Atherosclerosis is a chronic disease that serves as the underlying cause for most cardiovascular events globally. This condition involves the progressive hardening and narrowing of arteries due to the accumulation of atherosclerotic plaque. The formation of this structure within the body’s blood vessels is the mechanism behind heart attacks and ischemic strokes. Plaque development is a slow, inflammatory process that can take decades before causing an acute medical crisis.
What Atherosclerotic Plaque Is
Atherosclerotic plaque is a complex, composite structure that builds up within the artery wall. At its core lies a soft, necrotic lipid pool made primarily of cholesterol and fatty deposits. This core is highly inflammatory and contains the remnants of dead cells and immune factors. Surrounding this core is a layer of connective tissue and smooth muscle cells known as the fibrous cap.
The stability of the plaque depends on the characteristics of this cap. A stable plaque possesses a thick, robust fibrous cap and a smaller lipid core. Conversely, a vulnerable plaque is characterized by a large, soft lipid core, a high concentration of inflammatory cells, and a thin, fragile fibrous cap. Vulnerable plaques are the type most prone to rupture and cause sudden blockages. Over time, plaques may also accumulate calcium deposits, a process called calcification, which contributes to the hardening and stiffness of the artery wall.
The Step-by-Step Formation Process
Plaque formation begins with damage or dysfunction to the endothelium, the inner lining of the artery. This damage, often triggered by factors like high blood pressure, elevated LDL cholesterol, or tobacco smoke, makes the artery wall permeable. Low-density lipoprotein (LDL) cholesterol particles then infiltrate the damaged layer and become trapped within the artery wall.
Once trapped, these LDL particles undergo modification, such as oxidation, which signals an alarm to the body’s immune system. In response, white blood cells called monocytes are recruited from the bloodstream into the artery wall where they transform into macrophages. These macrophages attempt to clean up the invading lipids by engulfing the modified LDL cholesterol.
As the macrophages become engorged with fat, they transform into “foam cells,” which represent the earliest visible lesion of atherosclerosis, known as a fatty streak. The continued accumulation of foam cells, lipids, and cellular debris forms the growing lipid core of the plaque. To contain this mass, smooth muscle cells migrate from the deeper layer of the artery wall and proliferate, laying down a matrix of collagen and other materials. This effort to wall off the lesion results in the formation of the fibrous cap.
When Plaque Leads to Serious Events
Plaque can lead to serious cardiovascular events through two primary mechanisms: gradual narrowing or sudden rupture. Stable plaques, which grow slowly, can significantly narrow the artery, a condition known as stenosis. This restriction of blood flow limits the oxygen supply to the heart muscle, causing chest pain or discomfort called stable angina, especially during physical exertion. The symptoms resolve with rest because the blood supply is sufficient for the heart at lower workloads.
The most dangerous event occurs when a vulnerable plaque ruptures. The thin fibrous cap can tear or fissure under stress, exposing the lipid core contents to the circulating blood. The body interprets this exposure as a severe injury and immediately initiates the clotting cascade. Platelets rush to the site of the rupture and quickly form a blood clot, or thrombus, over the exposed material.
This blood clot can partially or completely block the artery within minutes. If the blockage occurs in a coronary artery, it cuts off the blood and oxygen supply to a section of the heart muscle, leading to a heart attack, also known as a myocardial infarction. Similarly, if the rupture and resulting clot occur in an artery supplying the brain, it causes an ischemic stroke. The event is not caused by the size of the plaque, but by its inflammatory composition and instability.
Strategies for Stabilizing and Managing Plaque
Managing atherosclerosis focuses on halting the progression of plaque and stabilizing existing vulnerable lesions. Lifestyle changes are foundational, starting with dietary modifications to reduce the intake of saturated and trans fats, which helps lower circulating LDL cholesterol. Regular physical activity and cessation of smoking are also important, as they improve endothelial function and reduce the inflammatory triggers that drive plaque formation.
Medical treatments play a major role in achieving plaque stabilization and reducing the risk of acute events. Statins are a primary class of medication used to lower LDL cholesterol, reducing the lipid content within the plaque. Beyond lowering cholesterol, statins also possess anti-inflammatory properties that can strengthen the fibrous cap, making the plaque more resistant to rupture. Antiplatelet medications, such as aspirin, are used to reduce the blood’s tendency to clot in the event of a rupture, minimizing the chance of a complete blockage. Other medications, including certain blood pressure drugs, may also contribute to plaque stability by improving vascular health and reducing arterial stress.