Historical data indicate that men develop coronary heart disease (CHD) 10 years before women. A recent study in the Journal of the American Heart Association indicates that this sex gap still remains.
Investigators analysed data from the Coronary Artery Risk Development in Young Adults (CARDIA) study, in which US adults aged 18–30 years enrolled in 1985–1986 and were followed through August 2020.
Among 5112 participants (54.5% female, 51.6% Black) with an average age of 24.8 years at enrolment and a median follow-up of 34.1 years, men had a significantly higher cumulative incidence of cardiovascular disease. They had higher cumulative incidence rates of the cardiovascular disease subtypes of CHD and heart failure compared with women, but no difference in stroke.
Men reached a 5% incidence of cardiovascular disease 7.0 years earlier than women (50.5 versus 57.5 years). CHD was the most frequent cardiovascular disease subtype, and men reached a 2% incidence 10.1 years earlier than women. There were no significant differences in the age at which men and women reached a 2% incidence for stroke (57.5 versus 56.9 years) or a 1% incidence for heart failure (48.7 versus 51.7 years)
Differences emerged in the fourth decade of life and were not explained after accounting for differences in cardiovascular health.
“Sex differences in cardiovascular disease risk are apparent by age 35, highlighting the importance of initiating risk assessment and prevention strategies in young adulthood,” said corresponding author Alexa Freedman, PhD, of the Northwestern University Feinberg School of Medicine.
Decades-long US study suggests prevention and screening should start earlier in adulthood
Pexels Photo by Freestocksorg
Men begin developing coronary heart disease – which can lead to heart attacks – years earlier than women, with differences emerging as early as the mid-30s, according to a large, long-term study led by Northwestern Medicine.
The findings, based on more than three decades of patient follow-up, suggest that heart disease prevention and screening should start earlier in adulthood, particularly for men.
“That timing may seem early, but heart disease develops over decades, with early markers detectable in young adulthood,” said study senior author Alexa Freedman, assistant professor of preventive medicine at Northwestern University Feinberg School of Medicine.
“Screening at an earlier age can help identify risk factors sooner, enabling preventive strategies that reduce long-term risk.”
Older studies have consistently shown that men tend to experience heart disease earlier than women. But over the past several decades, risk factors like smoking, high blood pressure and diabetes have become more similar between the sexes. So, it was surprising to find that the gap hasn’t narrowed, Freedman said.
To better understand why sex differences in heart disease persist, Freedman and her colleagues say it’s important to look beyond standard measures such as cholesterol and blood pressure and consider a broader range of biological and social factors.
Tracking heart disease from young adulthood
The study analysed data from the Coronary Artery Risk Development in Young Adults (CARDIA) study, which enrolled more than 5100 Black and white adults ages 18 to 30 in the mid-1980s and followed them through 2020.
Because participants were healthy young adults at enrollment, the scientists were able to pinpoint when cardiovascular disease risk first began to diverge between men and women. Men reached 5% incidence of cardiovascular disease (defined broadly to include heart attack, stroke and heart failure) about seven years earlier than women (50.5 versus 57.5 years).
The difference was driven largely by coronary heart disease. Men reached a 2% incidence of coronary heart disease more than a decade earlier than women, while rates of stroke were similar and differences in heart failure emerged later in life. “This was still a relatively young sample – everyone was under 65 at last follow-up – and stroke and heart failure tend to develop later in life,” Freedman explained.
Beyond traditional risk factors
The scientists examined whether differences in blood pressure, cholesterol, blood sugar, smoking, diet, physical activity and body weight could explain the earlier onset of heart disease in men. While some factors, particularly hypertension, explained part of the gap, overall cardiovascular health did not fully account for the difference, suggesting other biological or social factors may be involved.
A critical age: 35
One of the most striking findings was when the risk gap opened. The scientists found that men and women had similar cardiovascular risk through their early 30s. Around age 35, however, men’s risk began to rise faster and stayed higher through midlife. Heart disease screening and prevention efforts often focus on adults over 40. The new findings suggest that approach may miss an important window.
The authors highlight the relatively new American Heart Association’s PREVENT risk equations, which can predict heart disease starting at age 30, as a promising tool for earlier intervention.
The longer a person has type 2 diabetes, the greater the risk of cardiovascular disease. A new study from Karolinska Institutet, published in the journal Diabetes, shows that changes in red blood cells may be an important explanation, and identifies a specific molecule as a possible biomarker.
People with type 2 diabetes are at increased risk of heart attack and stroke, and the risk increases the longer they have lived with the disease. Previous research has shown that red blood cells can affect blood vessel function in diabetes. Now, a new study shows that the duration of the disease plays a decisive role in when and how these changes occur – and that long-term type 2 diabetes can make red blood cells directly harmful to blood vessels.
The researchers studied both animals and patients with type 2 diabetes. Red blood cells from mice with long-term diabetes and patients who had had the disease for over seven years had a harmful effect on blood vessel function. No such effect was seen in newly diagnosed individuals, but after seven years of follow-up, their blood cells had developed the same harmful properties. When the researchers restored the levels of microRNA-210 in the red blood cells, vascular function improved.
“What really stands out in our study is that it is not only the presence of type 2 diabetes that matters, but how long you have had the disease. It is only after several years that red blood cells develop a harmful effect on blood vessels,” says Zhichao Zhou, associate professor at the Department of Medicine, Solna, Karolinska Institutet, and lead author of the study.
The study points to microRNA-210 in red blood cells as a possible biomarker for early detection of the risk of cardiovascular complications. Researchers are now working to investigate whether this can be used in larger population studies.
“If we can identify which patients are at greatest risk before vascular damage has already occurred, we can also become better at preventing complications,” says Eftychia Kontidou, doctoral student from the same group and the first author of the study.
New research paves way for novel therapies to reverse heart failure
Human heart. Credit: Scientific Animations CC4.0
Pioneering research by experts at the University of Sydney, the Baird Institute and the Royal Prince Alfred Hospital in Sydney has shown that heart muscle cells regrow after a heart attack, opening up the possibility of new regenerative treatments for cardiovascular disease.
Following the publication of the study in Circulation Research, first author Dr Robert Hume, from the Faculty of Medicine and Health and Charles Perkins Centre, and Lead of Translational Research at the Baird Institute for Applied Heart and Lung Research, explained the significance of the finding:
“Until now we’ve thought that, because heart cells die after a heart attack, those areas of the heart were irreparably damaged, leaving the heart less able to pump blood to the body’s organs.
“Our research shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities.
“Although this new discovery of regrowing muscle cells is exciting, it isn’t enough to prevent the devastating effects of a heart attack. Therefore, in time, we hope to develop therapies that can amplify the heart’s natural ability to produce new cells and regenerate the heart after an attack.”
Though increased mitosis (a process in which cells divide and reproduce) after a heart attack has been observed in the heart muscles of mice, this is the first time the phenomenon has been demonstrated in humans.
Heart disease in Australia and the world
Cardiovascular disease is the leading cause of death globally, and is responsible for nearly a quarter (24 percent) of all deaths in Australia.
Heart attacks can eliminate a third of the cells in the human heart and, though survival rates have improved dramatically over the last decade thanks to therapeutic advancements, many patients still go on to develop heart failure, which can only be cured with a transplant. With approximately 144 000 heart failure patients in Australia and only 115 heart transplants per year, there is a huge disparity in what these patients need and the treatment that can be offered.
Pioneering techniques made research possible
The study is also the first in the world to use tissue samples taken from living patients during bypass surgery. These “pre-mortem” tissue samples were taken from consenting patients undergoing heart bypass surgery at the Royal Prince Alfred Hospital in Sydney.
The samples were collected from diseased and non-diseased parts of the heart using a method developed by Professor Paul Bannon and Professor Sean Lal, who work jointly at the University of Sydney, Royal Prince Alfred Hospital and The Baird Institute.
New therapies to regenerate the heart
Developing a technique to collect living tissue samples means the research team now has a laboratory model which they hope to use to unlock new treatments to regenerate the human heart.
Professor Sean Lal, senior author of the study from the School of Medical Sciences and heart failure cardiologist at the Royal Prince Alfred hospital, said: “Ultimately, the goal is to use this discovery to make new heart cells that can reverse heart failure.
“Using living human heart tissue models in our work means that we will have more accurate and reliable data to develop new therapies for heart disease.
“Already, our research using these samples has identified several proteins that have previously been shown to be involved in the regeneration of the heart in mice – which is a very exciting prospect to now translate to humans.”
Spending too long sitting raises the risk of heart disease and diabetes in people over 60, warns a major global review. Published in the Journal of Physical Activity and Health, the review analysed data from 28 international studies involving 82 000 people aged 60 and older.
It flags strong links between sitting time and worsening markers for chronic disease including high blood sugar, cholesterol, waist size, and blood pressure. And that’s even for people who exercise regularly.
That means — whether watching TV, using a tablet or reading a book — the longer older people sit, the higher their risk of major health problems like heart disease, stroke, and type 2 diabetes.
“This is a link we can’t ignore,” said Dr Daniel Bailey, Reader in Sedentary Behaviour and Health at the Department of Life Sciences, Brunel University of London. “You can meet the weekly exercise target, but if you spend the rest of the day sitting, your health is still at risk.”
In the UK, where more than 12 million people are aged 65 or older, older adults can spend up to 80% of their waking hours sitting down and longer during winter or for people with mobility issues. That means millions may be unknowingly accumulating risks day after day — a concern for families, carers, and health professionals.
One of the most revealing findings was that the harmful effect of sitting for long periods showed up even in otherwise healthy older adults, not just those already diagnosed with illness. Waist measurement, a major predictor of health risk, had the strongest, most consistent link with sitting time.
“We’re seeing these impacts in people who don’t yet feel unwell,” said Dr Bailey. “That means we have a chance to intervene early and protect health before problems start.”
Importantly, the study found limited protective effect from exercise alone. After accounting for how active people were, the damage from long hours of sitting remains.
“The evidence is clear. We urgently need strategies that don’t just encourage exercise, but also help people sit less throughout the day,” said Dr Bailey. “Simple changes make a difference —standing during phone calls, replacing some TV time with gardening or a stroll, or light chores around the house.”
The study by Brunel University of London, the University of Lincoln, Federation University in Australia, and the University of Bedfordshire is the most comprehensive analysis to date linking sedentary behaviour to cardiometabolic risk in later life. As the NHS contends with rising rates of diabetes and heart disease, it spells out to policymakers that keeping moving throughout the day is as vital as structured exercise.
Dr Bailey stressed the shared role of public services, community groups and healthcare professionals to help older people avoid sitting for long stretches: “From GP advice to local councils and charities, there’s a role for everyone in changing the message.”
A Scottish patient has become the first person in the world to receive a pioneering therapy aimed at improving outcomes for those having heart bypass surgery. The treatment involves precisely editing DNA in veins to be used during heart bypass surgery to boost the production of a protective protein.
The treatment could help extend the lifespan of blood vessels used during the surgery and significantly improve patient health, experts say.
Cause of failures in bypass surgery
Heart bypass surgery – an operation to improve blood flow to the heart – is a life-saving treatment for patients with coronary heart disease.
The process typically uses one artery and two or more veins as bypass grafts – healthy blood vessels used to bypass a narrowed or blocked artery – creating a new route for blood to flow.
Vein grafts used in this type of surgery can fail because they are not naturally designed to withstand the high pressure of blood flow from the heart.
Protecting vein grafts
The PROTECT study, led by NHS Greater Glasgow and Clyde and the University of Glasgow in collaboration with NHS Golden Jubilee and the University of Edinburgh, is trialling a new gene therapy designed to support newly grafted blood vessels.
The treatment will introduce a gene, which produces a protein called TIMP-3, into the vein to be grafted.
TIMP-3 is involved in tissue remodelling. Higher levels of the protein could help to prevent thickening and blockage of the blood vessel over time, scientists say.
Exciting milestone
The research team has developed a way to treat the graft directly at the time of surgery, safely and efficiently delivering the gene therapy to the affected tissue before grafting into the heart.
It is hoped the treatment will help to extend a patient’s healthy life expectancy and reduce the need for further surgeries, experts say.
Many people stop taking cholesterol-lowering statins because they experience muscle aches, weakness, and fatigue. A new study by Columbia researchers now suggests that at least for some people, the side effects arise when statins bind to a protein in muscle cells and cause a leak of calcium ions inside the cells.
“It is unlikely that this explanation applies to everyone who experiences muscular side effects with statins, but even if it explains a small subset, that’s a lot of people we could help if we can resolve the issue,” says Andrew Marks, chair of the Department of Physiology and Cellular Biophysics at the Vagelos College of Physicians and Surgeons.
About 10% of adults taking statins experience these muscular side effects.
“I’ve had patients who’ve been prescribed statins, and they refused to take them because of the side effects. It’s the most common reason patients quit statins, and it’s a very real problem that needs a solution,” says Marks.
Electron microscopy pinpoints statin-muscle interaction
Statins’ muscular side effects have puzzled researchers since the drugs hit the market in the late 80s. Statins are designed to lower cholesterol by binding to an enzyme involved in cholesterol synthesis. But statins also bind to other “off-target” molecules, and some previous studies have suggested that muscular side effects occur when statins bind to a specific protein in muscle.
With cryo-electron microscopy, a technique that can image molecules down to individual atoms, the researchers of the new study documented this binding and uncovered the precise details of the interaction.
Simvastatin molecules bind to two locations on a muscle protein, called the ryanodine receptor, which opens a channel in the receptor. The flow of calcium through the open channel could explain the muscular side effects of statins.
The images revealed two locations on the muscle protein, called the ryanodine receptor, where a statin called simvastatin binds, opening a channel in the receptor and allowing calcium to flow through.
The calcium leak could explain the muscular side effects of statins, Marks says, by weakening the muscle directly or by activating enzymes that degrade muscle tissue.
Building a better statin
The new images also suggest that statins could be redesigned so they do not bind the ryanodine receptor but retain their cholesterol-lowering ability.
Marks is now collaborating with chemists to create such a statin.
Plugging the calcium leak could be another option: Statin-induced calcium leaks in mice can be closed, the researchers showed, with an experimental drug developed in the Marks lab for other conditions involving calcium leaks.
These drugs are currently being tested in people with rare muscle diseases. If it shows efficacy in those patients, we can test it in statin-induced myopathies,” Marks says
A new ACC Scientific Statement on Inflammation and Cardiovascular Disease (CVD) highlights new groundbreaking research linking inflammation atherosclerotic cardiovascular disease (ASCVD) and provides consensus-based recommendations for evaluation, treatment and prevention reflecting this new era.
“The evidence linking inflammation with ASCVD is no longer exploratory but is compelling and clinically actionable,” write the authors, led by Writing Committee Chair George A. Mensah, MD, FACC. “The time for taking action has now arrived.”
Published in JACC, the Statement includes specific recommendations for screening, evaluation, and CVD risk assessment; inflammatory biomarkers in cardiovascular imaging; inflammation inhibition in behavioural and lifestyle risks; and anti-inflammatory approaches in primary and secondary prevention, as well as in heart failure and other cardiovascular diseases.
Among the key takeaways:
High-sensitivity C-reactive protein (hsCRP) is an inexpensive and widely available blood test. While there has been debate within the medical community regarding the utility of hsCRP, this statement details the data confirming its value in clinical decision making in primary and secondary prevention.
In patients with known CVD, hsCRP level is at least as predictive of future events as LDL cholesterol levels, even in patients treated with statin therapy.
The important role of lifestyle interventions to reduce systemic inflammation is emphasised, including regular exercise (at least 150 minutes/week), Mediterranean or DASH Diet, and intake of omega-3 fatty acids, including two to three meals per week of fatty fish high in EPA and DHA. This advice aligns with lifestyle management recommendations in the 2025 ACC/AHA High Blood Pressure Guideline
The Statement also discusses current challenges and opportunities based on the new evidence, exploring topics like the advancing field of cardioimmunology and areas for further research, such as the interplay between inflammation and key physiological systems, the role of novel special pro-resolving bioactive lipid molecules in promoting the resolution of inflammation and CVD risk reduction, and more.
The authors close with a call for action to “embrace anti-inflammatory interventions in patients with established ASCVD” and for clinical practice guidelines that implement “broad screening of primary and secondary prevention patients for hsCRP, in combination with LDL cholesterol.” Additionally, they note: “The time is also ripe for the development of strategies to promote increased physician awareness of the crucial role of inflammation in CVD and accelerate the adoption of evidence-based, guideline-directed anti-inflammatory therapy through dissemination and implementation research.”
Planned birth at term reduces the incidence of pre-eclampsia in women at high risk of the condition, without increasing emergency Caesarean or neonatal unit admission, according to new trial results.
The PREVENT-PE trial, led by researchers from King’s College London and King’s College Hospital NHS Foundation Trust, is the first to find that a strategy of screening for pre-eclampsia risk at 36 weeks of pregnancy, and then offering planned early term delivery according to the mother’s risk, can reduce the incidence of subsequent pre-eclampsia by 30%, compared with usual care.
The trial, funded by the Fetal Medicine Foundation (FMF), also found that the intervention did not increase the rates of birth by emergency Caesarean or neonatal care needs, and there was no evidence of other harms to mother or baby.
Pre-eclampsia is high blood pressure that develops during pregnancy, most commonly at term gestational age. Pre-eclampsia affects 2-8% of pregnancies worldwide and can be life-threatening – there are around 46,000 maternal deaths due to pre-eclampsia each year and around 500,000 foetal or newborn deaths.1
Pre-eclampsia usually develops after 20 weeks of pregnancy, or soon after the baby is born. While aspirin can be taken to significantly reduce the risk of developing pre-eclampsia before 37 weeks of pregnancy, there are no treatments available to reduce risk at term (37-42 weeks).
Building on findings from an earlier data analysis, the PREVENT-PE trial recruited over 8,000 women from King’s College Hospital and Medway NHS Foundation Trusts. Women were randomly allocated into one of two groups: the intervention group (risk assessment for pre-eclampsia, followed by planned early term delivery according to risk) and the control group (usual care at term).
Pre-eclampsia risk was assessed using a model developed by the FMF, which combines maternal demographics and history, with blood pressure, and specific markers in the blood.
Those at high risk of developing pre-eclampsia at term were offered planned birth at 37, 38, 39 or 40 weeks of pregnancy. Women considered to be at low risk received usual care, according to their hospital protocols and UK standards of care.
A 30% reduction in term pre-eclampsia, from 5.6% to 3.9%, is very important. It represents an even greater reduction in the number of pre-eclampsia cases than we can achieve for preterm pre-eclampsia with aspirin.Professor Kypros Nicolaides, founder and chairman of the Fetal Medicine Foundation, and senior author of the paper
This trial took place in busy NHS maternity units serving a highly diverse population, and often socially deprived communities where the burden of pre-eclampsia is greatest. The high level of participation and adherence shows that a personalised, risk-based approach is acceptable, practical, and aligns with what women want from their care. Achieving a 30% reduction in term pre-eclampsia, without increasing emergency Caesarean birth or neonatal admissions, represents a meaningful and reassuring improvement for women, babies, and maternity services.Dr Argyro Syngelaki, Reader in Maternal-Fetal Medicine at King’s College London and co-lead author of the paper
We will soon report on the health economic implications of the trial, as well as the experiences of women and staff who participated, to provide policy-makers with the information that they need to implement the trial intervention within the NHS.Professor Laura A. Magee, Professor of Women’s Health at King’s College London and co-author of the paper
Caffeine may have been unfairly portrayed as the villain in some heart rhythm disorders, according to a new study published in the Journal of the American Medical Association.
Longstanding medical advice has held that patients with atrial fibrillation (AF) should cut back on their caffeine intake – or eliminate it entirely – to improve their condition. Wong et al. conducted an investigation into the relationship between regular caffeinated coffee consumption and the recurrence of atrial fibrillation (AF) or atrial flutter.
The DECAF randomised clinical trial, conducted across five international centres, enrolled 200 patients with persistent AF who were successfully cardioverted and then randomised to either consume caffeinated coffee (averaging one cup daily) or abstain from coffee and caffeine for six months. But contrary to expectations, the caffeine group actually saw an improvement in symptoms.
