Patients treated with medication for benign prostatic hyperplasia at the time of a severe acute heart attack experienced fewer serious complications from the attack, according to a study from the University of Gothenburg.
Men likely suffer from more extensive heart attacks than women. Studies have shown that male sex hormones, such as testosterone, intensify inflammation during an acute heart attack and lead to a larger area of damage.
Inflammation is a key factor in the extent of heart damage when an acute heart attack is treated with balloon angioplasty, one of the most common methods for rapidly opening blocked vessels that supply blood to the heart muscle.
Protected after heart attack
The registry study, published in JAMA Network Open, shows that Swedish patients treated with finasteride for benign prostatic hyperplasia faced a lower risk of serious complications following an acute heart attack compared to patients matched to be as similar as possible in all respects other than the use of this specific drug.
Finasteride belongs to the class of drugs known as 5-alpha-reductase inhibitors, which reduce the size of an enlarged prostate. The drug blocks an enzyme that converts testosterone into dihydrotestosterone, a more potent and biologically active form of testosterone.
Among those treated with finasteride, the risk of serious complication was 20.8 percent, compared to 24.3 percent among the matched controls. Serious complications included, for example, cardiac arrest, severe signaling disturbances affecting heart rhythm and pumping ability, severely impaired left ventricular function, or death within 30 days.
Greater insight into the impact
The link between finasteride treatment and less severe complications following a heart attack aligned with the researchers’ hypothesis. However, no significant difference was observed for patients treated with hormone medication for prostate cancer.
Hannah Colldén, a pharmacist and researcher at the University of Gothenburg, comments:
“This result contributes to the exciting field of research into how sex hormones can affect the heart, for instance during a heart attack, but it has no direct impact on patient treatment at present.”
The study is based on the SWEDEHEART quality registry and national registers, including all men who suffered a severe acute heart attack, specifically an ST-elevation myocardial infarction (STEMI), and underwent balloon angioplasty. Those treated with drugs affecting male sex hormones (androgen-modulating agents) were matched with similar individuals who had also suffered a heart attack but did not receive that treatment.
For the past two decades, doctors have been using therapeutic hypothermia to prevent or treat brain injury in comatose survivors of cardiac arrest. The process involves cooling down the body, which slows the body’s metabolism and triggers other protective mechanisms that reduce brain damage. However, clinical trials of therapeutic hypothermia for out-of-hospital cardiac arrests have not consistently shown that the process works.
To get a clearer understanding, University of Michigan doctors and researchers led the Influence of Cooling duration on Efficacy in Cardiac Arrest Patient, or ICECAP, trial to determine if longer durations of cooling are more effective than those previously used. The largest US trial focusing on this question, ICECAP included 71 hospitals in the US between 2020-2025 and investigated adults who underwent cooling durations between six and 72 hours.
“We knew that cooling reduces brain injury, but we didn’t know how to make that work in a clinical environment,” said Robert Silbergleit, MD, Professor of Emergency Medicine.
“Most of the previous trials used limited durations of cooling, but longer durations were better in laboratory experiments. We wanted to study whether longer durations were more beneficial for adults with cardiac arrest.”
The study, published in JAMA, focused on 1158 patients, across different genders and races, whose heartbeats were restored with or without a defibrillator. It also included a range of injury severity seen in emergency departments. Patients who suffer cardiac arrests fall into two categories: those who have a sudden arrest, usually from a heart attack and those whose bodies have slowed down over time.
“The two situations created a lot of uncertainty in previous studies because those who have a sudden arrest are usually less sick and their hearts can be quickly restarted with defibrillators,” said William Meurer, MD, Professor of Emergency Medicine and Neurology.
“It was important to study both populations because sometimes doctors can give up hope for patients who had a longer period of CPR and never received a defibrillator shock.”
The study found that outcomes did not change when they underwent cooling for longer durations. Future analyses will explore whether duration of cooling was more important for some types of patients but not others. Additionally, the survival rate in the non-shockable patients was higher than in previous studies with cooling.
“Our study showed that some patients undergoing therapeutic hypothermia can wake up even after two weeks,” Meurer said. “Although it can be a difficult process to go through, it gives families and doctors hope.”
The team is conducting a similar study for paediatric cardiac arrest patients where they are looking at the benefits of cooling for up to four days.
A highly sensitive cardiac test brings traditional lab diagnostics to the field, when it’s most needed
Illustration of a portable cardiac troponin I testing system that wirelessly transmits results to a smartphone.Credit: AI-generated image
A person having a heart attack may be only feet from medical care but miles from the laboratory testing needed to confirm it. That gap matters, especially for rural patients, those in nursing homes, ambulances and other places where access to specialised diagnostics is limited.
In a paper published in Biosensors and Bioelectronics, an international team of researchers details a highly sensitive test designed to bring that molecular evidence closer to the patient.
“A heart attack doesn’t wait for laboratory results,” said lead author Sayantan Tripathy, assistant research scientist in Texas A&M University’s Optical and Bio-Sensing Laboratory in the College of Engineering. “By reducing the time needed to detect heart muscle damage, we’re helping clinicians move more quickly from uncertainty to action, not only in hospitals, but also in ambulatory and resource-constrained settings where rapid diagnostic tools are often unavailable.”
Clinicians may suspect a heart attack based on symptoms or an electrocardiogram, but confirming heart muscle damage has occurred often requires testing for cardiac troponin I, a protein released into the bloodstream when the heart is injured. The most sensitive versions of those tests typically rely on centralised laboratory equipment, creating a potentially dangerous delay between suspicion and certainty.
“Our goal is for emergency medical technicians in an ambulance to be able to take someone’s fingertip sample – just a small finger prick – put that sample into a cartridge that contains all of our components, plug this cartridge into our device, and then be able to run the test in five minutes,” said Dr Samuel Mabbott, associate professor of biomedical engineering and study co-author.
Faster heart attack diagnosis
Many of today’s troponin tests depend on expensive laboratory instruments and trained personnel. As a result, obtaining the information needed to confirm a heart attack can take time, especially when advanced laboratory resources are not immediately available.
“Our vision is to bring affordable and sensitive advanced molecular diagnostics closer to where care is delivered,” said Dr Gerard Coté, professor of biomedical engineering and director of Texas A&M’s Center for Remote Health Technologies and Systems. “The less distance between the patient and the information clinicians need, the faster critical decisions can be made.”
To create the test, the researchers designed a specific structured DNA molecule that remains inactive until it encounters cardiac troponin I. Once it detects the biomarker, it triggers a series of molecular reactions that amplify the signal, making it easier to detect even very small amounts of heart damage. The amplified signal is then measured using portable optical sensing technology.
The researchers say the technology requires additional development before it could be used in clinical practice. The original work takes approximately two hours to complete, but the current version of the technology has reduced the testing time to less than 25 minutes, and further work is underway to shorten it to under 15 minutes, improving its user applicability.
Still, the study points toward a future in which life-saving diagnostic information is no longer tied to a centralized laboratory and can instead move closer to the patients who need it most.
Every day, thousands of people worldwide suffer a heart attack, often leading to lasting damage to the heart muscle. New research from the University of Oslo suggests that targeting inflammation in the body helps protect the heart and improve recovery after a heart attack.
“In a small country like Norway alone, we see around 11 000 heart attacks every year,” says postdoctoral fellow Camilla Huse at the Research Institute for Internal Medicine, at University of Oslo and Oslo University Hospital. “Forty heart attacks every day is a lot.”
Fortunately, modern treatments are so effective that most patients survive a heart attack.
Inflammation damages the heart
However, a heart attack triggers a strong inflammatory reaction in the body. While this inflammation is part of the body’s natural response, it also causes damage to the heart muscle during a heart attack.
Such injury can lead to poorer health, a reduced quality of life and fewer working years for those affected. It also increases the risk of developing new heart diseases later in life.
So, how can we protect the heart during a heart attack?
Can anti-inflammatory medication improve heart attack treatment?
For some time, the researchers at the University of Oslo and Oslo University Hospital have been studying a medicine that blocks the effect of a substance that stimulates inflammation, a substance called IL-6. Previously, they have shown that administering this medicine in addition to established treatment for heart attacks has promising results: the patients suffered less damage to their hearts.
“This could be a new way of treating patients,” senior researcher Tuva Børresdatter Dahl says, and continues:
“To move forward with treatment, we need to understand what happens in the body when we block inflammation. Which processes inside the cells are affected by the medicine being tested? Which are not? And how does this relate to damage to the heart and to the improved recovery of the patient?”
How to investigate the effect of the treatment
The researchers conducted a study in which they examined the immune cells of 200 patients with STEMI. STEMI is a type of heart attack where the risk of serious complications is high.
The patients were randomly divided into two groups. Half of them received the anti-inflammatory medication, blocking the IL-6 signal, while the other half received a placebo, i.e. a treatment without any active ingredient.
The researchers then monitored how the treatment affected the immune cells in the blood. They also measured how much of the heart muscle was damaged.
Monocytes at the front line of our immune system
The researchers found that the treatment affects a type of immune cell called monocytes, which play an important role in all forms of inflammation.
“The monocytes are right at the front line of our immune system. They are among the first immune cells to arrive to the heart when a heart attack occurs,” Huse says.
Shortly after a heart attack, a strong inflammatory mobilisation occurs in the body, and monocytes flow to the heart muscle.
“The monocytes help to repair and clean up after a heart attack. But they can often get a little too eager. Thus, they also contribute to worsening the damage to the heart muscle after the heart attack,” she explains.
Reduced inflammation linked to better heart attack recovery
The study showed that the patients who received the anti-inflammatory medication had fewer monocytes in their blood shortly after the heart attack.
Normally, having high levels of these immune cells soon after a heart attack are linked to more heart damage and worse outcomes for the patients. Lower levels, on the other hand, are associated with less damage to the heart and better healing.
The researchers also found that the medicine made the cells in the heart muscle more resistant to damage, so that more heart cells survived the heart attack.
The study showed that patients who received the anti-inflammatory drug (dark blue) had fewer monocytes in their blood shortly after the heart attack. Illustration from the researchers.
Changing immune cell behaviour to protective
As a result of the treatment, the way the monocytes behave was also changed.
“The function of the monocytes changed, from being more harmful to becoming more protective. The “good” functions of the immune cells were strengthened,” Huse says.
“We believe that those functions are the reason why patients suffer less damage after the heart attack. The heart is helped towards recovery,” she adds.
The study also showed another important effect: mechanisms that normally draw inflammatory cells into the damaged area were prevented in the patients who received the medicine.
What could this mean for heart attack patients in the future?
The research provides new insight into how inflammation affects the heart during a heart attack, and how this treatment can protect the heart from damage following STEMI.
This creates an opportunity for anti-inflammatory drugs to become part of a standard treatment for heart attacks and give patients a better life afterwards.
“The study shows that monocytes play an important role in the development of heart attacks. We believe that affecting these cells, which the blocking of IL-6 does, is beneficial. It could be a new and important additional treatment for these patients,” Dahl points out.
Why mechanism-focused research matters
The researcher believes that more such in-depth studies are needed when new medicines are tested.
“They provide a better understanding of the mechanisms behind illness and how the medicine affects the body. It doesn’t just tell us whether a treatment has worked, but also why or why not.
“Such knowledge can make new treatment options possible. This type of research should therefore be prioritised in future clinical studies,” Dahl says.
Reference
Huse C, Murphy SL, Yang K, Balzer NR, Stokke MK, Anstensrud AK, et al. The effects of interleukin-6-receptor inhibition on monocytes in STEMI: a substudy of the ASSAIL-MI trial. EBioMedicine. 2025. doi:10.1016/j.ebiom. 2025.105960
By Julie Nybakk Kvaal, Institute of Clinical Medicine
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.”
International study supports combining advanced imaging to guide diagnosis and care
Photo by Joice Kelly on Unsplash
When Ashley Perlow felt a sharp pain shoot across her chest and into both wrists, she didn’t think it could be a heart attack. She was 36, a new mom, and otherwise healthy.
At the hospital, blood tests showed signs of a heart attack, but her arteries appeared normal.
Now, new research led by clinicians and researchers at NYU Grossman School of Medicine shows that in cases like hers, using two complementary heart imaging tests can identify the underlying cause of these heart attacks in most patients without coronary artery narrowing, helping guide diagnosis and medical treatment in a condition that often leaves patients without clear answers. The study is among the largest and most comprehensive to examine MINOCA, or myocardial infarction with non-obstructive coronary arteries, a condition that accounts for 6 to 15% of heart attacks and is about three times more common in women than men.
“When arteries are not badly blocked, it can be unclear what caused the event,” said Harmony R. Reynolds, MD, lead author and director of the Cardiovascular Clinical Research Center in the Leon H. Charney Division of Cardiology at NYU Langone Health. “What we show is that in most cases, we can find the underlying explanation, and most often it is a true heart attack. Our results support the need to do specialised imaging in all patients with MINOCA, because we could not reliably predict who will have specific imaging findings.”
The findings come from the Heart Attack Research Program (HARP), a large international, prospective study. The latest results were presented by Dr Reynolds as featured clinical research at the American College of Cardiology’s 2026 Annual Scientific Session and simultaneously published March 28 in Circulation.
Dr Reynolds and the team found that combining coronary optical coherence tomography (OCT) and a cardiac magnetic resonance imaging (MRI) identified the underlying cause of the heart event in 79 percent of study participants.
How Advanced Diagnostic Imaging Reveals the Cause
To better understand these cases in both women and men, researchers enrolled 336 patients across 28 international sites in the Unites States, Canada, and the United Kingdom. The median age of participants was 58 years, including 270 women and 66 men.
Using coronary OCT and cardiac MRI, researchers identified underlying causes, assessed how often each test provided a diagnosis, and examined differences between sexes.
During coronary OCT, a thin catheter is placed inside the coronary arteries to capture high-resolution images of the artery wall, helping detect plaque buildup or blood clots that may not appear on a standard angiogram. Cardiac MRI provides detailed images of the heart muscle, showing where damage has occurred and whether it is related to reduced blood flow, inflammation, or another cause.
Using both imaging techniques together, researchers identified a likely cause in 79% of patients.
Most (59%) had a typical heart attack mechanism related to reduced blood flow from plaque buildup, artery spasm or blood clotting, while 20% (67 patients) had conditions that mimic a heart attack, such as myocarditis, takotsubo syndrome, or other cardiomyopathies. These nonischaemic conditions require different treatment approaches than traditional heart attacks.
The new research builds on earlier work by Dr Reynolds and colleagues, published in 2020 in Circulation, that demonstrated the value of using the same imaging methods in a smaller group of women. The current study expands those findings to a larger, more diverse international population.
Implications for Patient Care
The findings provide important support for current clinical guidelines, which recommend additional imaging in these patients but have largely been based on expert consensus rather than large-scale data. The results also highlight the limitations of standard angiography, which shows blood flow but cannot detect problems within the artery wall or subtle heart muscle injuries.
The combination of OCT and cardiac MRI provided a significantly higher diagnostic yield than either test alone. The study also found that doctors cannot reliably predict which patients will benefit from one imaging test versus another based on symptoms, blood tests, or initial findings. Even patients with relatively low levels of cardiac biomarkers frequently had detectable heart damage on imaging.
“We had hoped to be able to tailor testing to individual patients,” said Dr Reynolds. “Instead, we found that comprehensive imaging is often necessary to get the full answer.”
Although MINOCA occurs more frequently in women, researchers found no significant differences in the underlying causes between women and men once the condition developed. This suggests that the disease process itself is similar once it occurs.
For Perlow, that clarity was critical. After months of unanswered questions, she was referred to Dr Reynolds at NYU Langone, where further evaluation and testing helped officially diagnose her condition as MINOCA and guide her care.
Findings suggest lifelong beta-blockers may be unnecessary in some patients
Human heart. Credit: Scientific Animations CC4.0
Among stable, relatively low-risk patients who had previously suffered a heart attack, discontinuing beta-blockers after at least one year was found to be non-inferior, or comparable, to continuing beta-blockers in terms of death, another heart attack or hospitalisation for heart failure, according to a study presented at the American College of Cardiology’s Annual Scientific Session (ACC.26).
Beta-blockers, which lower heart rate and blood pressure by inhibiting adrenaline and other hormones, have long been a mainstay of treatment to reduce the likelihood of subsequent cardiac events following a heart attack. However, many studies confirming their benefits were conducted decades ago, when procedures and medications for secondary prevention were more limited than they are today. More recent studies suggest the benefits of beta-blockers may vary depending on the overall health of a patient’s heart.
“In appropriately selected patients who survived a heart attack and do not have heart failure or left ventricular systolic dysfunction, routine continuation of beta-blockers indefinitely may not be necessary,” said Joo-Yong Hahn, MD, a cardiologist at Samsung Medical Center in Seoul, South Korea, and the study’s senior author. “In practice, for stable patients who are several years out from a heart attack, discontinuation can be considered through shared decision-making and with monitoring of blood pressure and heart rate. For patients with beta-blocker-related side effects – fatigue, dizziness, bradycardia, hypotension – the case for discontinuation is even stronger.”
The study evaluated 2,540 patients at 26 sites in South Korea between 2021 and 2024 who had no subsequent cardiac events after taking beta-blockers for at least one year following a heart attack. Participants’ average age was 63 years and 87% were men. At a median of 3.5 years following randomisation, the primary endpoint – a composite of all-cause death, recurrent heart attack or heart failure hospitalisation – occurred in 7.2% of those who discontinued beta-blockers and 9% of those who continued taking the medication. The results met the threshold for non-inferiority because of a lower rate of this composite endpoint in the group that stopped taking beta-blockers.
Discontinuation of beta-blockers was also found to be similar for secondary endpoints, including each of the components of the primary composite endpoint, new-onset atrial fibrillation, unfavourable changes in left ventricular function, changes in quality of life and serious adverse events.
“In current practice – where revascularisation rates are high and secondary prevention is strong – we expected that the incremental benefit of continuing beta-blockers indefinitely in stable patients might be small,” Hahn said. “We found that discontinuation did not worsen major outcomes, cardiac function or quality of life in this selected stable population.”
Since most study participants had been taking beta-blockers for several years before discontinuing, Hahn said that the results may not apply to patients who have been taking beta-blockers for a shorter amount of time. The study also does not definitively establish the earliest timepoint at which it is safe to stop taking beta-blockers.
The results were generally consistent across prespecified subgroups. However, women and patients with mildly reduced left ventricular ejection fraction made up a small proportion of the trial population, limiting the interpretation of results for these subgroups. In addition, the study was conducted only in South Korea, potentially limiting its generalisability to other areas of the world.
Hahn said future studies could help to clarify whether and when it is safe to discontinue beta-blockers among higher-risk groups, women and those with mildly reduced left ventricular ejection fraction and to better define the optimal timing of discontinuation. Pooled analyses across contemporary randomised trials could provide additional insights and help guide practice decisions. The researchers also plan to conduct further analyses to assess potential differences in health care costs.
The study was funded by the Patient-Centered Clinical Research Coordinating Center in the Ministry of Health and Welfare of the Republic of Korea.
It has long been known that heart attacks occurring in the morning are typically more serious than those that happen at night. While daily variations in stress hormone levels and blood pressure affect cardiac health, these are only part of the picture. There is also the diurnal variation in immune response involved: neutrophils, the body’s ‘first responders’, cause more inflammatory damage in the morning, causing havoc even as they neutralise pathogens.
“They’re the first sentinel, but they come fully loaded,” said Douglas Mann, MD, professor at Washington University School of Medicine in St Louis. “They’re shooting at everything and dumping a lot of toxic granules on the environment. They are indiscriminate in terms of their ability to destroy, and they take out healthy cells in the process.”
But exactly why they are more damaging at night has been a mystery. Now, researchers have found the reason behind this diurnal difference in destructiveness, and also how to tweak the ‘internal clocks’ of these white blood cells so that they cause less damage during sterile inflammation while still protecting against pathogens. Their findings are reported in the Journal of Exploratory Medicine, and are summarised in JAMA news.
Finding the pattern
The researchers, from Spain and Yale University, discovered that the timing of heart attacks significantly affects their severity due to a ‘neutrophil clock’ controlled by circadian rhythms. Neutrophils are more active during the day (activated by the Bmal1 protein) and less active at night (inhibited by the CXCR4 receptor).
Analysing more than 2000 patients with ST-segment elevation myocardial infarction, the researchers found that those who had an MI in the morning suffered worse cardiac damage than those who had them at night. Mouse experiments confirmed this pattern and showed that genetically disabling the Bmal1 protein reduced daytime neutrophil activity, protecting against severe cardiac injury.
This suggests a treatment strategy of tricking neutrophils into remaining in their nighttime inactive state, allowing doctors to reduce inflammation and lessen heart attack damage during daytime hours without compromising the immune system’s ability to fight infections.
Reducing cardiac damage without compromising the immune system
Mice engineered to have high levels of CXCR4 were given a drug compound, ATI2341, which bound to CXCR4 receptors. When heart attacks were induced, the mice showed reduced tissue damage. To test the neutrophils’ pathogen-fighting ability, they were also infected with Staphylococcus aureus or Candida albicans, but the mice were able to overcome the infection – the treated mice even tolerated the Candida infection better than the controls.
Mann explained why controlling the neutrophils was a better option. “Prior trials have tried to neutralise neutrophils or reduce neutrophil numbers entirely,” Mann noted. “But when you get rid of neutrophils, you’re also handcuffing the immune system. Before, it was considered an inevitability that neutrophils killing off infection also meant damaging a lot of tissue.”
The crucial question is of course whether this research in mice can translate to humans.
Luigi Adamo, MD, PhD, director of cardiac immunology at Johns Hopkins University who was not involved in the study, said that the study, one of the first use immune circadian rhythms to modulate inflammation, “offers new insight into neutrophils and a new way to look at this cardiac damage that might even apply to other types of sterile inflammation.”
Adamo struck a note of caution: the extremely low success rate in animal-to-human translation in cardioimmunology. “Immune cells are not always the same when you go from mice to humans,” he said.
Treatment implementation is a major obstacle
Even if this neutrophil clock alteration could be applied to humans, it would be difficult to administer since heart attacks strike without warning.
“If everyone took one of these drugs in the morning when they woke up, maybe it would make heart attacks less severe, but ‘preventive’ means you’re giving it chronically, and I don’t know what would happen with long-term stimulation of that receptor and other cell types,” Mann said. “Their data support the acute application, but in the long term, that’s a whole different story.”
As systemic treatment, the off-target effects of ATI2341 would need to be explored. He also struggled to envision a potential therapeutic solution.
“Today, when you have a heart attack, in most places with hospitals and well-developed health care systems, the patient gets an angioplasty,” Mann said. “The only time this drug could be given would be at the time of reperfusion, when you’re blowing up the balloon and opening up the clot.” Typically, ideal reperfusion timing is within two hours – but neutrophils probably do their damage within a matter of 30 minutes, Mann explained. “It’s a race against time, and I’m curious if [the researchers] can demonstrate that.”
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.
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.”
