We tend to picture coronary artery disease as an artery slowly narrowing as fatty material builds up. But the degree of narrowing tells only part of the story. What a plaque contains, how it changes over time and how it interacts with the surrounding artery all shape its clinical significance.
Research published in 2025 and 2026 is revealing how these patterns differ between men and women. It is also focusing attention on midlife, when the menopausal transition can change lipid metabolism and vascular health.
Together, these findings help explain why cardiovascular risk cannot be judged from a single cholesterol result, or from how obstructed an artery looks.
What is an atheroma?
An atheroma is a plaque that develops within the artery wall. It contains varying proportions of fatty material, inflammatory cells, connective tissue and calcium. Some plaques have a substantial lipid-rich core, while others are more fibrous or calcified.
Three measurements capture different aspects of the disease:
- Plaque volume: the total amount of plaque present.
- Plaque burden: the amount of plaque relative to the size of the vessel.
- Stenosis: the degree to which the channel carrying blood has narrowed.
These measurements are related but not interchangeable. Recent studies increasingly examine them together, alongside plaque composition, to assess risk more precisely.
Different patterns in men and women
A July 2025 study in Open Heart analysed coronary CT scans from 1,189 people with non-obstructive coronary artery disease, almost half of them women. These participants had coronary plaque without the degree of narrowing classed as obstructive disease.
Men had a greater proportion of fibrofatty plaque across all the age groups studied. Middle-aged and older men also had more CT-defined necrotic-core components, the areas associated with lipid accumulation and cellular debris.
Middle-aged and older women, by contrast, had greater proportions of fibrous and calcified plaque. Once vessel size was taken into account, however, these women also had a higher total plaque burden. The distinction matters because a smaller absolute amount of plaque can still represent a substantial burden within a smaller artery.
These are patterns within a particular population. They do not sort plaques into a "male type" and a "female type", and they do not show that a more fibrous or calcified plaque makes an individual's disease harmless.
Less plaque does not always mean proportionately less risk
A 2026 analysis of the PROMISE study adds another dimension. Researchers assessed 4,267 people with stable chest pain, 2,199 of them women, and followed outcomes over a median of 26 months.
Women were less likely to have detectable plaque and had lower total plaque volume, yet their plaque burden relative to vessel volume was similar to men's.
The link between plaque burden and later cardiovascular events also differed. In women, modelled risk began to rise at lower plaque burdens and climbed more steeply. The outcome combined death, myocardial infarction and hospitalisation for unstable angina.
This suggests the same plaque measurement may not carry the same meaning in women and men, which supports more individualised interpretation. It does not establish new universal treatment thresholds.
An August 2026 study of 5,412 patients also produced age- and sex-specific reference values for coronary plaque. Its authors stressed that these are descriptive benchmarks that still need validating against clinical outcomes.
Menopause and the conditions that favour plaque formation
The menopausal transition can alter several processes relevant to cardiovascular health. These include rises in LDL cholesterol and apolipoprotein B, changes in fat distribution and metabolic health, and remodelling of blood vessels.
These changes overlap with ageing. Blood pressure and glucose regulation may also worsen in midlife, but their trajectories cannot be attributed solely to falling oestrogen. Menopause acts within a wider picture of existing risk factors and years of cumulative exposure.
A large study in Nature Communications in November 2025 examined coronary CT scans from 16,300 patients in China. It found different age-related patterns of plaque burden: a relatively steady increase across age groups in men, and a curve that steepened with advancing age in women.
That pattern is compatible with a contribution from menopause, but association is not cause. The researchers compared people of different ages; they did not follow each woman's plaque across her final menstrual period. The findings cannot separate the effects of hormonal change from those of ageing, treatment or earlier risk exposure.
The useful conclusion is that menopause is a time when several influences on plaque development may shift together. It does not mean atherosclerosis begins at menopause, or that its progression is inevitable.
HDL: a more complicated picture
HDL is often called "good cholesterol", but the cholesterol carried in HDL particles is only one aspect of their biology.
The 2025 SWAN HDL study followed 279 women and examined HDL cholesterol efflux capacity in relation to the final menstrual period. Efflux capacity measures how effectively HDL accepts cholesterol from cells, a function relevant to cholesterol removal.
Higher efflux capacity was not consistently linked to better vascular health as women moved through menopause. The researchers assessed vascular health using arterial wall thickness, arterial stiffness and coronary calcium.
This does not show that HDL causes plaque, and a routine HDL cholesterol test does not measure efflux capacity. But it illustrates why HDL biology cannot be reduced to one reassuring number. In midlife, a favourable HDL result should be read alongside the rest of the lipid profile and the person's wider cardiovascular risk.
Rupture and erosion: two routes to a clot
Composition also matters because a clot can form by different mechanisms. In plaque rupture, the fibrous cap breaks and exposes the material beneath to the blood. In plaque erosion, a clot forms over a damaged surface without that rupture.
Earlier pathology studies linked erosion particularly with younger women, but the distinction is not a simple divide between the sexes. An invasive imaging study of 1,368 patients with acute coronary syndromes found similar overall proportions of rupture and erosion in women and men, while rupture and features of vulnerability increased with age in women.
This is useful context for the newer research: both mechanisms occur in both sexes, and age alters the comparison.
Cardiovascular health in menopause care
In clinical practice, these findings strengthen the case for considering cardiovascular health alongside menopausal symptoms.
A fuller assessment draws on blood pressure, the complete lipid profile, glucose regulation, smoking, family history, physical activity and sleep. The age at menopause also matters, as earlier menopause is recognised as a marker of increased cardiovascular risk.
Investigations should follow symptoms and individual risk. These studies do not establish a need for routine coronary plaque scanning in everyone.
Hormone therapy may be appropriate for menopausal symptoms after an individual assessment. However, current NICE guidance advises against prescribing HRT specifically to prevent cardiovascular disease. A hormonal contribution to vascular risk does not, on its own, show that HRT will prevent or reverse plaque.
At Wildberry Clinic, this research reinforces the value of considering endocrine, metabolic and cardiovascular health together, working alongside GPs and consultants. Midlife offers a chance to recognise changing risk and address it before cardiovascular disease becomes clinically apparent.
References
- Hondros CAB, et al. Age-stratified differences in coronary artery plaque phenotypes in women and men with non-obstructive coronary artery disease. Open Heart. 2025;12.
doi:10.1136/openhrt-2025-003371.
- Brendel JM, et al. Risk in Women Emerges at Lower Coronary Plaque Burden Than in Men: PROMISE Trial. Circulation: Cardiovascular Imaging. 2026;19.
doi:10.1161/CIRCIMAGING.125.019011.
- Breitbart P, et al. Coronary plaque burden and composition in an ESC guideline-selected outpatient CCTA cohort: age- and sex-specific percentile distributions. Clinical Research in Cardiology. Published 3 August 2026.
doi:10.1007/s00392-026-02993-5.
- El Khoudary SR, et al. Menopause Transition and Cardiovascular Disease Risk: Implications for Timing of Early Prevention. Circulation. 2020;142–e532.
doi:10.1161/CIR.0000000000000912.
- Yang X, et al. Deciphering age- and sex-specific patterns of coronary artery atherosclerosis from a large Chinese cohort. Nature Communications. 2025;16:10616.
doi:10.1038/s41467-025-64940-8.
- El Khoudary SR, et al. High-Density Lipoprotein Cardioprotection Function Deteriorates as Women Transition Through Menopause: The SWAN HDL Study. JACC: Advances. 2025;4:102131.
doi:10.1016/j.jacadv.2025.102131.
- Seegers LM, et al. Sex Differences in Culprit Plaque Characteristics Among Different Age Groups in Patients With Acute Coronary Syndromes. Circulation: Cardiovascular Interventions. 2022;15.
doi:10.1161/CIRCINTERVENTIONS.121.011612.
- NICE. Menopause: identification and management. NG23.
Cardiovascular disease prevention, recommendation 1.6.4. Accessed 30 September 2026.
This article provides educational information and does not replace individual medical assessment or treatment. New or persistent chest symptoms require medical attention.
