More Than Half of Adults Have Silent Plaque: What the REACT Study Means for You

October 4, 2026

Line up a hundred adults between 18 and 70, none of them with any history of heart disease, and scan the arteries in their necks, their groins, and their hearts. In a study published in August that did exactly that across the whole span of adult life, 57 of the hundred had plaque.

That is the finding from REACT, published August 29 in the New England Journal of Medicine and presented the same morning at the European cardiology congress in Munich. Investigators imaged 16,808 people in Denmark and Spain three ways, and more than half of them were walking around with atherosclerosis they knew nothing about. Among the 18-to-29-year-olds it was about one in thirteen. By the 60s it was more than nine in ten.

The question I get in clinic whenever a study like this makes the news is some version of “so do I have it?” If you are over 50, the odds say yes. What follows is what the study did, what it found, why the standard risk calculator flagged almost none of these people, and what I think you should and should not do about it, depending on whether you are 25, 45, or 65.

What the study did

REACT is a two-part project run jointly out of Rigshospitalet in Copenhagen and the Spanish national cardiovascular research center in Madrid, the CNIC, where Valentín Fuster’s group spent the previous decade running a smaller study called PESA that I’ll come back to. Its first part, the part published now, set out to answer a plain question. How common is silent plaque at each age of adult life, in each sex, and in which arteries?

They enrolled 16,808 adults aged 18 to 70 with no known heart or vascular disease, split into five age bands with roughly equal numbers of men and women in each, so the young were not drowned out by the old. Every participant got a three-dimensional ultrasound of the carotid arteries in the neck and the femoral arteries at the top of the leg, plus a CT angiogram of the heart’s own arteries with a calcium score. Plaque in any one of those territories counted as silent atherosclerosis. Average age was 45, and just over half were women. Funding came from the Novo Nordisk Foundation.

Three things make this study better than what came before it. Its size. Its age range, which starts at 18 where almost every earlier imaging study started at 40. And the fact that it looked in three places at once, so it can say where the disease shows up first and how it spreads, which no calcium-score study can do.

What it found

Fifty-seven percent. Exactly 57.1, with a confidence interval so narrow (56.3 to 58.0) that the number is not going to move. Sixty-three percent of men and 51 percent of women.

By age, the curve is the shape of an S. In the youngest band, 18 to 29, plaque was present in 8.7 percent of men and 6.7 percent of women. In the 30s it was already a third of men and a fifth of women. Men cross the halfway mark around 50 and women somewhat later. By 60 to 70 it is 98 percent of men and 92 percent of women, and at that age the person with clean arteries is the unusual one.

Where the plaque sat is as telling as how much of it there was. In young adults it was almost always in one place, and that place was usually the neck or the leg. The heart arteries came later. Isolated coronary plaque, meaning disease in the heart arteries and nowhere else, was rare at every age, 9 percent of men at most and 5 percent of women. Of the people who did have coronary plaque, about four in five had it in the neck or the leg as well. With each decade the plaques got bigger and the number of territories involved grew. By 60 to 70, more than half of the men and nearly a third of the women had plaque in all three places at once. Plaque volume, the investigators report, rose exponentially with age, which in plain terms means the growth compounds. A small plaque at 35 is a bigger plaque at 45 and a cluster of them at 55.

One detail is going to come up again, so I’ll flag it now. Among people in their 30s who had coronary plaque on the CT angiogram, about four in ten of the men and nearly half of the women had a coronary calcium score of zero. The plaque was there. It had not calcified yet. If you have read my post on why a zero calcium score doesn’t erase a high LDL, you already know why that figure stopped me.

The risk calculator missed almost everyone

Every participant 40 and over without diabetes also had a ten-year risk estimate from SCORE2, which is Europe’s version of the risk calculator American doctors use, built from age, sex, blood pressure, cholesterol, and smoking. Then the investigators asked a simple question. Of the people who had plaque on imaging, how many did the calculator flag as high risk?

About two in a hundred.

As a test for plaque, the high-risk label had a sensitivity of 1.9 percent. Loosen the bar to moderate risk or higher and it caught a third. Among people with plaque in both the heart arteries and the neck or leg arteries, the ones you would most want to find, fewer than four in a hundred were called high risk. The gap was widest in the young, and it did not close when the investigators set aside everyone already taking a cholesterol or blood pressure drug.

That reads as an indictment of the calculator. It is a narrower failure than it looks, because the calculator was never built to answer this question. A risk score estimates the probability that you will have a heart attack or stroke in the next ten years. Age carries most of the weight in that arithmetic, so a 42-year-old with an LDL of 170 and a father who had a heart attack at 55 comes out low risk, because few 42-year-olds have heart attacks in any given decade. The score is right about that, as far as it goes. It answers a question about the next ten years. Plaque in that man’s femoral artery answers a different one, about the previous twenty years and the next forty.

This is the distinction the whole calcium score conversation turns on, and REACT is the biggest demonstration of it yet. A calculator estimates. A scan looks.

For decades we have treated the estimate as if it were the diagnosis, and for people under 50 the estimate almost never comes out “high” no matter what is growing in their arteries.

Men first, then women catch up fast

Men ran ahead at every age, by the investigators’ estimate about five to ten years ahead. A 40-year-old man’s arteries looked roughly like those of a woman in her late 40s. Then something changes for women in midlife. In women the study describes a later but steeper climb, with the sharpest rise between 40 and 60, which is the window in which most women go through menopause.

The gap closes fast.

REACT did not set out to study menopause, so it cannot prove that menopause is the cause. The timing fits, and the wider evidence is split on how much of this is menopause itself and how much is simply age. The long-running SWAN study found artery-wall thickening and stiffening clustering in the last stretch of perimenopause independent of age, and the American Heart Association’s 2020 statement treats the transition as a window of accelerated risk. A British cohort of nearly 3,900 women found the thickening tracked a woman’s age alone. I have written about what changes in a woman’s heart risk after menopause, and the list is the recipe for plaque. LDL goes up. HDL often drops. Triglycerides rise, weight moves to the waist, and blood pressure climbs. REACT shows the plaque arriving on schedule.

For a woman in her late 40s or early 50s, the practical point is that the lipid panel from your 30s has expired. Numbers that were fine at 38 are often not fine at 52, and the arteries are keeping score.

The old evidence said the same thing

If 57 percent shocks you, it would not shock a pathologist. In 1953 army pathologists reported autopsies on 300 American soldiers killed in Korea, average age 22, and found coronary atherosclerosis of some degree in 77 percent of them. A Vietnam-era series found it in 45 percent. The most recent one, 3,832 service members who died between 2001 and 2011 at an average age of 27, found it in 8.5 percent, which is close to REACT’s figure for the under-30s. The pathologists’ bar for calling something plaque has also moved over those decades, so the three series are not strictly comparable. What REACT adds is a living population, measured in three territories with modern imaging, at every age from 18 up.

The imaging studies said the same thing once they had the tools. PESA, the Madrid study that REACT grew out of, scanned 4,184 bank employees aged 40 to 54 a decade ago and found plaque or coronary calcium in 63 percent, 71 percent of men and 48 percent of women. Among the ones the Framingham calculator rated low risk, 58 percent had plaque. And in a follow-up analysis of the 1,779 PESA participants with no conventional risk factors at all, no smoking, normal blood pressure, normal blood sugar, LDL under 160, half still had it, and LDL, at levels we call normal, independently predicted who did.

Sweden’s SCAPIS study ran CT angiograms on 25,182 people aged 50 to 64 and found coronary plaque in 42 percent, with onset running about ten years later in women, the same sex gap REACT saw. In the United States, the BioImage study put a carotid ultrasound and a calcium scan on 5,808 adults averaging 69 years old and found that either test improved risk prediction over the calculator alone. In MESA, the long-running American cohort of adults 45 to 84, about half had coronary calcium, and in a pooled analysis of nearly 20,000 Americans aged 30 to 45, between 7 and 26 percent did depending on sex and race, and calcium is the part of the plaque that shows up last. Nobody has scanned young Americans at REACT’s scale, so we do not have a REACT of our own. I would not take comfort in that. Denmark and Spain both have far lower obesity rates than we do.

Before you ask for a scan

The obvious reaction to a study like this is to ask for the scan. That is the one thing REACT did not test.

REACT is a prevalence study. It counted. It did not randomize anyone to be scanned or not scanned and then follow them for heart attacks, so it cannot tell us whether finding silent plaque at 32 and treating it changes what happens at 62. REACT-PROTECT, the project’s second phase, is the trial that will try. It is a randomized trial of imaging-guided prevention planned to run from 2027 to 2032, with a handheld ultrasound probe on the neck and leg as the screening tool. Until it reads out, anyone who tells you that screening healthy young adults with a scan is proven is ahead of the evidence, and some of the coverage has been.

The one large randomized trial of screening that does exist points the other way, or at least sideways. DANCAVAS, from Denmark, invited 16,736 men aged 65 to 74 to a package of screening that included a coronary calcium scan, an aneurysm check, and blood tests, and compared them with nearly 30,000 men who were not invited. After five and a half years, 12.6 percent of the invited group had died against 13.1 percent of the controls, a 5 percent relative difference that did not reach statistical significance. Strokes fell by about 7 percent, and in the younger half of the trial, men 65 to 69, deaths were 11 percent lower, which is the kind of signal that keeps the question open. That is in older men, where plaque is near universal and events are common.

Nobody has run the equivalent trial in 35-year-olds.

Guidelines reflect that. Our 2026 cholesterol guideline uses the calcium score for adults at intermediate risk, and some at borderline risk (men from 40, women from 45), when the statin decision is uncertain. A zero score in that group is a reason to hold off and repeat the scan in three to seven years. Any calcium at all is a reason to treat, and above 100 the recommendation is firm. It also says something REACT makes newly relevant, which is that a plaque in the carotid artery counts as a reason to treat even when the calcium score is zero. European guidelines likewise allow a calcium score, or a carotid or femoral plaque on ultrasound, to move a borderline person up a risk category. No major guideline anywhere recommends routinely imaging a healthy 30-year-old. The one carve-out is a lipid society statement that allows a calcium score before 40 for someone with a strong family history of early heart disease or several risk factors at once, and the US Preventive Services Task Force rates the evidence for the calcium score as a screening test insufficient.

Two more reasons the scan is the wrong first move under 40. A calcium score is the wrong instrument at that age. REACT showed more than four in ten 30-somethings with coronary plaque had a score of zero, so a zero in your 30s rules out much less than it does at 60. And a carotid ultrasound, which is the better test for the young and carries no radiation, is not something insurers pay for as a screening test, and when it finds a two-millimeter plaque the treatment is the same medication you could have started on the strength of your LDL and your family history without the scan.

What I would do with this at 25, 45, and 65

The lesson I take from REACT is the one this site keeps coming back to. Plaque is a cumulative process. Plaque in a 28-year-old’s femoral artery is the product of the LDL, the blood pressure, the cigarettes or the vape, and the blood sugar of the previous decade, and it will keep compounding for the next four. I have written about cumulative LDL exposure and why the years count at length. REACT is that argument in pictures.

At 25, I would not scan you, and I would not want you asking for it. I would want you to know five numbers. LDL first. Then Lp(a), which is genetic and needs measuring once in a lifetime. Blood pressure, measured properly, because half the people with high blood pressure don’t know it and under 40 it is three in four. A1c. And your waist, which tells you more than the scale does. If the LDL is high and a parent had a heart attack before 60, that is a conversation about treatment in your 20s, scan or no scan, and the 2026 guideline now explicitly supports thinking about lifetime trajectory in people that young. If you smoke or vape, stopping is the single biggest thing you can do for the next forty years, and no scan changes that.

At 45, this is the age where a calcium score earns its keep, for the person on the fence about a statin whose calculator says low or borderline. If the score is above zero, the question of whether you have the disease is settled and the conversation changes. If the score is zero, I treat it as a shorter warranty than most people assume, for the reasons in the zero-score post, and if your LDL is high I will usually still want to treat it. My bias runs toward treating the exposure early over waiting for a scan to find the scar, and REACT, with its plaques in the 30s that had not yet calcified, has hardened that bias. For a woman at this age, the menopause transition is the moment to recheck everything, because the numbers from your 30s no longer apply.

At 65, REACT says the odds you have plaque somewhere are better than nine in ten. The question is no longer whether. It is how much, where, and what you are doing about it. If you are not on a statin and have been told you are too old to start one, the STAREE trial answered that this summer. If you are on one, the LDL target for someone with documented plaque is lower than for someone without, under 70 in the 2026 guideline for anything beyond mild plaque, and that is a conversation to have with whoever manages your cholesterol, whether that is with me here in Encinitas or with your own cardiologist.

And at any age, if a scan has already found plaque and nobody explained it to you, the first thing to know is that most plaque never ruptures. Drugs that stabilize it work best when started before the first event, and REACT’s main message is that the first event is a long way downstream from where the disease begins.

Frequently Asked Questions

What is silent atherosclerosis?

Plaque in the wall of an artery, made of cholesterol, inflammatory cells, and scar tissue, in a person who has no symptoms and has never had a heart attack, stroke, or blocked artery. Silent means undetected, and undetected plaque is still plaque. Most heart attacks come from plaques that never narrowed the artery enough to cause chest pain, which is why the disease can be present for thirty years before it announces itself. In the REACT study, 57 percent of 16,808 adults aged 18 to 70 with no history of heart disease had it.

If more than half of adults have plaque, is it really a disease?

Yes, in the same way that high blood pressure is a disease even though nearly half of American adults have it. Being common does not make plaque safe. How much plaque a person carries predicts heart attacks and strokes better than the risk calculator does, and in the BioImage study people in the top third of carotid plaque burden had more than twice the event rate of people with none. What the 57 percent figure does change is the question. For most people past 50 the question is no longer whether there is plaque. It is how much, how fast it is growing, and whether the cholesterol and blood pressure feeding it are under control.

Should I get a scan to look for plaque?

It depends on your age and your risk. For adults 40 to 75 at intermediate risk, a coronary calcium score is the test the American guideline supports when the result would change the decision about a statin. Under 40, no major guideline recommends routine imaging (one lipid society allows a calcium score earlier for a strong family history of early heart disease), the calcium score misses much of the plaque at that age because it has not calcified yet, and no trial has shown that scanning healthy young adults prevents heart attacks. REACT’s second phase, a randomized trial planned for 2027 to 2032, is designed to answer exactly that question. In the meantime, knowing your LDL, Lp(a), blood pressure, and blood sugar gets you most of the way without a scan.

Can I have plaque in my 30s?

Yes. In REACT, about a third of men and a fifth of women aged 30 to 39 had plaque, usually in the neck or leg arteries and usually in one place. Among those who had plaque in the heart arteries, more than four in ten had a coronary calcium score of zero, which means a calcium scan would have called their arteries clean. At that age the right response is to treat the things that grow plaque, above all LDL, blood pressure, and smoking, and to do it early, because plaque volume compounds with every decade.

Why did the risk calculator miss so many people with plaque?

Because it was built to estimate the chance of a heart attack or stroke in the next ten years, and age dominates that estimate. Young and middle-aged people rarely come out high risk no matter what their cholesterol is, because few people their age have events in any given decade. In REACT, the SCORE2 calculator flagged 1.9 percent of the people with plaque as high risk. A calculator answers a question about the next ten years. A scan answers a question about what is already in the artery wall, which is the product of the previous twenty years.

Why do women catch up after menopause?

REACT found that men developed plaque five to ten years earlier than women and that women then climbed steeply between 40 and 60, the window in which most women go through menopause. REACT was not designed to test whether menopause is the cause, so it cannot prove it, and the wider research is split on how much is menopause itself and how much is age. The biology fits either way. After menopause, LDL rises, HDL often falls, triglycerides climb, weight shifts to the waist, and blood pressure goes up, and those are the raw materials of plaque. For a woman in her late 40s or 50s, the practical point is that cholesterol and blood pressure numbers from her 30s no longer apply and need rechecking.

If I have plaque, can it go away?

For most people the plaque itself does not disappear, and that is not the goal of treatment. In the Spanish PESA cohort, followed with repeat ultrasounds over six years, plaque regressed in 8 percent of the people who had it and progressed in a third, and higher LDL and blood pressure drove progression hardest in the youngest. Statins and the other LDL-lowering drugs shrink the soft, cholesterol-rich core of a plaque and thicken the cap over it, which is what makes it less likely to rupture and cause a heart attack. Calcium does not dissolve, and a calcium score can rise on a statin as soft plaque hardens, which is a sign of stabilization. Treatment aims to stop the plaque from growing and to make the plaque you have safer, and the evidence is clear that the earlier that starts, the more of a life it protects.

References

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Published on damianrasch.com. The above information was composed by Dr. Damian Rasch, drawing on individual insight and bolstered by digital research and writing assistance. The information is for educational purposes only and does not constitute medical advice.