Category: Cardiovascular Disease

Statins Cut Heart Attack and Stroke Risk in Older People by 30%

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A world-first clinical trial conducted by Monash University researchers has shown that cholesterol-lowering medication can reduce heart attack and stroke in people aged over 70 years.

Statins are commonly prescribed to manage high cholesterol in people up to 75 years, and are known to reduce the risk of heart attack and stroke. But until now it was unclear whether they were effective in older people.

New research from Monash University, published in the New England Journal of Medicine and presented concurrently at the European Society of Cardiology Congress 2026, found the medication decreases the risk of a first major cardiovascular event by 30 per cent for adults aged over 70 living independently.

The Statins in Reducing Events in the Elderly (STAREE) Trial is the first randomised controlled trial of statin therapy to examine whether the drugs could help in older people who have historically been overlooked in clinical trials.

This landmark, ten-year trial analysed the cardiovascular outcomes of almost 10 000 participants while they took either a statin or placebo.

Lead researcher Adjunct Professor Sophia Zoungas, from the Monash School of Public Health and Preventive Medicine, said the findings will change the way clinicians manage cardiovascular risk in older people.

“What we hope to see, now that we have provided such strong evidence, are updated treatment guidelines to help clinicians make use of this new finding,” Professor Zoungas said.

The global prevalence of cardiovascular disease is expected to almost double from 600 million in 2025 to more than one billion affected adults in 2050. An estimated 2 ,000 older Australians suffer from major cardiovascular events, like heart attack and stroke, each year. The risk increases with age, so people aged over 70 are automatically in a high risk category regardless of lifestyle or other factors.

“The risk of heart attack and stroke is a major concern for older people,” Professor Zoungas said. “Knowing there is a safe and effective measure for lowering that risk will be a huge reassurance to older people and their families.

“Anyone who has seen a loved one impacted by cardiovascular disease will know just how important prevention is.”

Co-author Professor Mark Nelson, a prominent general practitioner, Adjunct Professor at the Monash School of Public Health and Preventive Medicine and Research Fellow at Menzies Institute for Medical Research at the University of Tasmania, said this is critical evidence to support GPs in their decision-making around cardiovascular health in older people.

“This was a particularly important trial because it was conducted in the community, with more than 3400 GPs taking part across Australia,” Professor Nelson said. “In light of this new evidence, older patients should have a conversation with their GP about whether statins are an appropriate treatment for their cardiovascular health to help them remain fit and healthy.”

Read the research paper: http://doi.org/10.1056/NEJMoa2607314

Source: Monash University

Prostate Medication Linked to Fewer Complications After Heart Attack

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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.

Study: Androgen-Modulating Drugs and Severe Complications After ST-Elevation Myocardial Infarction

Source: University of Gothenburg

Study Finds Long-Term Benefits of Stroke Thrombectomy

Thrombophilia. Credit: Scientific Animations CC4.0.

A one-year follow-up analysis of a landmark clinical trial suggests that patients with severe strokes experienced better long-term outcomes after undergoing endovascular thrombectomy compared with medical management alone, according to findings published in JAMA.

The study evaluated ischemic stroke patients presenting with large-core infarcts, meaning a significant amount of brain tissue had suffered damage. These patients are historically considered less likely to benefit from mechanical clot removal because of the amount of brain damage that has already occurred by the time treatment begins, said Sameer A. Ansari, MD, PhD, professor and chief of Interventional Neuroradiology in the Department of Radiology, who was a co-author of the study.

While the original trial did not show meaningful benefit at 90 days, the newly reported one-year data show functional gains among patients who received thrombectomy. The results of the current study suggest longer-term follow-up was needed to fully understand the benefits of the procedure, Ansari said.

“At one year, it’s quite evident based on the statistical analysis that there’s significant benefit with thrombectomy,” said Ansari, also a professor in the Ken and Ruth Davee Department of Neurology and of Neurological Surgery.

In the study, investigators found that 23.6 percent of patients treated with endovascular thrombectomy achieved functional independence one year after their stroke, compared with 6.8 percent of patients who received medical management. Patients in the thrombectomy group were also significantly more likely to regain the ability to walk independently, with 35.4 percent achieving independent walking versus 18 percent in the medical-management group.

The multicentre trial enrolled patients at 47 US stroke centres who presented within 24 hours of symptom onset and had large strokes identified using noncontrast computed tomography (CT) imaging.

Patients who underwent thrombectomy also reported better quality of life one year after stroke, while one-year mortality rates were similar between the treatment groups.

The findings add to growing evidence from other large core interventional stroke trials that patients with extensive brain injury can still benefit from rapid thrombectomy to restore blood flow.

One possible explanation for the delayed benefit, Ansari said, is that recovery from severe stroke continues long after the standard 90-day assessment period used in most clinical trials.

“We know that people continue to improve after a stroke for the next one to two years,” Ansari said. “Three months has been an arbitrary standard used in prior stroke trials to assess benefit and functional outcomes after targeted interventions.”

Restoring blood flow may also support long-term neuroplasticity, the brain’s ability to reorganise and form new neural connections after injury, Ansari said. The study reported that patients who received thrombectomy continued to improve between 90 days and one year, while outcomes remained static or declined in the medical-management group.

While more research is needed to fully understand which large core stroke patients benefit most from thrombectomy, the results of the study may provide additional confidence that aggressive intervention can yield meaningful recovery for patients, even when improvement is not immediately apparent.

“What we’re seeing across multiple randomised controlled trials, endovascular thrombectomy remains a powerful intervention across a spectrum of stroke presentations,” Ansari said. “It gives clinicians more confidence to treat patients even with severe brain injury and to counsel their loved ones that the outcome benefit may require time to heal, hard work with physical therapy/rehabilitation, and family support.”

The study was supported by unrestricted grants from Medtronic, Cerenovus, Penumbra, Stryker and Genentech.

Original written by Olivia Dimmer

Source: Northwestern University

GLP-1 Drug Linked to Heart Benefits for High-risk Patients

Findings from clinical practice will help inform shared decision making

Human heart. Credit: Scientific Animations CC4.0

Adding the GLP-1 receptor agonist drug tirzepatide to standard care for patients with type 2 diabetes and heart disease is associated with a lower risk of a major cardiovascular event, such as a heart attack or stroke, finds a study published by The BMJ today.

Randomised trials and observational studies have shown non-inferior effects of tirzepatide compared to another GLP-1 receptor agonist, dulaglutide, for major adverse cardiovascular events (MACE) – a combined measure of heart attack, stroke, and death from any cause. But evidence on the effects of adding tirzepatide to standard care is more limited, resulting in uncertainty for both regulators and clinicians.

To address this, researchers analysed clinical practice data from two US health insurance claims databases between May 2022 and May 2025. They aimed to estimate the cardiovascular effects of adding tirzepatide to standard care for patients with type 2 diabetes, a body mass index of at least 25, and established heart disease by comparing the outcomes to sitagliptin, another diabetes drug.

Sitagliptin was chosen as a neutral placebo proxy based on several studies showing no effect on cardiovascular outcomes.

The main outcome of interest was a reduction in MACE, which was monitored from the first day of treatment up to one year, or until the individual stopped or switched treatment, or disenrolled from the health plan.

Factors including age, sex, race, body mass index, previous heart problems, other chronic conditions, and medication use were taken into account, and a technique called propensity score overlap weighting was used to balance out differences between the two groups to draw more reliable conclusions.

A total of 52,971 individuals were included in the analysis (average age 70 years; 51% female), of whom 35,353 started tirzepatide and 17,618 started sitagliptin.

At one year, the risk of MACE was 2.9% in the tirzepatide group and 4.4% in the sitagliptin group (a 32% relative reduction), and the researchers estimate that for every 70 patients starting tirzepatide, one case of MACE would be prevented.

For individual MACE components, tirzepatide was associated with a 33% lower risk of heart attack compared with sitagliptin, whereas ischaemic stroke showed no meaningful difference.

Infections requiring hospital admission were also lower with tirzepatide (one admission prevented for every 48 patients), as was infection related death (one death prevented for every 200 patients) and death from any cause (one death prevented for every 122 patients).

This is an observational study, but the researchers previously benchmarked their design, data, and analytics infrastructure against a randomised controlled trial before drawing conclusions about cause and effect.

They also acknowledge several limitations including a relatively short follow-up period, which may underestimate long term cardiovascular and safety effects, possible misclassification of treatment duration or outcomes, and findings may not apply to other healthcare systems or patients without established cardiovascular disease.

However, they conclude: “This study shows how trial-anchored evidence from clinical practice can estimate the expected cardiovascular benefit of initiating tirzepatide beyond standard background treatment and inform shared decision making.”

A linked editorial notes that while this study provides an important, transparent estimate of what initiating tirzepatide might achieve in routine care, it does not establish a mortality indication or define the best sequence for cardiometabolic therapy.

The authors say longer follow-up, randomised and pragmatic comparisons, and more studies of additive benefit on contemporary background treatment are needed. Furthermore, cardiovascular efficacy cannot benefit a population if cost, authorisation barriers, supply, and discontinuation prevent sustained treatment, they add.

As such, they conclude: “The signal is compelling; the causal and clinical placement questions remain open.”

Source: BMJ Group

Does Longer Therapeutic Hypothermia Improve Outcomes for Out-of-Hospital Cardiac Arrests?

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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.

Source: Michigan Medicine

Closing the Gap Between Suspecting a Heart Attack and Confirming it

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.

Source: Texas A&M University

Somatic Mutations Linked to Vascular Damage in Progeria

Angiogenesis. Credit: Scientific Animations CC BY-4.0

In the rare disease progeria, blood vessels deteriorate prematurely. A study from Karolinska Institutet shows how different cell types in the vascular wall undergo progressive changes and accumulate mutations over time. The findings are published in the journal Genome Medicine.

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder that causes remarkable premature ageing. Most patients die during their teenage years from cardiovascular disease, but the precise mechanisms underlying vascular damage remain unclear.

In the new study, researchers analysed cells from the aorta of mice carrying the same genetic mutation found in people with progeria. Using single-cell RNA sequencing, which enables gene activity to be studied in individual cells, they tracked how the vascular wall changes over time. In total, nearly 9000 cells from mice of different ages were analysed.

“This approach allows us to follow, step by step, how different cell types are affected throughout the course of the disease,” says Maria Eriksson, professor at the Department of Medicine, Huddinge, Karolinska Institutet.

Reduced numbers of smooth muscle cells

The researchers focused particularly on vascular smooth muscle cells, which provide blood vessels with strength and elasticity and are essential for normal vascular function. They observed that these cells gradually declined in number.

“Smooth muscle cells are progressively lost both in HGPS and during normal ageing. As these cells die, the vessel wall becomes weaker and more susceptible to disease,” says Lara Garcia Merino, doctoral student at the same department and first author of the study.

The study also showed that smooth muscle cells accumulated higher numbers of so-called somatic mutations, meaning genetic alterations that arise during an individual’s lifetime. The mutation burden was associated with increased cellular stress and activation of genes involved in DNA damage responses.

“This is the first evidence that the accumulation of somatic mutations is a hallmark of vascular disease in HGPS,” says Maria Eriksson.

Reveals a new mechanism

The findings link DNA damage to cellular stress, loss of cellular identity and cell death, thereby revealing a previously unrecognised mechanism driving irreversible vascular injury.

The researchers also found evidence that changes in cell behaviour may be influenced by signalling between different cell types within the vessel wall, suggesting that the process is not driven solely by alterations within individual cells.

“We see that cells undergo multiple changes over time, from stress to identity changes and ultimately cell death. Our results suggest that several different mechanisms interact in the development of vascular damage in progeria,” says Lara Garcia Merino.

The researchers believe that the findings may contribute to a better understanding of how vascular damage develops in progeria and underline the importance of initiating treatment early, before irreversible DNA damage has accumulated.

“New gene-editing approaches can correct the disease-causing mutation in HGPS, but correcting the mutation alone is unlikely to reverse damage in cells that have already accumulated a large number of somatic mutations. Early intervention is therefore essential,” says Maria Eriksson.

The study also provides new insights into the biological processes underlying normal vascular ageing. Several important similarities exist between HGPS and the cardiovascular disease that affects the general population. HGPS is therefore widely used as a model for understanding normal ageing and vascular disease.

The researchers emphasise that further studies are needed to confirm the findings in humans.

The study was conducted in collaboration with researchers from, among others, the Indian Institute of Technology in India and the University of Bergen in Norway. The research was funded by the Swedish Research Council, the European Research Council (ERC), the Swedish Cancer Society and the Center for Innovative Medicine, among others.

Source: Karolinska Institutet

Premature Menopause Is a High Blood Pressure Risk Factor

Large-scale study results call for earlier cardiovascular screening for women who experience menopause before age 40

Photo by Hush Naidoo on Unsplash

Women who reach menopause before age 40 face a meaningfully higher risk of developing high blood pressure than those who go through menopause after age 45, according to a new study of more than 107 000 women. Risk peaked among women who reached menopause prematurely between the ages of 25 and 35 years. The results of the study are published online today in Menopause, the journal of The Menopause Society.

Hormone shifts during the menopause transition are known to influence a woman’s overall disease risk, and earlier menopause has previously been linked to higher rates of coronary heart disease and stroke. However, evidence connecting the timing of menopause directly to hypertension has been inconsistent, with some prior meta-analyses finding an association and others finding none.

A key challenge has been separating the direct hormone effects of menopause from indirect effects driven by weight gain, metabolic changes, and other cardiovascular risk factors that tend to accompany the menopause transition.

To address this gap, researchers analysed data from 107 836 postmenopausal women enrolled in the UK Biobank between 2006 and 2010, following them for a median of nearly 15 years through the end of 2003. The study classified women by age at menopause – normal (after age 45), early (ages 40 to 45), and premature (before age 40) – as well as by type of menopause (natural vs surgical) and tracked new diagnoses of high blood pressure over time.

Over the follow-up period, 18 508 women (17.2%) were diagnosed with hypertension. The risk climbed steadily as age at menopause dropped: 16.6% of women with normal age at menopause developed hypertension, compared to 18.8% of women with early menopause and 22.6% of women with premature menopause. After adjusting for more than 50 variables – including weight, lifestyle habits, family history, and lab values – women with premature menopause still had a 12.3% higher risk of developing hypertension than women who reached menopause after age 45.

A further analysis modelling age at menopause on a continuous scale found that risk peaks not at the traditional premature-menopause cutoff of age 40 but between the ages 25 and 35, suggesting the cardiovascular risk associated with premature menopause may be concentrated in an even younger group of women than previously defined. Surgical menopause was associated with higher hypertension rates in initial analyses, but that association did not hold once other risk factors were considered.

Based on these findings, the study authors recommend that clinicians treat age at menopause as a distinct cardiovascular risk factor, particularly for women who reach menopause before age 40. In addition to individualised counselling on hormone therapy, they point to earlier identification and management of high blood pressure as an opportunity to help reduce long-term cardiovascular risk in this group of women.

“The results of this study highlight the potential adverse long-term health outcomes associated with premature menopause, and in particular, the need to regularly screen for cardiovascular risk factors such as hypertension. Use of hormone therapy is also routinely recommended in women with premature menopause at least until the natural age of menopause unless contraindications exist,” says Dr Stephanie Faubion, medical director for The Menopause Society.

Source: The Menopause Society

Cardiovascular Risk Factors that Drive Rupture-prone Plaques in Coronary Arteries

Source: Wikimedia CC0

Cardiovascular risk factors are linked to higher risk of heart disease, but it has been unknown how they are related to abrupt closure of the coronary arteries leading to heart attack and sudden cardiac death. A new study by Mass General Brigham Heart and Vascular Institute investigators finds that people with higher modifiable risk factors burden such as high blood pressure, high cholesterol, diabetes, smoking and obesity have more widespread buildup of plaques in major coronary arteries. Furthermore, these modifiable factors were associated with more unstable, high-risk plaques that are prone to rupture and cause heart attacks. Results are published in JACC: Advances.

“The higher the number of vulnerable, or rupture-prone plaques, the greater the chance that one of them will trigger an adverse event,” said senior author Ik-Kyung Jang, MD, PhD, at the Mass General Brigham Heart and Vascular Institute. “Our findings highlight the importance of early, intensive and sustained interventions to control the modifiable risk factors and prevent future events.”

To better understand how modifiable risk factors and non-modifiable risk factors (including age, sex and family history of heart disease) influence dangerous plaque buildup, the research team examined plaque burden and plaque characteristics across all three major coronary arteries. They analysed 534 plaques in 131 patients who underwent optical coherence tomography (OCT), an intravascular imaging modality that can visualise plaques at high resolution.

The researchers reported that patients with more risk factors had more plaques across all three coronary arteries. In addition, greater number of modifiable risk factors was associated with fewer stable plaques and more prevalent vulnerable plaque features such as lipid plaques with thin fibrous caps that are susceptible to disruption. In contrast, non-modifiable risk factors were associated with more stable plaque phenotypes.

The authors note that prospective research involving larger cohorts, including patients who have previously been treated for blocked coronary arteries, is needed to generalise their findings.

Source: Mass General Brigham

Pregnancy Complications Linked to Long-term Risk of Peripheral Artery Disease

Study of over 2 million women finds an association between adverse pregnancy outcomes and an increased risk of PAD up to 46 years after delivery

Image by Scientific Animations, CC4.0

Women who experience pregnancy complications such as gestational diabetes, preeclampsia, or preterm delivery have a significantly increased long-term risk of developing peripheral artery disease (PAD) later in life, according to a new study published July 21st in the open access journal PLOS Medicine by Casey Crump of the University of Texas, US, and colleagues.

PAD, a condition in which narrowed arteries reduce blood flow to the limbs, affects more than 230 million people worldwide and is a strong predictor of future stroke, ischaemic heart disease, and premature mortality. Adverse pregnancy outcomes have been identified as risk factors for other cardiovascular diseases, but their association with long-term PAD risk had not been well established.

In the new study, researchers analysed data from 2 201 446 women who had a singleton delivery in Sweden between 1973 and 2015, following them for PAD diagnoses from nationwide inpatient, outpatient, and primary care records through 2018. Five adverse pregnancy outcomes were examined: preterm delivery, small for gestational age, preeclampsia, other hypertensive disorders of pregnancy, and gestational diabetes.

In 54 million person-years of follow-up, 13 211 women (0.6%) were diagnosed with PAD, at a median age of 62. All five adverse pregnancy outcomes were independently associated with increased PAD risk. At 30–46 years after delivery, adjusted hazard ratios were highest for gestational diabetes (HR 3.83, 95% CI 3.20–4.59), followed by small for gestational age (HR 1.74, 95% CI 1.65–1.83), other hypertensive disorders (HR 1.61, 95% CI 1.21–2.15), preterm delivery (HR 1.58, 95% CI 1.48–1.70), and preeclampsia (HR 1.28, 95% CI 1.20–1.37). Women with multiple adverse pregnancy outcomes had further increases in risk. These findings were largely unexplained by shared familial factors in co-sibling analyses.

“Because this was a relatively young cohort, the risks of PAD following adverse pregnancy outcomes may be even higher as women reach older ages when PAD is more likely to manifest,” the authors write. “Women with pregnancy complications may warrant early cardiovascular risk assessment and long-term clinical follow-up given their higher subsequent risk of PAD.”

The authors add, “Pregnancy is a “natural stress test” that may reveal higher cardiovascular risks in early adulthood. In a population of > 2 million women, we found that all 5 major adverse pregnancy outcomes (preterm delivery, small for gestational age, preeclampsia, other hypertensive disorders, and gestational diabetes) are independently linked with higher risks of peripheral artery disease up to 46 years later. Women with pregnancy complications need early and long-term follow-up with their physician to reduce their lifetime risk of peripheral artery disease and other cardiovascular diseases.”

Provided by PLOS