Plaque buildup in arteries is a gradual process where fatty deposits, cholesterol, calcium, and cellular waste accumulate inside your artery walls, narrowing the space blood flows through. The medical term is atherosclerosis, and it starts earlier than most people realize. For most people, the process begins in childhood and worsens with age, with risk climbing significantly after 45 in men and 55 in women.
How Plaque Forms Inside Your Arteries
The process starts with damage to the inner lining of an artery. High blood pressure, smoking, high blood sugar, or chronic inflammation can all cause this initial injury. Once the lining is damaged, inflammatory cells rush to the site and release chemical signals that attract cholesterol particles and cellular waste to the injured spot.
LDL cholesterol (the “bad” kind) plays a central role. LDL particles slip into the artery wall and get trapped there, where they become chemically altered through oxidation. These modified LDL particles trigger even more inflammation, calling in white blood cells called monocytes. The monocytes transform into macrophages, which swallow the cholesterol and clump together. Over time, this mass of cholesterol-gorged cells, calcium, and fibrin (a clotting protein) forms a deposit called plaque.
As plaque grows, the artery lining becomes increasingly leaky, allowing even more LDL to enter and get trapped. The plaque essentially creates a self-reinforcing cycle: damage attracts cholesterol, cholesterol causes more inflammation, and inflammation causes more damage.
What Plaque Is Made Of
Arterial plaque isn’t a single substance. It’s a mix of fatty deposits, cholesterol, cellular waste products, calcium, and fibrin. The exact composition matters because it determines whether a plaque is dangerous in the short term or more of a slow, long-term problem. Plaques that are mostly calcium and dense scar tissue tend to be stable. Plaques with a large core of dead cells and fat, covered by only a thin cap, are the ones that can rupture suddenly and cause a heart attack or stroke.
Stable vs. Unstable Plaque
Not all plaque carries the same risk. Stable plaques are heavily calcified, rich in dense collagen, and lack a large core of dead tissue. They narrow the artery gradually and may cause symptoms like chest pain during exercise, but they’re less likely to trigger a sudden cardiac event.
Unstable plaques are a different story. These have a large necrotic core (a pool of dead cells and fat) covered by a thin fibrous cap, sometimes as thin as 65 micrometers. Immune cells actively break down the cap from the inside. Small bleeds within the plaque itself can enlarge the necrotic core and weaken the structure further. When the cap finally tears open, the contents spill into the bloodstream and trigger a blood clot. That clot can block the artery entirely within minutes, causing a heart attack or stroke. This is why someone with no prior symptoms can have a sudden, severe cardiac event.
Calcification patterns offer a clue about stability. Large, solid sheets of calcium are actually a marker of stable plaque. Scattered, fragmented specks of calcium are more common in unstable plaques. About two-thirds of the calcium found at the site of dangerous plaques appears in this fragmented pattern.
Where Plaque Builds Up and What It Causes
Plaque can develop in arteries throughout your body, and the location determines which disease it causes.
- Heart arteries: Coronary artery disease (CAD), the most common form, restricts blood flow to the heart muscle and is the leading cause of heart attacks.
- Leg and arm arteries: Peripheral artery disease (PAD) most often affects the legs, causing pain, cramping, or weakness when walking. It can also affect the arms or pelvis.
- Neck arteries: Carotid artery disease reduces blood flow to the brain and is a major cause of stroke.
Who Is Most at Risk
High blood pressure is the single most impactful modifiable risk factor. In the United States, it accounts for more atherosclerosis-related deaths than any other changeable factor. Over time, elevated pressure physically damages artery walls, creating the entry points plaque needs to start forming.
Smoking and secondhand smoke exposure are responsible for nearly one-third of deaths caused by coronary heart disease. Diabetes damages artery linings through persistently high blood sugar. Inflammatory conditions like rheumatoid arthritis and psoriasis injure blood vessels through chronic, body-wide inflammation. A sedentary lifestyle is directly linked to the unhealthy cholesterol levels that feed plaque growth.
Genetics play a meaningful role too. Familial hypercholesterolemia, an inherited cholesterol disorder, affects about 1 in 300 people and can cause dangerously high LDL levels from birth. Black Americans face a 30% higher risk of death from heart disease compared to white Americans, and people of South Asian descent also carry elevated risk. Diet high in saturated fat raises cholesterol levels, and heavy alcohol use increases total cholesterol.
How Plaque Buildup Is Detected
A coronary calcium scan is one of the most straightforward ways to measure plaque. It uses a CT scanner to detect calcified plaque in the heart’s arteries and produces a number called an Agatston score.
- Score of 0: No calcium detected. Low chance of heart attack in the near future.
- Score of 100 to 300: Moderate plaque deposits. Relatively high risk of heart attack or other heart disease over the next 3 to 5 years.
- Score above 300: More extensive disease and higher heart attack risk.
Your score can also be expressed as a percentile comparing you to others of the same age and sex. A calcium score at or above the 75th percentile is linked with significantly higher heart attack risk. It’s worth noting that calcium scoring only detects calcified plaque. Soft, unstable plaque won’t show up on this test, which is why a zero score doesn’t guarantee completely clean arteries.
Can Plaque Be Reversed?
Plaque buildup was once considered a one-way street, but aggressive cholesterol-lowering treatment can actually shrink it. Clinical trials comparing high-intensity cholesterol-lowering therapy to lower-intensity treatment have consistently shown plaque regression in the more aggressive treatment groups. In one notable trial (GLAGOV), patients who added a powerful cholesterol-lowering medication to their existing treatment saw plaque volume shrink by 2.9% over 76 weeks, compared to just 0.4% with standard therapy alone.
How far you lower LDL cholesterol matters. Patients who brought their LDL below roughly 70 mg/dL saw plaque volume increase by only 4.6% over the study period, while those with LDL at or above that threshold saw an 11.6% increase. Getting LDL low enough doesn’t just slow the disease; it can shift the balance toward shrinkage.
Current guidelines from the American Heart Association and American College of Cardiology set different LDL targets depending on your overall risk. For people at the highest risk (10% or greater chance of a cardiovascular event in the next 10 years), the goal is to cut LDL by at least 50%, ideally to below 70 mg/dL. For people at moderate risk, the target is below 100 mg/dL. For those at low risk, lifestyle changes like improving diet, increasing physical activity, and quitting smoking are the first-line approach.
Even without medication, lifestyle changes meaningfully slow plaque progression. Regular physical activity improves cholesterol profiles, reduces blood pressure, and lowers inflammation. Reducing saturated fat intake directly lowers LDL levels. Quitting smoking allows damaged artery linings to begin healing, removing one of the primary triggers for new plaque formation.