An atheroma is a buildup of fat, cholesterol, immune cells, and cellular debris inside the wall of an artery. It forms beneath the inner lining of the vessel, not on the surface like a scab. Over time, this buildup can harden, narrow the artery, or rupture suddenly, which is what triggers most heart attacks. About 73% of coronary artery blood clots are caused by a ruptured atheroma.
What an Atheroma Looks Like Inside
An atheroma is not simply a blob of cholesterol stuck to an artery wall. It has a layered structure. At its center sits a soft, fatty core made primarily of oxidized cholesterol, dead immune cells, and other cellular debris. This is called the necrotic core. Surrounding and capping that core is a layer of fibrous tissue, essentially a scar-like shell made of smooth muscle cells and structural proteins.
The stability of an atheroma depends heavily on the balance between these two components. A thick, sturdy fibrous cap over a small fatty core is relatively stable and less likely to cause problems. A thin cap stretched over a large, inflamed core is dangerous. Plaques with a fibrous cap thinner than 65 micrometers (roughly the width of a human hair) are classified as vulnerable, meaning they are prone to rupturing and triggering a blood clot.
How Atheromas Form
The process starts with damage to the inner lining of an artery. This lining, called the endothelium, is a single layer of cells that acts as a barrier between your blood and the artery wall. High blood pressure, smoking, high blood sugar, and other factors can injure or weaken that barrier, creating gaps where blood components seep into the artery wall.
Once the lining is compromised, cholesterol particles (particularly LDL, the “bad” cholesterol) penetrate into the wall and become trapped. The body treats this as a threat: immune cells rush in to clean up the cholesterol, swallow it, and become bloated “foam cells.” These foam cells accumulate and form what’s known as a fatty streak, the earliest visible stage of an atheroma. At the same time, platelets in the blood stick to the damaged area and release chemical signals that cause smooth muscle cells in the artery wall to multiply. Those muscle cells produce fibrous tissue, thickening the wall further.
This entire process unfolds over years and decades. The atheroma slowly grows as more cholesterol deposits, more immune cells arrive and die, and more fibrous tissue forms. Eventually the center of the plaque becomes a pool of dead cells and fat, while the cap overhead may thin out from ongoing inflammation.
Why Most Atheromas Cause No Symptoms
Atheromas are remarkably common, and the vast majority produce no symptoms at all. Intravascular ultrasound studies of heart donor arteries found that 17% of people under age 20 already had measurable plaque in at least one coronary artery. By age 40, that number climbed to over 70%. By age 50, it reached 85%. Standard angiograms (the X-ray images doctors use to look at arteries) missed all of these early plaques in people under 30, even though ultrasound clearly detected them.
The reason atheromas stay silent for so long is that arteries can remodel outward to accommodate the growing plaque, maintaining blood flow even as the wall thickens. Symptoms like chest pain or shortness of breath typically don’t appear until the artery is narrowed by about 70% or more, or until a plaque ruptures.
Stable Versus Vulnerable Plaques
Not all atheromas carry the same risk. The critical distinction is between stable and vulnerable plaques.
Stable plaques tend to have thick fibrous caps, smaller fatty cores, and less active inflammation. They may narrow an artery gradually, potentially causing predictable chest pain during exertion (stable angina), but they are less likely to rupture suddenly.
Vulnerable plaques are the opposite: large necrotic cores, thin fibrous caps, and heavy infiltration by inflammatory cells. These are the plaques responsible for most heart attacks and strokes. When a vulnerable plaque ruptures, the contents of its fatty core spill into the bloodstream, triggering a blood clot that can block the artery within minutes. Plaque erosion, where the surface wears away without a full rupture, is the second most common cause of sudden artery blockage.
The Role of Calcification
Calcium deposits within atheromas add another layer of complexity. Large, dense calcium deposits deep within a plaque generally act as stabilizers, creating a hard shell that may actually reduce the risk of rupture. Patients with heavily calcified plaques tend to have fewer acute symptoms than those with less calcified ones.
Small, scattered calcium specks (called spotty or microcalcifications) tell a different story. These represent active, inflammation-driven calcification and are more common in people experiencing acute heart events like heart attacks. Superficial calcifications near the inner surface of the artery are independently associated with plaque rupture and bleeding within the plaque, likely because they create uneven mechanical stress. Elongated calcium particles can increase local stress on the cap by nearly four times.
Key Risk Factors
The well-known drivers of atheroma formation include high LDL cholesterol, high blood pressure, smoking, diabetes, and obesity. But one lesser-known risk factor deserves attention: a blood particle called lipoprotein(a), or Lp(a). Unlike regular LDL, Lp(a) levels are almost entirely determined by genetics and are not reduced by standard cholesterol-lowering medications.
Lp(a) is more prone to oxidation and penetrates artery walls more easily than regular LDL, making it even more effective at fueling foam cell formation and plaque growth. Elevated Lp(a) independently predicts a first heart attack or stroke in people with no prior cardiovascular disease. Critically, elevated Lp(a) can be present even when all other cholesterol numbers look normal, which means some people carry significant atheroma risk that routine blood work won’t catch. In people already taking cholesterol-lowering therapy, high Lp(a) becomes an even stronger predictor of remaining cardiovascular risk, since other lipid levels have been addressed.
How Atheromas Are Detected
Because most atheromas are silent, detection often depends on imaging rather than symptoms. The main tools fall into two categories: noninvasive and invasive.
CT coronary angiography is the primary noninvasive option. It can reveal calcium deposits and plaque within the coronary arteries without threading a catheter into the heart. A coronary artery calcium score, derived from a CT scan, provides a rough measure of total plaque burden.
For more detailed evaluation, doctors use catheter-based imaging. Intravascular ultrasound (IVUS) provides cross-sectional images of the artery wall and detects calcium deposits with about 89 to 90% sensitivity. Optical coherence tomography (OCT) offers even finer resolution and is considered the best tool for identifying blood clots and measuring fibrous cap thickness. Near-infrared spectroscopy (NIRS) is the only imaging method specifically validated for detecting fatty, lipid-rich plaque. Combining IVUS with NIRS provides the most complete picture of plaque composition.
Can Atheromas Shrink?
For decades, atheroma was considered a one-way street: plaques could grow or stabilize but never truly reverse. That view has changed. A meta-analysis of lipid-lowering therapy trials found that coronary plaques measurably shrank when LDL cholesterol was brought below 80 mg/dL, with the most consistent regression seen below 70 mg/dL. Maintaining HDL cholesterol (the “good” cholesterol) above 45 mg/dL at the same time further improved results.
This regression is modest in absolute terms. Plaques don’t disappear, but they become smaller and, more importantly, more stable. The fibrous cap thickens, the lipid core shrinks, and inflammation quiets down. The practical takeaway is that aggressive cholesterol lowering doesn’t just slow atheroma progression. It can partially reverse it, reducing the chance that a plaque will rupture.
Achieving these cholesterol targets typically involves medication combined with dietary changes, exercise, and smoking cessation. The specific treatment approach varies based on overall cardiovascular risk, not just cholesterol numbers alone.