Silent Atherosclerosis in Young Adults: What the REACT Study Changes—and What It Does Not

An artery does not wait for a risk calculator to label someone “high risk.” Silent atherosclerosis can begin in young adulthood, years before chest pain, breathlessness, a heart attack or stroke. That does not mean every young adult with plaque will have an event. It means something more actionable: cardiovascular prevention should begin before symptoms do.

The international REACT study has put new numbers around that reality. Among 16,808 adults aged 18–70 without known atherosclerotic cardiovascular disease, investigators detected plaque in 57.1% of the study cohort (95% CI, 56.3–58.0). In participants aged 18–29, prevalence was 8.7% in men and 6.7% in women—roughly 1 in 13.

What the REACT study actually measured

REACT enrolled 16,808 adults in Spain and Denmark who had no known atherosclerotic cardiovascular disease. The cohort used five prespecified age groups with approximately balanced numbers of women and men. The overall figure therefore describes this cohort; it is not a population-weighted estimate for either country.

Investigators looked directly for plaque in several vascular territories:

• three-dimensional ultrasound of the carotid arteries in the neck;
• three-dimensional ultrasound of the femoral arteries in the groin;
• coronary CT angiography to image the heart’s arteries.

The protocol also assessed conventional risk factors, laboratory markers, retinal images and samples for omics research. In younger participants, disease was usually peripheral and confined to one territory. Plaque burden and multiterritorial involvement increased with age, while isolated coronary disease was uncommon.

The project was funded by the Novo Nordisk Foundation, with in-kind support from Philips and Zeiss. Disclosing these relationships does not invalidate the result, but it belongs in a complete critical appraisal. The age pattern is also cross-sectional: it can show differences between age groups, not prove which mechanism—including menopause—caused them.

What “silent atherosclerosis” means

Atherosclerosis is the gradual accumulation of lipids, inflammatory cells, fibrous tissue and, over time, calcium within the arterial wall. “Silent” means plaque is detected before a person has a clinical diagnosis or attributable symptoms.

It does not automatically mean that a major obstruction is present, a heart attack is inevitable, a cardiac procedure is needed or one blood biomarker has diagnosed arterial disease. Plaque is evidence of subclinical disease and accumulated exposure. Its relevance depends on location, burden, distribution and the person’s wider risk profile.

What REACT changes—and what it cannot yet change

REACT strengthens a useful clinical idea: waiting until 10-year risk becomes high may be late for some younger adults. Decades of exposure to elevated LDL, atherogenic particle burden, smoking, high blood pressure or diabetes can matter even when age keeps near-term risk estimates low.

But REACT-DETECT is an observational baseline analysis. It detected disease; it did not compare universal screening with standard care or demonstrate fewer clinical events. That question belongs to REACT-PROTECT, a second phase planned for 2027–2032 if funding is secured. Its planned primary endpoint is plaque progression—a surrogate—not heart attacks, strokes or mortality.

The careful conclusion is twofold: cumulative exposure deserves earlier attention, but current evidence does not support turning vascular ultrasound or CT into routine population screening.

Earlier prevention does not mean more testing

For most people, the first prevention layer is less dramatic than a scan and more useful:

1. Personal and family history: premature cardiovascular disease, hypertension, diabetes, kidney disease, premature menopause, pre-eclampsia, chronic inflammatory conditions and medication.
2. Exposure: smoking or nicotine, inactivity, diet, disrupted sleep, alcohol and sustained stress.
3. Repeatable measurements: blood pressure and, where useful, weight and waist circumference.
4. Standard laboratory testing: a lipid profile, glucose or HbA1c, and kidney function when indicated.
5. Risk refiners: lipoprotein(a) at least once in adulthood, and ApoB when particle burden may clarify risk.
6. Validated risk estimation: use a tool appropriate to country and age without mistaking a 10-year percentage for a person’s full lifetime trajectory.

VO₂ max measures cardiorespiratory fitness and can guide training, but it does not detect plaque. Biological-age clocks and emerging biomarkers do not diagnose atherosclerosis either.

Decision table: what may make sense for whom

Situation	High-value first step	Vascular imaging?
Age 18–39, no symptoms or major risk factors	Family history, blood pressure, lipids, glucose, one-time Lp(a) and lifestyle	Not routinely
Premature family history, very high LDL, diabetes, smoking, kidney disease or multiple enhancers	Early clinical review; consider ApoB and secondary causes	Only if the result could change management
Borderline/intermediate risk or near a treatment threshold in midlife	Estimate risk, review enhancers and preferences	A coronary calcium score or arterial plaque imaging may be a selective tie-breaker
Treatment is already clearly indicated	Optimise prevention and follow-up	Do not image merely to confirm an established decision
Chest pain, new breathlessness, exertional symptoms or a neurological deficit	Prompt diagnostic assessment	This is not screening; the test depends on the presentation

The 2025 ESC/EAS update treats arterial plaque or elevated CAC as risk modifiers for selected people at low or moderate risk and near a treatment threshold. It also states that coronary imaging and CAC are not broad screening tests. The 2026 ACC/AHA guidance mainly positions CAC as a decision aid when uncertainty remains, particularly in men from age 40 and women from age 45 with borderline or intermediate risk.

The risks and limits of plaque imaging

• Carotid and femoral ultrasound does not use ionising radiation, but results depend on technique, equipment and standardised definitions.
• Coronary CT angiography uses radiation and iodinated contrast; it may be unsuitable in pregnancy, contrast allergy or some kidney conditions.
• Any imaging programme can generate incidental findings, false positives, anxiety and further tests.
• Detecting plaque does not by itself establish which treatment offers net benefit to one person.
• Repeating imaging without a clinical question may add cost without improving outcomes.

Before ordering a test, ask: What would we do differently if the result were normal, intermediate or clearly abnormal? If the answer is “nothing,” it is probably not the right test. Our preventive medicine guide explains how to structure that decision.

What you can do now to reduce cumulative risk

There is no single protocol that erases all plaque. There are evidence-based ways to reduce the exposures that drive it and lower cardiovascular risk:

• do not smoke or vape nicotine; seek structured support if stopping is difficult;
• build meals around a Mediterranean-style pattern with vegetables, whole fruit, legumes, nuts, olive oil, fish and whole grains;
• aim for 150–300 minutes of moderate aerobic activity or 75–150 minutes of vigorous activity each week, plus strength training on at least two days, adjusted for health and capacity;
• identify and treat high blood pressure, dyslipidaemia and abnormal glucose;
• protect regular sleep and assess possible sleep apnoea;
• use medication—including statins or other lipid-lowering therapy—after reviewing absolute risk, expected benefit, adverse effects, interactions and preferences.

An article cannot prescribe exercise intensity or medication. Both depend on baseline risk, age, tolerance, other conditions and shared goals.

Earlier prevention, with less noise

The useful message from REACT is not “get a coronary CT while young.” It is this: identify the exposures affecting arterial health early enough to change the trajectory.

At Progevita, that means organising history, validated risk, laboratory data, functional capacity and lifestyle first. If imaging can resolve a real decision, it can be considered selectively with the appropriate specialist. If it will not change management, it does not add precision—it adds noise.

If you want to understand cardiovascular risk without accumulating tests, a clinical assessment can help separate what is worth measuring now, what can wait and which result would genuinely change your plan.

Sources

1. Bundgaard H et al. Prevalence of Silent Atherosclerosis across Adult Life. New England Journal of Medicine. 2026.
2. Bundgaard H et al. REACT-DETECT study design. American Journal of Preventive Cardiology. 2026.
3. Ibáñez B, Bundgaard H. REACT initiative and planned REACT-PROTECT protocol. European Heart Journal. 2025.
4. American College of Cardiology. Official ESC 2026 REACT summary.
5. 2025 ESC/EAS focused update on dyslipidaemias, arterial plaque and coronary calcium.
6. ACC/AHA. 2026 guideline for managing lipids and cholesterol.
7. World Health Organization. Physical activity recommendations.

Method: narrative review of the primary study, its protocol and current clinical guidance. Cohort prevalence is not presented as a national estimate, and plaque detection is not equated with screening benefit. Sources and search results checked on 23 September 2026. This article is educational and does not replace medical assessment.