Category: Cardiovascular Disease

Categories : Cardiovascular Disease Emergency MedicineTags :

Naloxone Use During Cardiac Arrest Linked to Improved Survival

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Study shows benefits to drug often used for opioid overdose reversal

Photo by Mikhail Nilov

A new study by emergency medicine researchers at UC Davis Health set out to assess the effects of naloxone administration by first responders treating patients with out-of-hospital cardiac arrest (OA-OHCA).

The study, published in Jama Open Network, found naloxone administration during resuscitation by emergency medical service (EMS) personnel was associated with improved outcomes in patients with suspected OA-OHCA.

“This study provides important real-world evidence that naloxone may offer benefit even after cardiac arrest has occurred.”

David Dillon, study author

What the data shows

For this retrospective cohort study (looking back at existing patient records), researchers collected data from the California Resuscitation Outcomes Consortium between 2021 and 2022. In total, 3811 patients with suspected OHCA were treated by EMS.

Researchers found that people who received naloxone, a medication better known for reversing opioid overdoses, had higher rates of survival from the time they were treated by EMS to the time they were discharged from the hospital. The patients also benefitted from return of spontaneous circulation (ROSC) and favourable neurological outcomes compared to those who did not receive the drug.

The key findings included:

  • Survival to hospital discharge was higher among those receiving naloxone (8.1%) compared to those who did not (4.4%). 
  • Naloxone use was associated with a 2.8% absolute increase in survival, after accounting for patient and clinical factors. 
  • People treated with naloxone had improved neurologic outcomes (+3.2%) and ROSC (+3.3%).
  • Benefits were even greater among those with EMS-suspected drug-related cardiac arrest, with survival improvements approaching 8–9%.

The study also found that the association between naloxone and improved outcomes was weakened in certain situations – particularly among patients who required epinephrine during resuscitation. This suggests that timing, patient condition or resuscitation complexity may influence effectiveness.

Addressing a critical gap

Opioid overdose deaths in the United States have surged over the past two decades, contributing to a growing number of cardiac arrests outside the hospital. While naloxone is widely used to reverse opioid overdoses, its role during cardiac arrest has remained unclear and is identified by the American Heart Association as a key evidence gap.

“This study provides important real-world evidence that naloxone may offer benefit even after cardiac arrest has occurred,” said David Dillon, assistant professor of emergency medicine at UC Davis Health and one of the study’s authors. “While these findings are promising, randomised controlled trials are needed to determine whether naloxone directly improves survival in opioid-associated cardiac arrest.”

By Liam Connolly

Source: UC Davis Health

Categories : Cardiovascular Disease Diet and NutritionTags :

Common Food Preservatives Linked to Hypertension and Heart Disease

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Photo by Erik Mclean

Eating foods that contain common preservative food additives may increase the risks of high blood pressure and cardiovascular disease, according to research published in the European Heart Journal.

The research was led by Dr Mathilde Touvier, a research director at INSERM (the French National Institute for Health and Medical Research), and Anaïs Hasenböhler, PhD student, both from the Nutritional Epidemiology Research Team at the Université Sorbonne Paris Nord and Université Paris Cité, France.

Ms Hasenböhler said: “Food preservatives are used in hundreds of thousands of industrially processed foods. Experimental studies suggest that some preservative food additives may be harmful to cardiovascular health, but we have not had enough evidence on the impact of these ingredients in humans. As far as we know, this is the first study of its kind to investigate the links between a wide range of preservatives and cardiovascular health.”

The research is part of a larger study, called NutriNet-Santé, and included 112 395 volunteers from across France. Every six months, the volunteers told researchers everything they ate and drank over a period of three days.

Researchers carried out detailed analyses of the ingredients of all the food and drink, including any preservatives. They also tracked the volunteers’ health for an average of seven to eight years to see if they developed high blood pressure or any cardiovascular disease.

Researchers found that 99.5% of the volunteers had consumed at least one food preservative within the first two years of taking part.

Overall, they found that people who ate the largest amounts of ‘non-antioxidant’ preservatives had a 29% higher risk of hypertension, compared to those who ate the least, and a 16% higher risk of cardiovascular disease, including heart attack, stroke and angina. People who ate the most antioxidant preservatives had a 22% higher risk of hypertension. Non-antioxidant preservatives are designed to stop harmful microbes, such as mould and bacteria, from growing, whereas antioxidant preservatives are designed to stop oxidation, which means the food will not turn brown or become rancid.

Researchers also looked at 17 of the most commonly eaten preservatives and found that eight of these were specifically linked to high blood pressure. These were: potassium sorbate (E202), potassium metabisulphite (E224), sodium nitrite (E250), ascorbic acid (E300), sodium ascorbate (E301), sodium erythorbate (E316), citric acid (E330) and extracts of rosemary (E392). Ascorbic acid (E300) was also specifically linked to cardiovascular disease.

Dr Touvier added: “This study has some limitations inherent to its observational design. However, the findings are based on highly detailed data, and we have taken account of other factors that can increase or lower the risk of cardiovascular disease. Experimental research in the literature consistently suggested that preservatives may cause oxidative stress in the body or affect the way the pancreas works.

These results suggest we need a re-evaluation of the risks and benefits of these food additives by the authorities in charge, such as the EFSA in Europe and the FDA in the USA, for better consumer protection. In the meantime, these findings support existing recommendations to favour non-processed and minimally processed foods, and avoid unnecessary additives. Doctors and other healthcare professionals play a key role in explaining these recommendations to the public.”

The researchers are now looking at how food additives and ultra-processed foods may affect signs of inflammation, oxidative stress, metabolic profile in the blood and the composition of the gut microbiota. This may help them to understand why additives may increase the risks of disease.

Source: European Society of Cardiology

Categories : Cardiovascular Disease Surgeries & ProceduresTags :

Younger Adults Face Risks With ‘Quick-Fix’ for Heart Valve Surgery

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University of Rochester Medicine researchers urge collaborative decision making

Artificial heart valve. Credit: Scientific Animations CC4.0

Growing demand for a minimally invasive aortic valve replacement by adults under 65 with aortic stenosis may put many at greater risk for potentially more complicated heart surgeries later, according to University of Rochester Medicine research published in The Annals of Thoracic Surgery.

Scientists recommend patients work with a multidisciplinary heart care team to assess their short- and long-term needs when facing surgery.

The procedure, transcatheter aortic valve replacement (TAVR), is less invasive than open heart surgery, offering a faster recovery. Since its introduction in 2011, TAVR is the recommended alternative for frail adults over 65 who cannot withstand surgical aortic valve replacement (SAVR) and younger adults whose mortality risk is high.

However, analysis of the Vizient Clinical Database of nearly 14 000 aortic stenosis cases between 2018 and 2023 showed nearly half of the lowest risk patients under 65 underwent TAVR despite the recommendation that they undergo SAVR. And SAVR can be performed using less invasive techniques that can reduce recovery times.

“It’s not surprising that people want a ‘quick fix’ that lets them get back to their normal routine. However, TAVR is not without risks,” said Laurent G. Glance, MD, lead author and professor of Anesthesiology and Perioperative Medicine. “The bioprosthetic valve can wear out or leak and lead to additional complicated surgeries later.” 

Aortic stenosis is diagnosed when the aortic valve gets thick and narrow, restricting blood flow, forcing the heart to work harder. It causes shortness of breath, fatigue, dizziness and can lead to heart failure.

The TAVR technique delivers the new valve through a catheter in the groin and threaded through the femoral artery into the heart. Once inside, it is placed and expanded inside the failing valve.

Researchers reviewed hospital practice data and risk calculations and concluded “the marked use of TAVR among low-risk younger patients…may not represent the optimal long-term strategy for young patients.”

Explanting and replacing a failed TAVR valve requires SAVR, the open surgical approach, which the younger patients initially aimed to avoid. They face potentially slow and painful recovery and face risk of serious complications such as life-threatening stroke.

Co-author and chief of Cardiac Surgery Peter Knight, MD, said the rapid adoption of TAVR for younger adults has outpaced the data to assess durability of the valve and long-term patient outcomes. 

“Careful decision-making is needed and patients should do their homework and talk with their physicians,” Knight said. “You have to look at the short- and long-term needs when making this important choice.”

Source: University of Rochester Medical Center

Categories : Cardiovascular DiseaseTags :

Self-reported Family History Often Underestimates Relatives’ Heart Attacks

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A new study from Karolinska Institutet shows that people’s own reports of heart attacks in the family only partially correspond with register data. The findings suggest that heart attacks among relatives are often underreported, particularly for events occurring early in life.

Asking patients about cardiovascular disease in the family is common practice in both research and clinical risk assessment. But how reliable is this information? Researchers at Karolinska Institutet have investigated this by comparing self-reported family history with Swedish national registers. 

The study included just over 25 000 participants from the Swedish SCAPIS cohort. Participants were asked to state whether their parents or siblings had suffered a heart attack, and the information was then compared with diagnoses in the Patient and Cause of Death Registers.

The results, published in the European Journal of Epidemiology, show that the agreement between self-reported data and register data was only moderate. 

“Our findings show that data from questionnaires only capture part of the occurrence of heart attacks in families,” says Agnes Wahrenberg, researcher at the Department of Clinical Research and Education and resident physician at Södersjukhuset. The study forms part of her doctoral thesis.

For heart attacks in close relatives, the sensitivity was 57.6 per cent, meaning that many cases identified in the registers were not reported in the questionnaires. Misreporting was more common for cases of heart attack occurring early in life.

At the same time, the study highlights the unique opportunities that Swedish health registers offer for research into hereditary cardiovascular disease.

“These registers can be used to supplement and validate family history information in both large cohorts and future register studies,” says Per Svensson, associate professor at the same department and senior physician at Södersjukhuset.

Despite these limitations, the researchers emphasise that self-reported information remains valuable, as it is easy to obtain and can help identify individuals at increased risk in everyday clinical practice.

“It can be difficult to know exactly which diseases have occurred in relatives, particularly further back in time. The Swedish registers are a unique complement to studies on family history and cardiovascular disease, as they enable a more comprehensive assessment of disease in relatives”, says Agnes Wahrenberg.

Source: Karolinska Institutet

Categories : Cardiovascular DiseaseTags :

AFib Found to Cause Profound Changes in Both Atria

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Human heart. Credit: Scientific Animations CC4.0

New research findings from the University Medical Center Göttingen (UMG) show that both atria undergo profound changes in cases of persistent atrial fibrillation. Until now, the left atrium was considered the primary site of the disease. The results of the international study were published in the journal Cardiovascular Research.

Atrial fibrillation is the most common persistent heart rhythm disorder worldwide, and is caused by chaotic electrical activity in the atria. As a result, the heart beats irregularly and often too fast. Many patients suffer from palpitations, shortness of breath, reduced physical performance, or exhaustion. The so-called persistent form of atrial fibrillation is particularly problematic, as the arrhythmia no longer resolves on its own. Over time, this leads to structural and functional changes in the heart tissue. The condition significantly increases the risk of stroke, heart failure, and premature mortality. Until now, research and treatment have focused primarily on the left atrium and the pulmonary veins that drain into it, which are considered major triggers of atrial fibrillation. 

A research team at the University Medical Center Göttingen (UMG) investigated whether and to what extent the right atrium is also affected by long-term atrial fibrillation. The study shows that the right atrium also undergoes profound remodelling processes and increasingly resembles the left atrium. 

“The results suggest that persistent atrial fibrillation must be understood as a disease of both atria,” says Dr Aiste Liutkute, the study’s first author. “This could also explain why established therapies are often not permanently successful in cases of long-standing atrial fibrillation.” 

The Approach

The research team analysed tissue samples from the right and left atria of patients with persistent atrial fibrillation, which had been collected during heart surgery. Samples from non-transplanted donor hearts with no known cardiac arrhythmias served as the control group.

Using state-of-the-art mass spectrometry techniques, the scientists examined thousands of proteins simultaneously to identify disease-related changes in heart tissue. Mass spectrometry is a high-resolution analytical method that allows molecules to be precisely identified and quantified based on their mass. This makes it possible to determine which proteins are present in heart muscle cells and how their composition changes in the presence of disease. For the study, the researchers first created a comprehensive reference library of the human heart proteome. The proteome refers to the totality of all proteins in a tissue or cell. Proteins perform central functions in the body and provide insight into which biological processes are active in the cells. In addition to the proteome analyses, the team examined the scarring of heart tissue under a microscope, confirmed notable protein changes using biochemical methods, and identified blood markers that indicate stress on the heart.

The Results

The analyses show that, in cases of persistent atrial fibrillation, the right atrium exhibits pathological changes similar to those in the left atrium. In both atria, the researchers found increased tissue scarring, a breakdown of important heart muscle structures, and clear signs of cellular stress and remodeling processes. These changes impair normal electrical signal transmission in the heart and may contribute to the persistence of atrial fibrillation. At the same time, many of the molecular differences that normally exist between the right and left atria disappeared. For instance, the right atrium lost typical protein markers that normally characterize its specific function and increasingly took on features of the left atrium, including proteins associated with altered energy metabolism and structural remodeling of heart muscle cells.

Source: University Medical Center Göttingen

Categories : Cardiovascular DiseaseTags :

Up to 10 Hours of Exercise a Week Needed for Substantial Heart Benefits

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Current exercise guidelines are too low, suggest researchers

Photo by Ketut Subiyanto on Pexels

Adults should aim to do between 560 and 610 minutes a week of moderate to vigorous physical activity to achieve a substantial reduction in the risk of heart attacks and stroke, suggest the findings of an observational study published online in the British Journal of Sports Medicine.

This is between 3-4 times higher than the current public health recommendation that adults do at least 150 minutes a week of moderate to vigorous physical exercise such as brisk walking, running or cycling.

People who are less fit need to do slightly more exercise than those who are very fit to get the same cardiovascular benefits, the study suggests.

The researchers say that the current one-size fits-all advice on exercise may need to be changed and replaced with personalised targets according to an individual’s fitness level.

Cardiorespiratory fitness varies greatly and is a strong predictor of cardiovascular health. Low cardiorespiratory fitness is strongly associated with an increased risk of heart attacks, strokes and early death, the researchers point out.

A simple way to assess cardiorespiratory fitness is by measuring VO2 max – the maximum rate of oxygen the body consumes and uses during intense exercise. This measures how efficiently the heart, lungs and muscles deliver and use oxygen.

Less fit individuals need to do more exercise to get the same benefits

Researchers from Macao Polytechnic University, China, set out to look at how both exercise levels and cardiorespiratory fitness, as measured by VO2 max, affected the risk of cardiovascular disease.

The study included data from 17 088 people who were taking part in a UK Biobank study between 2013 and 2015. The average age was 57 years and 56% were female and 96% were white.

The study participants wore a device on their wrist for seven consecutive days to record their typical exercise levels and had completed a cycle test to measure their estimated VO2 max.

Data on smoking status, alcohol intake, self-related health and diet, body mass index, resting heart rate and blood pressure were also included in the analysis.

During an average follow up period of 7.8 years, there were 1233 cardiovascular events, including 874 atrial fibrillation, 156 myocardial infarction, 111 heart failure and 92 stroke events.

Those adults who met the 150 minute a week guideline on exercise experienced a modest 8-9% reduction in cardiovascular risk, the study found. This was consistent across all levels of fitness.

In order to achieve substantial protection, classed as a greater than 30% risk reduction, between 560 and 610 minutes of moderate to vigorous exercise a week was needed. However, this level of exercise was only achieved by 12% of people in the study.

The analysis found that those individuals with the lowest fitness needed approximately 30-50 additional minutes per week compared with those with high fitness to achieve equivalent benefits.

For example, to achieve a 20% reduction in the risk of cardiovascular events, 370 minutes of moderate to vigorous exercise was needed for those at the lowest fitness compared to 340 minutes for those at the highest fitness levels.

The researchers say, “This finding highlights the steeper challenge faced by deconditioned populations.”

This is an observational study and as such no firm conclusions can be drawn about cause and effect. The researchers acknowledge that the study group could have been healthier and fitter than the general population. Another limitation was that cardiorespiratory fitness was estimated and sedentary time or less vigorous exercise was not measured.

The researchers say their findings confirm that current guidelines provide a robust universal minimum for cardiovascular protection. But they add that there should be stratified advice to help guide motivated patients to do more to protect their heart health.

“Future guidelines may need to differentiate between the minimal moderate to vigorous exercise volume required for a basic safety margin and the substantially higher volumes necessary for optimal cardiovascular risk reduction,” they conclude.

Source: The BMJ Group

Categories : Cardiovascular Disease ExerciseTags :

Swimming Beats Running for Strengthening the Heart, Study Finds

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By Maria Fernanda Ziegler  |  Agência FAPESP – A study conducted on an animal model by researchers at the Federal University of São Paulo (UNIFESP) in Brazil demonstrated that swimming is more effective than running in promoting healthy heart growth and improving the strength with which the heart muscle (myocardium) contracts.

“Swimming and running are two excellent ways to improve cardiorespiratory health and protect the heart muscle, but we wanted to know if one could be even more beneficial than the other. We found that, although both increase respiratory capacity, swimming goes a step further by combining functional and molecular adaptations that make the heart stronger and more efficient,” says Andrey Jorge Serra, a professor at UNIFESP and coordinator of the study supported by FAPESP. 

The study, published in the journal Scientific Reports, demonstrates that swimming promotes greater modulation of microRNAs that control various heart adaptations, such as cardiac cell growth, the formation of new blood vessels (angiogenesis), protection against cell death, and the regulation of contractility and responses to oxidative stress, compared to running training.

MicroRNAs are molecules that regulate the expression of messenger RNAs, which are responsible for protein synthesis.

“Although several studies had already examined the expression of microRNAs regulated by aerobic training in general, little was known about expression patterns when swimming and running were compared in the same experimental setting. Therefore, this study reveals that there’s a distinction in cardiovascular effects between these two modalities,” says Serra.

In the study, the mice underwent an eight-week training protocol consisting of daily 60-minute sessions five days a week. The rats were divided into three groups: one that did not train, one that only ran, and one that only swam. Since running and swimming are very different forms of exercise, the comparison between the training regimens was not based on the speed the animals reached but rather on the relative intensity of the effort, as measured by maximum oxygen consumption (VO₂ max) – an indicator that assesses the body’s ability to capture, transport, and utilize oxygen during physical activity.

According to the results, running and swimming improved physical fitness similarly: between the first and last training sessions, VO₂ max increased by more than 5%. However, only swimming promoted significant structural changes in the heart, such as increases in cardiac and left ventricular mass. Running did not show relevant differences compared to the sedentary animals.

“People’s choice of sport depends largely on personal preference, aptitude, and enjoyment. But our results show that swimming may have a special impact in situations involving myocardial recovery, cardiac rehabilitation, and above all, scientific research. This is also relevant because studies on aerobic exercise often use running and swimming interchangeably, and we now know that the effects aren’t the same,” Serra explains.

Before and after the training period, the researchers administered a series of tests to evaluate various aspects of cardiac health, including cardiorespiratory capacity, fitness, and the structure and function of the heart and myocardium.

The study also analyzed the gene expression and protein pathways involved in physiological cardiac hypertrophy and the mechanisms involved in identifying regulatory microRNAs.

“Although we don’t yet know why this change occurs at the molecular level, of the microRNA, we were able to delve deeply into and investigate the molecular pathways that control physiological hypertrophy,” the researcher adds.

The article “Swimming is superior to running in inducing physiological cardiac hypertrophy and enhancing myocardial performance” can be read at nature.com/articles/s41598-026-36818-2.

Source: FAPESP

Categories : Cardiovascular DiseaseTags :

Digoxin Benefits Heart Failure Patients, Study Shows

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Right side heart failure. Credit: Scientific Animations CC4.0

Analyses supporting the use of digitalis glycosides in patients with heart failure were presented in a Late-Breaking Science session at Heart Failure 2026, [1–3] the annual congress of the Heart Failure Association of the European Society of Cardiology.

Investigations from researchers at University Medical Center Groningen, Netherlands, evaluated the effects of the digitalis glycosides, digoxin and digitoxin, in patients with heart failure (HF) and reduced or mildly reduced left ventricular ejection fraction (HF(m)rEF). 

“Digoxin is the oldest drug in cardiovascular medicine, but there has been uncertainty about its value in HF(m)rEF management,” explained Principal Investigator, Professor Dirk van Veldhuisen. “In the DIG trial, published in 1997, digoxin had a neutral effect on the primary endpoint of mortality, but a 28% reduction in heart failure hospitalisations (a secondary endpoint) was observed. Later analyses from DIG showed that lower serum digoxin levels were associated with a favourable effect, while higher digoxin levels worsened prognosis. [4] We conducted the DECISION trial to investigate whether low-dose digoxin has positive effects on cardiovascular outcomes in patients with HF(m)rEF receiving contemporary guideline-recommended treatments.”[1]

The double-blind DECISION trial was conducted at 43 sites in the Netherlands (NCT03783429). Patients with symptomatic mild-to-moderate HF(m)rEF (left ventricular ejection fraction <50%). were randomised to low-dose digoxin or placebo, with a target serum digoxin concentration of 0.5–0.9 ng/mL.  Both patients with sinus rhythm and atrial fibrillation were enrolled. The primary outcome was a composite of total worsening HF events (defined as total hospitalisations or total urgent hospital visits for worsening HF) and cardiovascular mortality. A total of 1001 patients were randomised. The mean age of the participants was 73 years, 28% were women, and 29% had atrial fibrillation.

Low-dose digoxin did not significantly reduce the primary outcome. Over a median follow-up of 36.5 months, 238 primary-outcome events occurred in 131 of 500 patients in the digoxin group, while 291 primary-outcome events occurred in 152 of 501 patients in the placebo group (rate ratio [RR] 0.81; 95% confidence interval [CI] 0.61 to 1.07; p=0.133). Although not statistically significant, the total number of worsening HF events was lower in the digoxin group than in the placebo group (RR 0.76; 95% CI 0.54 to 1.05). Cardiovascular mortality was similar with digoxin and placebo (hazard ratio [HR] 0.93; 95% CI 0.69 to 1.26). Low-dose digoxin was generally well tolerated and safe.

Last year, results were published from the DIGIT-HF trial, which studied another digitalis glycoside, digitoxin, in patients with advanced HF and reduced ejection fraction. [5] Treatment with digitoxin led to a lower risk of death from any cause or hospital admission for worsening HF.

A second presentation at Heart Failure 2026, by Associate Professor Kevin Damman, demonstrated positive overall benefits with digoxin/digitoxin in a meta-analysis of the DECISION, DIGIT-HF and DIG trials. [2] Across 9,013 patients, digitalis glycoside treatment reduced the risk of the primary endpoint of time to cardiovascular death or first worsening HF event compared with placebo (HR 0.85; 95% CI 0.80 to 0.90; p<0.001). This reduction was mostly attributable to the effect on time to the first worsening HF event (HR 0.75; 95% CI 0.69 to 0.81; p<0.001). There was no statistically significant heterogeneity by trial, treatment period or type of digitalis glycoside. In addition, the effect was not attenuated in patients who were already receiving full guideline-directed HF treatment. 

A third presentation, by Professor Peter van der Meer, found that digoxin withdrawal was associated with clinical deterioration. [3] This was a prespecified blinded analysis that followed patients who stopped taking study medication at the end of the DECISION trial, and were subsequently followed for another 6 weeks. Across 587 patients, there were more cardiovascular deaths and HF events in patients after withdrawal of digoxin than after placebo withdrawal (RR 7.37; 95% CI 1.56 to 34.88; p=0.012). 

Summing up the evidence, Professor van Veldhuisen concluded, “In patients with HF(m)rEF, low-dose digitalis glycosides seem to be an effective additional medical treatment option, which are cheap, safe and easy to use. The totality of the evidence supports the role of low-dose digoxin in the contemporary management of HF, with caution warranted when it is stopped.”

References

[1] ‘Low-dose digoxin in heart failure’ presented during the Hottest trials (2) session on 10 May at 13:15 to 14:15 in Room 3, with simultaneous publication in Nature Medicine: https://doi.org/10.1038/s41591-026-04406-6.


[2] ‘DECISION/DIGIT-HF/DIG study level meta analysis’ presented during the Hottest trials (2) session on 10 May at 13:15 to 14:15 in Room 3.


[3] ‘Blinded withdrawal of digoxin or placebo’ presented during the Hottest trials (2) session on 10 May at 13:15 to 14:15 in Room 3. 


[4] Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997;336:525−533.


[5] Bavendiek U, Großhennig A, Schwab J, et al. Digitoxin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2025;393:1155–1165.

Source: European Society of Cardiology

Categories : Cardiovascular DiseaseTags :

Cause of Bicuspid Aortic Valve Revealed in Genetic Study

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Photo by Sangharsh Lohakare on Unsplash

New clues from genetic research may help explain what causes the most common heart defect present at birth. Researchers in Sweden have identified rare DNA changes during foetal development that can lead to a condition known as bicuspid aortic valve (BAV).

Pelin Sahlén

Publishing in Nature Communications, a team of researchers from KTH Royal Institute of Technology and Karolinska Institutet identified nearly 30 times more potential genes linked to BAV than previously known. The aortic valve has three cusps; a bicuspid aortic valve is a valve with only two cusps.

The study offers a clearer picture of how heart valves form, says Pelin Sahlén, an associate professor at KTH Royal Institute of Technology whose former student Artemy Zhigulev led the study as his PhD project.

“These findings expand our understanding of the genetic complexity of BAV and raise hope for new ways to improve how genetic risk is assessed,” Sahlén says.

People born with BAV often go on to develop complications, such as a narrowing of the valve or enlargement of the aorta. More than half will undergo surgery at some point in their lives.

But the underlying causes have long remained unclear. Earlier research showed a small number of cases are caused by changes in genes that contain the instructions for making proteins – the molecules that carry out most of the work in a cell. This explained only about 10% of all cases, says the study’s co-author Hanna Björck, associate professor at Karolinska Institutet.

“Most patients had no known genetic cause,” she says.

The new study shifted attention to a different part of the DNA – the regulatory regions of the genome that act like switches, turning important genes on or off during early development. The researchers studied tissues close to heart valves from eight people with BAV and eight people with normal valves.

Rather than focus on genes themselves, Sahlén says they used a technique called HiCap, for targeted 3D genome mapping to examine how the DNA is arranged inside the cell and how regulatory regions connect to key developmental genes.

They found that rare mutations in the regulatory parts of DNA are likely to play a major role in causing BAV. Each patient in the study had different mutations, but many of these mutations disrupted the same important genes that shape the aortic valve in the foetus, Zhigulev says.

“This suggests that even though the mutations vary, they interfere with the same developmental processes,” he says.

One of the surprising discoveries is that adult tissues retain traces of what went wrong during foetal development, Sahlén says. Harmful changes that happened before birth can be detected decades later. The finding indicates adult tissue samples can be used to study problems that originally occurred in the early stages of life.

By David Callahan

Source: KTH Royal Institute of Technology

Categories : Cardiovascular DiseaseTags :

A New Explanation for the Rise in Heart Disease Risk After Menopause

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A new study points to gene regulation as a key factor in post-menopausal cardiovascular risk

Photo by Anthony Shkraba on Pexels

Scientists at Virginia Tech say that the increased risk of cardiovascular disease after menopause may stem not only from declining hormone levels, but also from how those changes influence gene activity.

In a new paper published in the journal Cells, researchers examine growing evidence that declining oestrogen levels can alter epigenetics, the system that controls when genes turn on and off. These changes may help explain why rates of heart disease, diabetes, and other metabolic conditions rise sharply in women after menopause.

In addition, the study identifies a potential link between oestrogen loss, changes in gene regulation, and cardiovascular health. The epigenome, the full set of chemical modifications that regulate gene activity without altering DNA, has been studied extensively in breast cancer, but far less is known about how these mechanisms operate in the heart and cardiovascular system, according to  Sumita Mishra, senior author of the study and assistant professor at the Fralin Biomedical Research Institute at VTC.

The findings suggest that oestrogen-related gene regulation pathways, long studied in cancer biology, may also play an important role in cardiometabolic health. Heart disease is the leading cause of death for women, and risk increases during and after the menopause transition, according to the National Heart, Lung, and Blood Institute.

“For years, we’ve focused on oestrogen loss as the primary driver of increased heart disease risk after menopause,” Mishra said. “What’s becoming clear is that the story is more complex. By reframing menopause-related health risks around gene regulation, this work points to new directions for future treatments that may extend beyond hormone therapy to more directly target these regulatory pathways.”

In addition, genetic predisposition and environmental factors, such as diet, exercise, and metabolic disease, likely interact with these pathways to shape cardiovascular risk after menopause, beyond what hormone replacement alone can address.

Rather than identifying a single new mechanism, the results of the study offer a new way of understanding the problem by connecting hormone loss to longer-term changes in how the body regulates interconnected systems involved in cardiovascular and metabolic health.

The study also highlights that many existing interventions used to manage cardiometabolic disease in postmenopausal women, including lipid-lowering therapies, glucose-lowering agents such as GLP-1 receptor agonists and SGLT2 inhibitors, and lifestyle interventions such as diet and exercise, may intersect with gene regulatory pathways influenced by oestrogen.

Emerging evidence suggests that these strategies can modulate metabolic and inflammatory signalling networks and, in some cases, the way DNA is packaged and regulated, helping to link current therapies to menopause-associated biological changes.

The researchers also highlight a gap in current knowledge, noting that much of the mechanistic evidence comes from laboratory and preclinical studies, and that more research in humans is needed to understand how these processes unfold over time.

Looking ahead, ongoing studies in the Mishra laboratory will focus on understanding how metabolic and gene-regulatory pathways are integrated in cardiometabolic disease, including in postmenopausal health. 

The new study also aligns with ongoing research in the Mishra laboratory focused on heart failure with preserved ejection fraction (HFpEF), a form of heart disease that disproportionately affects women and becomes more prevalent after menopause. HFpEF is closely linked to obesity and metabolic dysfunction and remains a major unmet clinical challenge.

In related work published in Hypertension, the Mishra team investigated how oestrogen-dependent signaling pathways in the heart and vasculature are altered after menopause, contributing to changes in vascular function and metabolic regulation. 

Together, these findings emphasise a broader research focus on how hormonal signalling interacts with molecular pathways that govern cardiometabolic health in postmenopausal women. This growing body of work may help guide the development of more targeted strategies to prevent and treat cardiovascular disease in this population.

Mishra is a member of the Center for Exercise Medicine Research and the Center for Vascular and Heart Research at the Fralin Biomedical Research Institute. She is also an assistant professor in the Department of Human Nutrition, Foods, and Exercise in the College of Agriculture and Life Sciences.

By John Pastor

Source: Virginia Tech