Tag: myocardial infarction

Categories : Cardiovascular Disease Lab Tests and ImagingTags : Leave a comment

Dual Imaging Identifies Cause of Heart Attack in Patients Without Blocked Arteries

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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.

Source: NYU Langone Heath

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Stopping Beta-Blockers After Heart Attack is Safe for Low-Risk Patients

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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.

This study was simultaneously published online in the New England Journal of Medicine at the time of presentation.

Source: American College of Cardiology

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Why Heart Attacks in the Morning Have Worse Outcomes

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Human heart. Credit: Scientific Animations CC4.0

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.”

Source: JAMA

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Men’s Heart Attack Risk Climbs by Mid-30s, Years Before Women

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Decades-long US study suggests prevention and screening should start earlier in adulthood

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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.

By Ben Schamisso

Source: Northwestern University

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Human Heart Regrows Muscle Cells After Heart Attack, World-first Study Shows

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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.”

The research was published in Circulation Research.

Source: The University of Sydney

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Even Low-intensity Smoking Increases Risk of Heart Attack and Death

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Study of 300 000 people finds just two to five cigarettes per day increases risk of death by 60%

Photo by lil artsy

An analysis of data from almost two dozen long-term studies finds that even low-intensity smokers have a substantially higher risk of heart disease and death compared to people who never smoked, even years after they quit. Michael Blaha of the Johns Hopkins Ciccarone Center for Prevention of Cardiovascular Disease, USA, and colleagues report these findings November 18th in the open-access journal PLOS Medicine.

Previous research has shown that smoking cigarettes increases a person’s risk of developing cardiovascular disease, but the exact relationship between how heavily a person smokes and their risks is still unclear, especially for low-intensity smokers. Today, more people are smoking fewer cigarettes, but it’s still important to understand the cardiovascular risks and long-term benefits of quitting, even for individuals who aren’t smoking a pack a day.

Blaha’s team analysed data from more than 300 000 adults enrolled in 22 longitudinal studies – which involve following groups of individuals over time – for up to 19.9 years. In that time, they documented more than 125 000 deaths and 54 000 cardiovascular events, such as heart attacks, strokes and heart failure. The analysis showed that even very low-intensity smoking, defined as two to five cigarettes per day, was associated with a 50% higher risk of heart failure and a 60% higher risk of death from any cause, compared to never smoking. A person’s risk of cardiovascular events dropped most substantially in the first decade after quitting smoking and continued to decrease over time. However, even up to three decades later, former smokers may still exhibit higher risk compared to those who never smoked.

Considering that even occasional or very low-intensity smoking significantly increases a person’s risk of cardiovascular disease and death, the researchers conclude that quitting smoking at younger ages is the best way to decrease your risk, rather than reducing the number of cigarettes smoked each day. These findings reinforce established public health guidelines – that smokers should quit as early as possible instead of just cutting back – and emphasize the importance of smoking prevention programs.

The authors add, “This is one of the largest studies of cigarette smoking to date using the highest quality data in the cardiovascular epidemiology literature. It is remarkable how harmful smoking is – even low doses of smoking confer large cardiovascular risks. As far as behaviour change, it is imperative to quit smoking as early in life as possible, as the among of time passed since complete cessation from cigarettes is more important prolonged exposure to a lower quantity of cigarettes each day.”

Provided by PLOS

Press preview: https://plos.io/4nES58Z

In your coverage, please use this URL to provide access to the freely available paper in PLOS Medicine: https://plos.io/4nIQAXN

Contact: Michael Blaha, mblaha1@jhmi.edu

Image caption: Researchers assess the impact of when one quits smoking and their health outcomes later on.

Image credit: lil artsy, Pexels (CC0, https://creativecommons.org/publicdomain/zero/1.0/)

High-resolution image link: https://plos.io/3VIPLCA

Citation: Tasdighi E, Yao Z, Dardari ZA, Jha KK, Osuji N, Rajan T, et al. (2025) Association between cigarette smoking status, intensity, and cessation duration with long-term incidence of nine cardiovascular and mortality outcomes: The Cross-Cohort Collaboration (CCC). PLoS Med 22(11): e1004561. https://doi.org/10.1371/journal.pmed.1004561

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Stem Cell Therapy Linked to Lower Risk of Heart Failure After a Heart Attack

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Technique may be a valuable add-on procedure for patients with weak heart function after a heart attack, say researchers

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

Patients with weak heart function who receive stem cell therapy shortly after a heart attack are at lower risk of developing heart failure and related hospital stays compared with standard care, finds a clinical trial published by The BMJ.

The researchers say the findings suggest this technique may be a valuable add-on procedure for this particular group of patients after a heart attack to prevent subsequent heart failure and reduce the risk of future adverse events.

Advances in heart attack management have improved survival rates considerably, but this has also led to rising rates of subsequent heart failure. While recent studies have indicated that stem cell therapy may reduce rates of heart failure after a heart attack, clinical trials are needed to confirm these benefits.

To address this gap, the researchers set out to assess the impact of delivering stem cells directly into coronary arteries (known as intracoronary infusion) after a heart attack on the development of heart failure over three years.

Their findings are based on 396 patients (average age 57-59 years) with no previous heart conditions at three teaching hospitals in Iran. They had all experienced a first heart attack (myocardial infarction) leading to extensive heart muscle damage and weakened heart function – where the left ventricle, the heart’s main pumping chamber, is too weak to pump blood out to the body as effectively as it should.

Of these, 136 patients in the intervention group received an intracoronary infusion of allogenic Wharton’s jelly derived mesenchymal stem cells within 3-7 days of their heart attack in addition to standard care. The remaining 260 control group patients received standard care alone.

Factors such as age, sex, baseline heart function, smoking status, obesity, existing high blood pressure, diabetes, or kidney problems were taken into account, and patients were monitored for an average of 33 months.

Compared with the control group, intracoronary infusion of stem cells was associated with reduced rates of heart failure (2.77 vs 6.48 per 100 person years), readmission to hospital for heart failure (0.92 vs 4.20 per 100 person years), and a combined measure of cardiovascular death and readmission for heart attack or heart failure (2.8 vs 7.16 per 100 person years).

The intervention did not have a statistically significant effect on readmission to hospital for heart attack (1.23 vs 3.06 per 100 person years), death from any cause (1.81 vs 1.66 per 100 person years), or cardiovascular death (0.91 vs 1.33 per 100 person-years).

However, by six months heart function in the intervention group showed a significantly greater improvement from baseline at six months compared with the control group.

This was a large trial with long term follow-up and clinically meaningful outcome measures, but the researchers acknowledge several limitations to their findings. These include the inability to do a sham procedure for the control group, which would have allowed for a double blinded study design instead of a single blinded format. Nor did they assess heart failure biomarkers or investigate the physiological effects of the intervention on heart tissue.

Nevertheless, they say these results suggest that this technique “may serve as a valuable adjunctive procedure after myocardial infarction to prevent the development of heart failure and reduce the risk of future adverse events.”

Additional trials confirming this finding are needed as well as further research “to explore the underlying mechanisms of mesenchymal stem cells therapy and to optimise its application in clinical practice,” they add.

Source: BMJ Group

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Some Heart Attack Patients Can Benefit From Screening for Helicobacter Pylori

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Not all acute myocardial infarction patients should be offered routine screening for the stomach ulcer bacterium Helicobacter pylori. However, it is possible that some patient groups with an elevated risk of post-infarction gastrointestinal bleeding benefit from such a test, concludes a large-scale study from Karolinska Institutet and Södersjukhuset published in the journal JAMA.

Upper gastrointestinal bleeding is a serious complication that affects approximately two per cent of patients within a year of a myocardial infarction.

“It’s associated with increased mortality and the risk of recurring cardiovascular events,” says the study’s lead author Robin Hofmann, senior consultant at the Department of Cardiology, Södersjukhuset, and associate professor at the Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet. “We therefore wanted to examine if screening for the common Helicobacter pylori bacterium, which causes gastritis and gastric ulcers, can reduce the risk of bleeding. This is currently not routine practice.”

The randomised study included almost 18 500 myocardial infarction patients at 35 hospitals in Sweden. Half the group was tested for the bacterium and treated with antibiotics and protein pump inhibitors by their doctors if testing positive, while the other half received routine care without an extra test or treatment.

Effective in anaemic patients

After almost two years’ follow-up, the researchers found that there were slightly fewer individuals in the screening programme who had suffered gastrointestinal bleeding, but not enough to make the difference statistically significant. However, they found a positive effect of the screening when studying specific sub-groups of patients, such as those with anaemia or kidney failure. A particularly positive effect was observed in patients with moderate to severe anaemia, who suffered gastrointestinal bleeding at roughly half the rate if they underwent screening.

“Our results suggest that screening for Helicobacter pylori does not need to be done routinely for all individuals following a heart attack,” says Dr Hofmann. “On the other hand, testing and treatment could be a meaningful complement for selected patient groups with an elevated risk of bleeding.”

The researchers will now go on to study the long-term effects and try to identify which groups will benefit most from screening.

Source: Karolinska Institutet

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New Studies Explore Early Aspirin Withdrawal and Tailored Antiplatelet Strategies Following PCI

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Percutaneous coronary intervention.
Percutaneous coronary intervention. Credit: Scientific Animations CC4.0

Early withdrawal of aspirin following successful percutaneous coronary intervention (PCI) for acute coronary syndrome and in low-risk patients following an acute myocardial infarction (MI) was the focus of two separate hot line trials presented at ESC Congress 2025. A third trial provided insights into early escalation and late de-escalation of antiplatelet therapy after complex PCI.

In the NEO-MINDSET trial, simultaneously published in NEJM, researchers in Brazil randomised approximately 3400 patients within the first four days of hospitalisation following a successful PCI to either stop treatment with aspirin and receive potent P2Y12 inhibitor monotherapy (ticagrelor or prasugrel) or to receive dual antiplatelet therapy (DAPT) that included aspirin and a potent P2Y12 inhibitor for 12 months.

At 12 months, the primary endpoint of death from any cause, MI, stroke or urgent revascularisation had occurred in 119 patients in the monotherapy group and in 93 patients in the DAPT group (p = 0.11 for noninferiority). Researchers also noted that major or clinically relevant nonmajor bleeding occurred in 33 patients assigned to monotherapy vs 82 patients assigned to DAPT. Stent thrombosis occurred in 12 patients in the monotherapy group and in 4 in the dual antiplatelet therapy group.

“We failed to demonstrate the noninferiority of aspirin-free monotherapy initiated immediately after PCI with regard to the ischaemic primary endpoint over 12 months,” said Principal Investigator Pedro Lemos, MD. “Results from the landmark analysis suggest that the excess ischaemic risk with monotherapy occurred in the first 30 days, with comparable outcomes thereafter. Bleeding appeared to be lower at both 30 days and 12 months with monotherapy versus DAPT.”

In TARGET-FIRST, also simultaneously published in NEJM, P2Y12-inhibitor monotherapy was noninferior to continued DAPT with respect to the occurrence of adverse cardiovascular and cerebrovascular events among low-risk patients with acute MI who had undergone early complete revascularisation and had completed one month of DAPT without complications. It also resulted in lower incidence of bleeding events.

Nearly 2000 patients from 40 centres in Europe were randomised to receive P2Y12-inhibitor monotherapy or to continue DAPT for 11 months. A primary-outcome event occurred in 20 patients (2.1%) in the P2Y12-inhibitor monotherapy group and in 21 patients (2.2%) in the dual antiplatelet therapy group (p = 0.02 for noninferiority). Major bleeding occurred in 2.6% of the patients assigned to P2Y12-inhibitor monotherapy group compared with 5.6% of those assigned to DAPT (p = 0.002 for superiority). The incidence of stent thrombosis and serious adverse events appeared to be similar in the two groups, researchers said.

Principal Investigator Giuseppe Tarantini, MD, noted that no previous randomised trials have assessed early aspirin discontinuation in acute MI patients who achieve early, complete revascularisation with modern stents. “These results reflect the benefits of modern stents, high procedural success and optimal medical therapy, making early aspirin discontinuation feasible in this selected population,” he said.

The TAILORED-CHIP trial found early escalation and late de-escalation of antiplatelet therapy is not beneficial in patients with high-risk anatomical or clinical characteristics undergoing complex PCI.

Researchers in South Korea randomised approximately 2000 patients to standard DAPT (clopidogrel plus aspirin for 12 months) or a tailored antiplatelet strategy consisting of early escalation (low-dose ticagrelor at 60mg twice daily plus aspirin for 6 months) followed by late de-escalation (clopidogrel monotherapy for 6 months).

Overall findings showed no significant difference in the incidence of major ischemic events at 12 months with tailored therapy compared with standard DAPT. However, the incidence of clinically relevant bleeding was significantly higher with tailored therapy, according to study investigators.

“Our results suggest that a tailored strategy in patients undergoing complex high-risk PCI does not provide a net clinical benefit,” said Principal Investigator Duk-Woo Park, MD, PhD, FACC. “We observed an increase in bleeding complications without a significant reduction in ischaemic events. This challenges the notion that ‘more is better’ even in carefully selected patients at high ischaemic risk.”

Source: American College of Cardiology

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Clinical Trial Challenges 40-year-old Standard of Care for Heart Attack Patients

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Human heart. Credit: Scientific Animations CC4.0

Beta-blocker therapy showed no evidence of an effect on all-cause death, reinfarction or heart failure admission in patients with myocardial infarction (MI) managed invasively who had left ventricular ejection fraction (LVEF) ≥ 40%, according to late-breaking research from the REBOOT trial presented in a Hot Line session today at ESC Congress 20251 and simultaneously published in the New England Journal of Medicine. 

Explaining the rationale for the REBOOT trial, Principal Investigator, Professor Borja Ibáñez from the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) and Fundación Jiménez Díaz University Hospital, Madrid, Spain, said: “Beta-blockers have long been a foundational treatment after acute MI; however, supporting evidence is derived from trials that predate modern standards of care − before the time of routine reperfusion, invasive management, potent antiplatelet therapies and statins. Re-examining the role of beta-blockers is warranted, particularly among patients with uncomplicated MI and LVEF > 40% in whom the benefits of beta-blockers are not well established, unlike with reduced LVEF (≤ 40%).”  

The investigator-initiated randomised open blinded-endpoint REBOOT trial was conducted at 109 centres across Spain and Italy. Patients with MI (with or without ST-segment elevation) were eligible for enrolment if they underwent invasive management during the index hospitalisation and had a predischarge LVEF > 40%, with no history or signs of heart failure. Patients were randomised 1:1 to beta-blocker or no beta-blocker therapy. The primary endpoint was a composite of all-cause mortality, nonfatal reinfarction or heart failure admission. 

Among 8505 patients who underwent randomisation, the mean age was 61 years and 19.3% were women. A total of 10% had a prior MI and 12% were on beta-blocker treatment before the index hospitalisation. 

After a median follow-up of 3.7 years, the primary composite outcome of all-cause death, nonfatal reinfarction or heart failure admission occurred in a similar proportion of patients in each group: 22.5/1000 patient-years in beta-blocker group and 21.7/1000 patient-years in the no beta-blocker group (hazard ratio [HR] 1.04; 95% confidence interval [CI] 0.89 to 1.22; p=0.63). 

All-cause mortality occurred in 11.2 and 10.5/1000 patient-years on beta-blocker therapy and no-beta blocker therapy, respectively (HR 1.06; 95% CI 0.85 to 1.33). Nonfatal reinfarction occurred in 10.2 and 10.1/1000 patient-years, respectively (HR 1.01; 95% CI 0.80 to 1.27), while heart failure admission occurred in 2.7 and 3.0/1,000 patient-years, respectively (HR 0.89; 95% CI 0.58 to 1.38).  

Regarding safety, admission for stroke occurred in 2.6/1000 patient-years in the beta-blocker group and 1.7/1000 patient-years in the no beta-blocker group (HR 1.50; 95% CI 0.90 to 2.49). Admission for symptomatic advanced atrioventricular block occurred in 0.5 of patients in the beta-blocker group and 0.4/1000 patient-years of patients in the no beta-blocker group (HR 1.18; 95% CI 0.40 to 3.50). 

There appeared to be an absence of benefit with beta-blockers across the prespecified subgroups. However, fewer events were noted in patients with mildly reduced LVEF (40−49%) on beta-blockers vs no beta-blockers, although low patient numbers limit interpretability. Women experienced overall more events, especially when on beta-blockers. 

Professor Ibáñez concluded: “Beta-blocker therapy showed no evidence of benefit across the study population of patients with MI managed invasively who had LVEF > 40%. However, as also presented today at ESC Congress, a meta-analysis of data from four trials, including REBOOT, suggest there may be a positive signal in patients with mildly reduced LVEF (40−49%).2” 

Source: European Society of Cardiology