An atheroma is a buildup of fatty material inside the wall of an artery. It starts as a small deposit along the artery’s inner lining and, over years or decades, grows into a thickened patch of cholesterol, immune cells, calcium, and other debris that narrows the vessel and restricts blood flow. Atheromas are the core feature of atherosclerosis, the disease behind most heart attacks and strokes.
What an Atheroma Is Made Of
A healthy artery has a smooth inner lining called the endothelium. When that lining gets damaged, whether from high blood pressure, smoking, high blood sugar, or other stressors, fats and immune cells begin collecting in the artery wall. Over time this collection hardens into a structured deposit with two main parts: a soft, lipid-rich core and a tougher outer shell called a fibrous cap.
The core contains cholesterol, dead cells, inflammatory immune cells, and proteins. Smooth muscle cells in the artery wall produce collagen, elastin, and other connective tissue that form the fibrous cap over the top. Calcium also accumulates inside the deposit, which is why advanced atheromas sometimes show up on imaging as hardened, calcified spots. The mix of soft fat and hard calcium within a single plaque is what makes atheromas unpredictable: some stay quiet for years, while others rupture suddenly.
How Atheromas Form
The process begins when LDL cholesterol particles slip through damaged spots in the artery lining and become trapped in the wall beneath. Once there, these particles undergo chemical changes (oxidation) that make them toxic to surrounding tissue. The body responds by sending white blood cells called monocytes into the artery wall, where they mature into macrophages, essentially cleanup cells designed to swallow the damaged cholesterol.
The problem is that macrophages take in far more oxidized LDL than they can handle. A single receptor on their surface is responsible for roughly 75% of the cholesterol they absorb. Overloaded with fat, they swell into what researchers call foam cells, and eventually die. Their contents spill out, forming the soft, necrotic core of the atheroma. This cycle repeats: more cholesterol infiltrates, more immune cells arrive, more foam cells die, and the deposit grows larger year after year.
Who Has Them and When They Appear
Atheromas are far more common than most people realize, and they usually develop long before any symptoms appear. In the Framingham Heart Study, MRI scans of over 300 adults with no cardiovascular symptoms found that 40% already had visible atheroma in their aorta. Among men under 50, about 18% had detectable plaque. By ages 60 to 69, nearly half of both men and women showed evidence of buildup, and by age 70 and older the rate climbed to roughly 57% in men and 69% in women.
These numbers reflect “subclinical” disease, meaning the atheromas hadn’t yet caused noticeable problems. The takeaway is that atheroma formation is extremely common with age and often progresses silently for decades before it either narrows an artery enough to cause symptoms or ruptures to trigger an acute event.
Stable vs. Unstable Plaques
Not all atheromas carry the same risk. The distinction between stable and unstable plaques determines whether an atheroma quietly restricts blood flow or suddenly causes a heart attack or stroke.
A stable atheroma typically has a thick fibrous cap, dense calcification, and relatively little soft lipid core. These plaques may narrow the artery significantly, sometimes enough to cause symptoms like chest pain during exertion, but they’re less likely to rupture. One common stable form is the fibrocalcific plaque, which is heavily calcified and rich in collagen with minimal necrotic material inside.
An unstable (or “vulnerable”) atheroma looks very different. It has a large, soft lipid core covered by a dangerously thin fibrous cap, often less than 65 micrometers thick. That cap contains fewer smooth muscle cells and less collagen, making it structurally weak. It’s also infiltrated with inflammatory immune cells that actively degrade the cap from within. Studies of ruptured plaques found that the average cap thickness at the point of rupture was just 23 micrometers, with 95% measuring under 64 micrometers. In fragmented or speckled patterns of calcification, about 67% of the calcium was associated with unstable lesions, while dense, sheet-like calcification was a marker of stability.
When an unstable cap tears open, the fatty, protein-rich core is suddenly exposed to flowing blood. This triggers a blood clot that can partially or completely block the artery within minutes, causing a heart attack if it happens in a coronary artery, or a stroke if it happens in an artery feeding the brain.
What Happens as Atheromas Progress
The consequences depend entirely on where the atheroma sits and how it behaves. In the coronary arteries, a growing plaque gradually limits blood supply to the heart muscle, producing chest tightness or pain during physical effort. In arteries supplying the brain, it raises the risk of stroke or transient ischemic attacks (brief episodes of stroke-like symptoms). In the kidney arteries, atheroma can contribute to high blood pressure and eventually kidney damage.
Rupture isn’t the only way an atheroma causes trouble. In some cases the endothelial surface over the plaque erodes away without the cap fully tearing. This “plaque erosion” still exposes the underlying tissue to blood and can trigger clot formation. A third mechanism involves calcified nodules that protrude through the cap into the bloodstream, also provoking clots. Together, rupture, erosion, and calcified nodules account for most acute cardiovascular events.
How Atheromas Are Detected
Because atheromas produce no symptoms until they’ve grown large or ruptured, detection usually relies on imaging. CT angiography is one of the most common tools, capable of identifying high-risk plaque features in the coronary arteries including the degree of narrowing, calcification patterns, and soft plaque composition. A simpler version, the coronary calcium score, uses a quick CT scan to measure how much calcium has accumulated in your heart arteries, serving as a rough gauge of overall plaque burden.
MRI offers a different advantage: it can distinguish between plaque components in greater detail, helping characterize whether a plaque has a large lipid core, a thin cap, or signs of inflammation. Nuclear imaging techniques go a step further by using radioactive tracers that highlight areas of active inflammation or early plaque development at the molecular level. Ultrasound, particularly of the carotid arteries in the neck, is a simpler and widely available screening option that measures artery wall thickness and can spot larger plaques.
Can Atheromas Shrink?
Yes, to a degree. A large body of clinical trial evidence shows that cholesterol-lowering medications can induce measurable plaque regression. In studies using intravascular ultrasound to directly image the inside of coronary arteries, treatment reduced the volume of noncalcified, fatty, and necrotic core components of plaques in a dose-dependent way: more aggressive cholesterol lowering produced greater shrinkage. Adding a second cholesterol-absorbing medication to the regimen produced further regression, with studies showing plaque volume reductions ranging from about 3% to nearly 14%.
Just as important as shrinking the plaque is stabilizing it. Treatment shifts the composition of an atheroma away from a large, soft lipid core toward a more fibrous, calcified structure that is less prone to rupture. In practical terms, the goal isn’t necessarily to eliminate every trace of plaque but to convert dangerous, vulnerable atheromas into stable ones that are unlikely to cause acute events.
What Drives Atheroma Growth
The major modifiable risk factors are the same ones behind cardiovascular disease broadly: high LDL cholesterol, high blood pressure, smoking, diabetes, and physical inactivity. Each of these damages the artery lining or increases the amount of cholesterol available to infiltrate the wall, or both. Chronic inflammation plays a central role too. The immune response that creates foam cells and weakens fibrous caps is amplified by conditions like obesity, poorly controlled blood sugar, and smoking.
Age and genetics also matter. The Framingham data show a clear, steady increase in plaque prevalence with every decade of life, and some people develop significant atheroma even with relatively favorable risk profiles due to inherited tendencies toward high cholesterol or vascular inflammation. That’s why atheroma prevention focuses on controlling what you can: keeping cholesterol and blood pressure in range, staying physically active, not smoking, and managing blood sugar if you have diabetes.