugs were doing something important in the heart, but the target responsible for those effects had remained elusive.”

The findings could have important implications for future drug development. While SGLT2 inhibitors are highly effective, they can cause side effects such as urinary tract infections, dehydration, and, in rare cases, diabetic ketoacidosis.  “One of the most exciting possibilities is developing drugs that directly target PANK1,” Arany said. “That could allow us to capture the heart benefits while potentially avoiding some of the side effects associated with current therapies. We’re actively working on that now.”

Source: Penn Medicine

Categories : Cardiovascular Disease UrologyTags :

New ESC Guidelines Recommend all Heart Disease Patients are Tested for Kidney Disease

On By ModernMedia
Chronic kidney disease (CKD). Credit: Scientific Animations CC4.0

The first-ever European Society of Cardiology Guidelines on the management of cardiovascular disease and chronic kidney disease have been developed in collaboration with the European Renal Association. The new guidelines were published online in the European Heart Journal [1] and presented at ESC Congress 2026 on 29 August.[2] 

Chronic kidney disease (CKD) is defined as the presence of abnormalities of kidney structure or function present for at least 3 months, with implications for health.[4] It has been estimated there are around 100 million people in Europe with CKD,[5] all of whom are at increased risk of a wide range of cardiovascular diseases (CVD) as a result of their kidney problem. 

“The disability and lifetime lost to each disease are profound, but CKD can accelerate CVD and vice versa, resulting in cardiovascular events and the need for dialysis much earlier in life,” said Task Force Chair, Associate Professor Kevin Damman from University Medical Centre Groningen, Netherlands. “The good news is that there have been major advances over the last few years, which mean there are now several simple treatments that can substantially lower the risk of both cardiovascular and kidney complications.” 

Task Force Chair, Professor William Herrington from the University of Oxford, UK, noted: “Many patients with CKD are treated by the cardiology community and the new ESC Guidelines aim to increase the use of kidney function and urine albumin testing in patients with CVD. With improved screening, more at-risk patients can be identified and the most appropriate treatments for both CKD and CVD can be prescribed.” 

The Task Force developed the ‘STAMP on CKD’ acronym, which stands for: Screen, Triage, Address CKD Risk, Modify CVD management and Plan health services. The first step is screening all patients with CVD at diagnosis for CKD using blood and urine tests (estimated glomerular filtration rate from blood creatinine plus urine albumin-to-creatinine ratio). A key message on triage is the accurate assessment of risk of kidney failure and accurate assessment of CVD risk using validated scoring systems that incorporate kidney function. 

Addressing risk means ensuring the early use of proven cost-effective risk-modifying therapies that have been shown to slow CKD progression and reduce the risk of cardiovascular events. “Early use of drugs called RAS inhibitors and SGLT2 inhibitors alongside statin-based therapy are particularly important and effective,” explained Associate Prof. Damman. 

The guidelines highlight key areas where modifications to CVD management are needed in the context of CKD, including recommendations for medications that are permitted in patients who may not be able to clear standard treatments from their bodies due to decreased kidney function.  

Finally, appropriate planning of health services ensures that services are set up to recognise high-risk patients and provide timely access to care from cardiologists and nephrologists. “Active and efficient communication between specialties is often necessary due to the complexities associated with CKD,” noted Prof. Herrington. “Engagement of patients and family/caregivers in the multidisciplinary care process also helps to ensure patients’ priorities are met, improve their experience and promote patient-centred care.” A version of the new guidelines for patients aims to give individuals the knowledge and confidence to be involved in shared decision-making with healthcare providers.[3] 

The Task Force Chairs concluded, “CVD and CKD are major burdens on patients, healthcare systems and society. The key messages in these guidelines should be noted by all relevant healthcare stakeholders and policymakers, and research planned to fill several gaps in the evidence. Raising awareness will help realise the hope that the guidelines will lead to important individual and societal improvement for those with, or at risk of, CVD and CKD.” 

References

[1] 2026 ESC Guidelines for the management of cardiovascular disease and chronic kidney disease. Eur Heart J. 2026. doi:10.1093/eurheartj/ehag098. 

[2] 2026 ESC Guidelines for the Management of Cardiovascular Disease and Chronic Kidney Disease presented at ESC Congress 2026 on 29 August from 13:45 to 15:00 in Munich, the Main Auditorium (Hall B3). 

[3] ESC Guidelines for the management of cardiovascular disease and chronic kidney disease: What patients need to know. Available on the Patient Versions of ESC Guidelines webpage. 

[4] Kidney Disease Improving Global Outcomes CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105:S117–S314.  

[5] GBD Chronic Kidney Disease Collaboration. Global, regional, and national burden of chronic kidney disease, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2020;395:709–733. 

Source: European Society of Cardiology

Categories : Cardiovascular DiseaseTags :

Patients are Missing out on the Cardiovascular Benefits of Antihypertensives

On By ModernMedia
Credit: Pixabay CC0

The true impact of missing doses of blood pressure-lowering medication will be demonstrated in a presentation at ESC Congress 2026.[1] 

Approximately 1.4 billion adults worldwide aged 30–79 years are estimated to have high blood pressure (hypertension),[2] one of the most significant risk factors for disease burden.[3] Despite the proven benefits of blood pressure-lowering medication in reducing cardiovascular events, around half of patients do not take them as prescribed.[4] 

“We have evidence that poor adherence to antihypertensive medication is associated with worse outcomes,[5]” explained presenter, Miss Qianqian Yang from the University of Oxford, UK. “However, previous data has come from observational studies and could be confounded by other factors. We undertook an analysis of randomised trial data to assess the true impact of adherence on the benefits of antihypertensive treatment.” 

A meta-analysis was conducted of patient-level data from 91 339 participants in nine trials where an antihypertensive regimen (intervention group) was compared with another treatment (comparator group: either placebo or a less-intensive regimen). Participants who took at least 80% of their assigned treatment were classified as having higher adherence, while those who took less than 80% were classified as lower adherence. 

“A decline in adherence over time was apparent, even in the structured setting of trials,” noted Miss Yang. Overall, the proportion of patients classified as having higher adherence was 88% in the first year and only 79% by year five. 

In patients with higher adherence, systolic blood pressure was reduced by 5.2mmHg in the intervention group vs. the comparator group. In patients with lower adherence, the reduction was only 3.0mmHg. 

Next, the researchers studied the impact of adherence on major cardiovascular disease defined as stroke, myocardial infarction or ischaemic heart disease and heart failure causing death or hospitalisation.  

The incidence of major cardiovascular disease was significantly reduced by 11% in the intervention group vs the comparator group in patients with higher adherence, but there appeared to be no significant reductions in patients with lower adherence. 

“Notably, our results reinforce the saying that ‘drugs don’t work in patients who don’t take them.’ Patients with lower adherence derived little or no cardiovascular benefit, whereas those with higher adherence had greater reductions in blood pressure and prevention of cardiovascular events,” said Miss Yang. 

According to the authors, adherence assessment and education should be more prominent in hypertension management. In addition, strategies that help improve adherence should be promoted. These include simplifying regimens, using single-pill combinations to reduce the medication burden and using longer-acting agents where the effect of an occasional missed dose is less. 

Commenting on the findings, Professor Felix Mahfoud, Chair of the ESC Communication Committee, said: “For years, we have neglected non-adherence to medication as a cause for uncontrolled hypertension. Assessment of adherence should become a routine part of hypertension care so patients do not miss out on life-saving benefits. As healthcare providers, we are here to have open, non-judgemental conversations with our patients about any barriers they may have to taking medication, to help improve adherence.” 

References

[1] ‘Adherence to antihypertensive therapy and cardiovascular outcomes: an individual participant data meta-analysis of randomised controlled trials’ presented during the New therapeutic strategies targeting renin-angiotensin-aldosterone system in hypertension session at ESC Congress 2026 on 30 August from 08:15 to 09:45 in Room Vienna (ICM). 

[2] World Health Organization, 2025. Global report on hypertension 2025-High stakes: turning evidence into action.  

[3] GBD 2023 Disease and Injury and Risk Factor Collaborators. Burden of 375 diseases and injuries, risk-attributable burden of 88 risk factors, and healthy life expectancy in 204 countries and territories, including 660 subnational locations, 1990−2023: a systematic analysis for the Global Burden of Disease Study 2023. Lancet. 2025;406:1873−1922. 

[4] Abegaz TM, Shebab S, Gebreyohannes EA, et al. Nonadherence to antihypertensive drugs: A systematic review and meta-analysis. Medicine (Baltimore). 2017;96:e5641. 

[5] Chowdury R, Khan H, Heydon E, et al. Adherence to cardiovascular therapy: a meta-analysis of prevalence and clinical consequences. Eur Heart J. 2013;34:2940−2948. 

Source: European Society of Cardiology