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Atherosclerosis: What Arterial Plaque Is and How It Builds Up

Atherosclerosis: What Arterial Plaque Is and How It Builds Up

Arterial plaque is a buildup of cholesterol, immune cells, scar-like tissue and, later, calcium inside the wall of an artery. The process is called atherosclerosis. It is not sludge stuck to the inside of a pipe. It grows within the wall itself.

Plaque builds slowly, usually over decades, and most of it never causes a symptom. The danger is that a plaque can tear open without warning and trigger a clot. That is how most heart attacks happen.

Key takeaways

  • Plaque is a buildup of cholesterol, immune cells, scar-like tissue and later calcium that grows within the artery wall.
  • It builds over decades and usually causes no symptoms.
  • Most heart attacks happen when a plaque tears or erodes and a clot forms, not from slow narrowing alone.
  • No single test shows all plaque, and a calcium score of zero cannot rule out soft plaque.
  • Lowering ApoB particles, controlling blood pressure and blood sugar, and not smoking reduce risk, but nobody can promise to clear your arteries.

How plaque starts

Cholesterol travels through your blood inside small particles. The ones that can cause plaque each carry one copy of a protein called ApoB, which is why an ApoB test is a count of those particles.

Some of these particles pass through the inner lining of the artery and get trapped in the wall. The more particles in your blood, and the more years they circulate, the more get trapped. A consensus review covering more than 200 studies and over 2 million people concluded that these particles cause atherosclerotic heart disease, and that the risk grows with both the level and the years of exposure.1

Your immune system reacts to the trapped particles. White blood cells move in, swallow the cholesterol and swell with fat. This is the earliest visible stage, called a fatty streak. Our guide to inflammation and heart disease explains this immune reaction in more detail.

How it builds over decades

Plaque is not a problem that begins in middle age. In an autopsy study of people aged 2 to 39 who died mostly from accidents, fatty streaks and early plaques were already present and increased with age and with the number of risk factors.2

From there the process is slow. Fat-filled cells die and leave a soft, fatty core. The artery lays down a cap of fibrous tissue over the core, a little like a scar. Over time, calcium is deposited in older parts of the plaque.

High blood pressure, smoking, diabetes and inherited factors such as a high Lp(a) level all speed this up.

Healthy artery open channel Early deposit particles enter the wall Soft plaque grows within the wall Calcified plaque visible on a calcium scan
Plaque builds inside the artery wall over decades. A calcium scan sees only the last stage; soft plaque that has not calcified does not appear on it.

Soft plaque and calcified plaque

You will often hear plaque described as soft or calcified. Most people with plaque have a mix of both.

TypeWhat it isWhat to know
Soft (non-calcified) plaqueA fatty core covered by a fibrous cap, with no calcium yetUsually the earlier stage. It does not show up on a calcium score.
Calcified plaqueOlder plaque in which calcium has been depositedEasy to see on a CT scan. It marks how much plaque has built up over time.
Mixed plaqueSoft and calcified parts togetherCommon. Most people with plaque have some of each.

Why most plaque causes no symptoms

An artery can make room for plaque. As a plaque grows, the wall often expands outward, so the channel where blood flows stays open for a long time.

Symptoms such as chest tightness with effort tend to appear only when a plaque narrows the channel enough to limit blood flow. Many plaques never reach that point. This is why you can feel well, pass a physical and still have plaque. Our article on silent heart disease looks at this more closely.

Why rupture, not just narrowing, causes heart attacks

It is natural to picture a heart attack as an artery that slowly closed. More often, something sudden happens.

The cap over a plaque tears, or the surface wears away. Blood touches the material inside and forms a clot within minutes. The clot can block the artery. Pathology studies show that plaque rupture is the most common cause of a heart attack, with surface erosion of a plaque as the other main cause.3

The plaques that rupture tend to have a large fatty core and a thin, inflamed cap. They are not always the ones causing the tightest narrowing. That is why a test that looks only for blockages can miss risk, and why prevention focuses on the total amount of plaque and the factors that drive it.

How plaque is found, and what the tests miss

No single test shows all of your plaque. Each one sees part of the picture.

Coronary artery calcium (CAC) score. A quick CT scan of the heart without contrast dye. It measures calcified plaque in the heart's arteries. It cannot see soft plaque. In one large registry of people with symptoms and a calcium score of zero, 13% had non-obstructive plaque on a more detailed CT scan and 3.5% had an artery narrowed by half or more.4 A zero is reassuring, but it is not proof of clean arteries.

Carotid ultrasound. An ultrasound of the neck arteries can show plaque there and measure the thickness of the artery wall (CIMT). It looks at the neck, not the heart, so it is an indirect clue. A meta-analysis of 11 population studies found that carotid plaque predicted future heart attacks more accurately than wall thickness did.5 US guidance from 2013 does not recommend routine CIMT measurement for predicting a first cardiovascular event.6

Blood tests. ApoB, Lp(a) and other markers do not show plaque. They show how strong the forces building it are.

Can plaque be slowed?

Be careful with anyone who promises to clear your arteries. What the evidence supports is more modest and still valuable: lowering the number of ApoB particles, controlling blood pressure and blood sugar, and not smoking reduce the risk of heart attack and stroke.

The goal is to slow new plaque and lower the chance that existing plaque causes trouble. The right plan depends on your own numbers and should be made with your clinician.

Your next step: learn what the tests can tell you

If you want to know whether you have plaque, read our guide to the coronary calcium score, which explains who the scan may help and where it stops being useful.

You can also answer the three quick questions in the Cardio Res-Q screener on our program page to see whether a closer evaluation makes sense for you.

Cardiovascular Risk Screener

Are You a Candidate for Cardio Res-Q?

Three quick questions about the risk factors we screen for. Your answers stay between you and the clinic.

Frequently asked questions

At what age does plaque start?

Earlier than most people think. Autopsy studies have found fatty streaks and early plaques in children and young adults, and more of them in those with more risk factors. Plaque that matters for heart attacks usually takes decades to develop, which is why the years before symptoms are the best time to act.

Is soft plaque more dangerous than calcified plaque?

Plaques that rupture tend to have a large fatty core and a thin cap, so soft plaque is often described as less stable. In practice most people have both kinds, and a high calcium score is a sign of more plaque overall. Neither type should be read alone.

Can you have plaque with normal cholesterol?

Yes. A standard panel measures the cholesterol inside particles, not the number of particles, and it does not capture inherited Lp(a), blood pressure, diabetes, smoking or inflammation. Any of these can drive plaque even when the usual numbers look fine.

Does a calcium score of zero mean I have no plaque?

It means no calcified plaque was seen. That is reassuring, especially in middle age and later, but soft plaque does not show on this scan. A zero is also less reassuring if you have diabetes, smoke or have a strong family history.

Related reading

This article is for general education and is not medical advice. Decisions about testing and medication should be made with your clinician. If you have chest pain or other symptoms of a heart attack, call 911.

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About Dr. Kenneth Varano, D.O.
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YoungerMeMD is a physician-led practice in Anti-Aging, Functional and Preventive Medicine, and your care is delivered by our whole clinical team. That team works under Medical Director Kenneth Varano, D.O., who brings over 30 years in clinical medicine and more than 20 years in age management and functional medicine — using science-backed, patient-focused strategies that restore balance, vitality, and health longevity.

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Barbara Dougherty, MSN, CRNP, is a Board-Certified Family Nurse Practitioner and Certified Menopause Practitioner (MSCP) specializing in optimizing hormones, and improving cardio-metabolic health. 

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References

  1. Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2017. PMID 28444290 · doi:10.1093/eurheartj/ehx144↩
  2. Berenson GS, et al. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa Heart Study. N Engl J Med 1998. PMID 9614255 · doi:10.1056/NEJM199806043382302↩
  3. Falk E, et al. Update on acute coronary syndromes: the pathologists' view. Eur Heart J 2013. PMID 23242196 · doi:10.1093/eurheartj/ehs411↩
  4. Villines TC, et al. Prevalence and severity of coronary artery disease and adverse events among symptomatic patients with coronary artery calcification scores of zero undergoing coronary computed tomography angiography: results from the CONFIRM registry. J Am Coll Cardiol 2011. PMID 22079127 · doi:10.1016/j.jacc.2011.10.851↩
  5. Inaba Y, et al. Carotid plaque, compared with carotid intima-media thickness, more accurately predicts coronary artery disease events: a meta-analysis. Atherosclerosis 2012. PMID 21764060 · doi:10.1016/j.atherosclerosis.2011.06.044↩
  6. Goff DC Jr, et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014. PMID 24239921 · doi:10.1016/j.jacc.2013.11.005↩
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