Atherosclerosis is a condition characterized by the buildup of a waxy substance called plaque inside the arteries. These arteries are blood vessels responsible for carrying oxygen-rich blood from the heart to other parts of the body. This plaque accumulation can gradually narrow and stiffen the arteries, impeding blood flow over time. The disease often progresses silently for many years, showing no outward symptoms until significant narrowing or a complication occurs.
Initial Triggers of Atherosclerosis
The development of atherosclerosis begins with damage or dysfunction to the endothelium, the inner lining of the arteries. This endothelial dysfunction makes the arterial wall more permeable and susceptible to the entry of various substances. Several factors can contribute to this initial injury.
High blood pressure, for instance, exerts excessive force against the arterial walls, leading to physical stress and microscopic damage to the endothelial cells. Similarly, elevated levels of low-density lipoprotein (LDL) cholesterol, often referred to as “bad” cholesterol, can directly impair endothelial function. The presence of these high LDL particles within the bloodstream can initiate changes in the arterial lining.
Smoking introduces numerous toxic chemicals into the bloodstream, which directly harm endothelial cells and promote inflammation. Chronic high blood sugar levels, common in individuals with diabetes, also contribute significantly to endothelial damage. These damaging factors compromise the usually smooth and protective endothelial surface.
The Inflammatory Response and Lipid Infiltration
Following initial endothelial damage, the body initiates an inflammatory response within the arterial wall. This process involves the recruitment of immune cells to the site of injury. Monocytes, a type of white blood cell, are attracted to the dysfunctional endothelium and adhere to its surface.
Once attached, these monocytes migrate into the sub-endothelial space, the layer just beneath the arterial lining. Within this space, they transform into macrophages, immune cells that engulf substances. Simultaneously, LDL cholesterol particles infiltrate the arterial wall.
These infiltrated LDL particles undergo oxidation, a chemical modification that makes them more reactive and recognizable by macrophages. The macrophages then take up these oxidized LDL particles, accumulating lipids within their cytoplasm. This lipid accumulation transforms the macrophages into “foam cells,” named for their foamy appearance under a microscope.
The accumulation of these lipid-laden foam cells within the arterial wall represents early atherosclerotic lesions. These foam cells contribute to the expanding lesion, releasing inflammatory molecules that sustain inflammation. This process establishes a localized inflammatory state within the artery.
Plaque Formation and Growth
The accumulation of foam cells marks the beginning of the fatty streak. Over time, these fatty streaks can progress into more complex atherosclerotic plaques. This progression involves the continued influx of inflammatory cells and lipids, alongside changes in the arterial wall structure.
Smooth muscle cells migrate from the artery’s middle layer into the inner layer where the fatty streak forms. These migrating smooth muscle cells then proliferate, meaning they multiply, contributing to the growing lesion. They also produce extracellular matrix components, such as collagen and elastin, which provide structural support to the developing plaque.
This combination of accumulating foam cells, proliferating smooth muscle cells, and extracellular matrix forms a fibrous cap over a core of lipids and cellular debris. The fibrous cap acts as a protective layer, separating the plaque’s contents from the bloodstream. Over many years, the plaque can continue to grow, gradually narrowing the artery’s lumen, the open space through which blood flows. Calcium deposits can also accumulate within the plaque, leading to calcification, which makes the artery stiffer and less elastic.
Plaque Rupture and Its Consequences
While many atherosclerotic plaques remain stable, a concern arises when a plaque becomes “vulnerable” and susceptible to rupture. Vulnerable plaques have a thin fibrous cap covering a large, soft lipid-rich core. This makes them unstable and prone to mechanical stress.
When a vulnerable plaque ruptures or erodes, its thrombogenic (clot-forming) contents are exposed to the bloodstream. This exposure triggers the body’s clotting cascade, a series of events designed to stop bleeding. Platelets, small blood cells involved in clotting, adhere to the exposed plaque material and become activated.
The activated platelets then aggregate, forming a plug, and initiate the formation of a blood clot (thrombus) on the surface of the ruptured plaque. This thrombus can rapidly grow, severely or even completely blocking the artery. If this blockage occurs in the coronary arteries supplying the heart, it can lead to a heart attack (myocardial infarction). A similar event in the carotid or cerebral arteries can result in an ischemic stroke, depriving brain tissue of oxygen and nutrients.