Atherosclerosis is a chronic inflammatory disease characterized by the buildup of plaque within artery walls. This plaque is a complex mixture of fats, cholesterol, calcium, and other cellular debris. Plaque formation leads to a thickening and hardening of the artery walls. In its early stages, this condition often remains undetected, as symptoms do not appear until arteries become significantly narrowed or blocked.
Initial Triggers for Plaque Formation
The process of plaque formation begins with damage or dysfunction to the endothelium, the smooth inner lining of the arteries. This delicate layer can be injured by factors such as high blood pressure, elevated low-density lipoprotein (LDL) cholesterol, tobacco smoke toxins, and high blood sugar levels from diabetes.
When the endothelium is damaged, it triggers an inflammatory response within the arterial wall. This response involves the recruitment of immune cells, such as monocytes and T cells, to the injury site. These cells infiltrate the arterial wall.
How Plaque Develops
Following initial endothelial injury, LDL cholesterol particles accumulate within the damaged arterial wall. Once inside, these LDL particles can undergo oxidation, becoming oxidized LDL (Ox-LDL).
Ox-LDL attracts monocytes, a type of white blood cell, to the area. These monocytes then differentiate into macrophages, which are large immune cells. Macrophages engulf the oxidized LDL, transforming into lipid-laden “foam cells.”
The accumulation of these foam cells within the intima, the innermost layer of the artery, forms a “fatty streak.” This early, visible sign of atherosclerosis may appear in individuals as young as their 20s. At this stage, the fatty streak does not significantly protrude into the artery or impede blood flow.
As the process continues, smooth muscle cells from the middle layer of the artery wall, known as the media, migrate into the intima. These cells proliferate and produce extracellular matrix components like collagen and elastic tissue, contributing to plaque growth.
A fibrous cap, composed of smooth muscle cells and connective tissue, forms over the accumulating plaque. This cap stabilizes the plaque, containing the fatty core beneath it. Over time, calcium deposits can also accumulate within the plaque, leading to calcification and hardening of the arterial wall.
As the plaque grows, it bulges into the lumen, the inner channel of the artery, narrowing the vessel and reducing blood flow, potentially restricting oxygen-rich blood delivery to tissues and organs.
Key Contributors to Plaque Formation
Several factors accelerate the development of atherosclerotic plaque. High levels of LDL cholesterol are a primary contributor because these particles can easily accumulate and become oxidized within arterial walls. Conversely, low levels of high-density lipoprotein (HDL) cholesterol also play a role, as HDL helps remove cholesterol from the arteries.
High blood pressure, or hypertension, damages the endothelial lining of the arteries, making them more susceptible to plaque formation. The constant force of high pressure can cause microscopic injuries, initiating the inflammatory cascade.
Diabetes, characterized by elevated blood sugar levels, can also injure the inner layers of the arteries, promoting plaque buildup. Excess glucose can lead to inflammation and contribute to endothelial dysfunction.
Smoking and exposure to secondhand smoke introduce toxins that directly damage blood vessels and accelerate plaque formation and growth. Obesity and a lack of physical activity are associated with unhealthy cholesterol levels and an increased risk of high blood pressure and diabetes. Genetic predispositions, such as a family history of early cardiovascular disease or inherited cholesterol disorders like familial hypercholesterolemia, can also increase susceptibility to plaque formation.
Health Impacts of Plaque Formation
The presence and progression of atherosclerotic plaque can have significant health consequences. As plaque builds up, it narrows the arteries, a condition called stenosis, which reduces blood flow to organs and tissues. This reduced blood flow can lead to symptoms such as chest pain or discomfort, especially during physical activity.
A major risk occurs when plaque ruptures. If the fibrous cap covering the plaque breaks open, the inner contents are exposed to the bloodstream. This exposure can trigger the formation of a blood clot, known as a thrombus.
A blood clot can partially or completely block the artery, cutting off blood flow. If this blockage occurs in arteries supplying the heart, it can cause a heart attack. A blockage in arteries leading to the brain can result in a stroke. Plaque formation in arteries supplying the limbs can lead to peripheral artery disease, causing pain and potential tissue damage.