Medical & Clinical Reviews

Description

Atheroma, as described in medical literature, refers to plaque deposits that build up inside artery walls, a key contributor to the progression of atherosclerosis. These deposits comprise cholesterol, fats, calcium, cellular debris and inflammatory cells. The process of atheroma formation initiates with damage to the endothelium, the inner lining of arteries. This damage can stem from factors like hypertension, smoking, elevated cholesterol levels, or diabetes. When the endothelium is compromised, it becomes permeable to Low Density Lipoprotein (LDL) cholesterol particles circulating in the bloodstream. LDL cholesterol infiltrates the arterial wall, undergoes oxidative changes, and triggers inflammation. Attracted to the injured site, macrophages engulf oxidized LDL particles, forming foam cells. These foam cells accumulate along with calcium and cellular waste, initiating the formation of a fatty streak, the initial stage of atheroma. As the process continues, smooth muscle cells from the arterial wall migrate into the fatty streak. These cells proliferate and produce collagen which stabilizes the plaque. With the buildup of smooth muscle cells, collagen, and other substances, the fatty streak evolves into a more advanced atheromatous plaque over time.

Atheromatous plaques

Atheromatous plaques are defined by their distinct composition and structure within artery walls. They typically consist of a lipid core containing cholesterol crystals, lipids, and cellular debris. Surrounding this core is a fibrous cap composed of smooth muscle cells, collagen and other connective tissue components. Calcification, marked by the deposition of calcium salts within the plaque, can render the plaque rigid and more prone to rupture. The presence of inflammatory cells, particularly macrophages, contributes to plaque instability and progression. The stability and size of the fibrous cap play critical roles in determining the risk associated with atheromatous plaques. Plaques with a thick fibrous cap are considered stable and less likely to rupture, thereby reducing the risk of acute complications such as myocardial infarction (heart attack) or stroke. Conversely, plaques with a thin or weakened fibrous cap are deemed vulnerable, increasing the likelihood of rupture and subsequent formation of blood clots (thrombosis). Depending on their location and size within the arteries, atheromatous plaques can lead to various clinical complications. In the coronary arteries, these plaques can restrict blood flow to the heart muscle, resulting in symptoms like angina (chest pain) or myocardial infarction. Plaques in the carotid arteries that supply blood to the brain may cause Transient Ischemic Attacks (TIAs) or strokes. In peripheral arteries, such as those in the legs, atheroma can lead to symptoms like claudication (leg pain during walking) or critical limb ischemia.

Clinical management of atheroma

Clinical management of atheroma centers on plaque progression and associated complications. This approach primarily includes lifestyle adjustments such as adopting a heart-healthy diet, engaging in regular exercise, quitting smoking and effectively managing conditions like hypertension and diabetes. Medications like statins, which lower cholesterol levels and antiplatelet agents, which diminish the risk of blood clot formation, are standard prescriptions aimed at stabilizing plaques and preventing cardiovascular events. Ongoing research endeavors seek to deepen our understanding of the molecular mechanisms that drive atheroma formation and progression. This involves investigating genetic predispositions, inflammatory pathways and novel therapeutic targets that could potentially halt or reverse plaque accumulation. Advanced imaging technologies such as intravascular ultrasound and optical coherence tomography provide more precise insights into plaque morphology and composition, aiding in risk assessment and treatment planning.