Atherosclerosis is defined by the slow, silent accumulation of material within the walls of arteries. This process centers on the formation of atheromatous plaque, a complex lesion that underlies many serious cardiovascular diseases globally. The plaque forms in the arterial wall, progressively narrowing the vessel and compromising blood flow. Understanding the composition, development, and consequences of this plaque is fundamental to grasping the progression of heart attacks, strokes, and other related health events.
What Atheromatous Plaque Is
Atheromatous plaque, or atheroma, is an abnormal, localized accumulation of material that develops exclusively within the subendothelial space of medium and large arteries. This space, known as the tunica intima, is located just beneath the single layer of endothelial cells lining the vessel. The plaque is composed of multiple biological components trapped within the artery wall.
At its core, the atheroma features a pool of accumulated lipids, primarily cholesterol, which forms a necrotic core. Surrounding this lipid core are foam cells, which are macrophages that have engulfed large amounts of oxidized low-density lipoprotein (LDL) cholesterol. The plaque also contains cellular debris, calcium deposits, and migrating smooth muscle cells. This entire structure is covered by a fibrous cap, a layer made of collagen and smooth muscle cells that separates the volatile inner core from the flowing blood.
The Progression of Plaque Formation
The biological mechanism of plaque formation is a chronic inflammatory process initiated by damage to the artery’s inner lining. This process begins with endothelial dysfunction, where the protective inner layer of cells becomes impaired due to factors like high blood pressure or toxins from smoking. The dysfunctional endothelium becomes more permeable, allowing LDL cholesterol particles to infiltrate and accumulate within the subendothelial space.
Once trapped in the artery wall, these LDL particles undergo oxidation, becoming chemically modified. In response, circulating white blood cells called monocytes are recruited to the site, where they migrate into the arterial wall and transform into macrophages. These macrophages attempt to clear the oxidized LDL by engulfing it through scavenger receptors, leading to their transformation into lipid-filled foam cells.
The accumulation of foam cells creates the initial lesion, known as a fatty streak. As the process continues, smooth muscle cells from the middle layer of the artery migrate to the site of injury and begin producing collagen and other fibrous materials. This production forms the fibrous cap over the fatty core, marking the development of a mature atheromatous plaque. The inflammation also promotes the accumulation of calcium, which contributes to the hardening and stiffening of the artery wall over time.
Major Health Conditions Caused by Plaque
Atheromatous plaque causes health problems through two distinct mechanisms: gradual narrowing and sudden rupture. The slow growth of the plaque progressively narrows the artery’s lumen, a condition known as stenosis, which restricts blood flow and oxygen supply to downstream tissues. Narrowing in the coronary arteries, which supply the heart muscle, leads to Coronary Artery Disease (CAD) and can cause symptoms like stable angina, or chest pain during exertion.
The second mechanism involves the plaque becoming unstable and rupturing. Unstable plaques have a large, soft lipid core and a thin, weak fibrous cap. When this cap tears, the highly thrombogenic contents of the plaque’s core are exposed to the bloodstream. This exposure instantly triggers the body’s clotting cascade, leading to the rapid formation of a thrombus, or blood clot, on top of the ruptured plaque.
If this clot grows large enough, it can suddenly block the artery, resulting in an acute event. A complete blockage in a coronary artery causes a myocardial infarction (heart attack). If the blockage occurs in an artery leading to the brain, such as the carotid artery, it causes an ischemic stroke. Plaque formation in the arteries supplying the limbs, especially the legs, causes Peripheral Artery Disease (PAD), leading to pain and potentially tissue death due to lack of oxygen.
Key Factors Driving Plaque Development
The initiation and acceleration of atheromatous plaque formation are strongly linked to several modifiable and non-modifiable factors that promote endothelial damage. High levels of cholesterol, specifically elevated LDL cholesterol (dyslipidemia), are a primary driver because they increase the concentration of particles available to infiltrate the artery wall and become oxidized. High blood pressure (hypertension) damages the delicate inner endothelial lining of the artery by subjecting it to increased physical stress. This continuous stress makes the endothelium more susceptible to injury and subsequent infiltration of LDL particles.
Smoking is another significant factor, as the toxins in cigarette smoke directly injure the endothelial cells and trigger an inflammatory state throughout the circulatory system. Chronic high blood sugar associated with diabetes similarly damages the blood vessel lining, contributing to endothelial dysfunction and accelerating the inflammatory process. Chronic inflammation, often linked to conditions like obesity or other inflammatory diseases, also plays a role by sustaining the immune response within the arterial wall that drives plaque growth. These factors combine to create an environment where the arteries are continuously damaged and the body’s inflammatory response is constantly activated, fueling the progression of plaque buildup.