What Is Atherosclerosis?

Atherosclerosis is a chronic inflammatory disease of the arteries characterized by the accumulation of lipids, immune cells, and fibrous material within the inner wall of blood vessels, forming structures called plaques. It is among the leading causes of cardiovascular morbidity and mortality worldwide, underpinning conditions such as coronary artery disease, stroke, and peripheral artery disease. The condition develops silently over decades, making early detection and mechanistic understanding central concerns for both clinical medicine and biomedical engineering.

The disease draws its scientific foundations from vascular biology, immunology, and fluid mechanics. Biomedical engineers contribute through computational modeling of blood flow, imaging analysis, and the development of diagnostic and therapeutic devices.

Plaque Formation and Endothelial Dysfunction

Atherosclerosis begins when the endothelium, the single-cell layer lining arterial walls, is exposed to mechanical or chemical stressors such as disturbed blood flow, elevated low-density lipoprotein (LDL) cholesterol, or hypertension. Endothelial dysfunction allows LDL particles to infiltrate the arterial intima, where they undergo oxidation and trigger an immune response. Monocytes recruited from circulation differentiate into macrophages, which engulf oxidized LDL and transform into lipid-laden foam cells. As described in pathophysiology reviews published through the NIH's PubMed Central, this cascade of lipid retention and inflammation is the foundational mechanism by which plaques are initiated. Over time, smooth muscle cells migrate into the intima, adding a fibrous cap over the growing lipid core.

Disease Progression and Plaque Vulnerability

Early plaques, known as fatty streaks, are largely asymptomatic. As the disease progresses, plaques enlarge and calcify, narrowing the arterial lumen and reducing blood flow. The clinical risk arises less from gradual obstruction and more from plaque rupture: when a thin fibrous cap overlying a large necrotic lipid core tears, the exposed contents trigger rapid thrombus formation, potentially causing myocardial infarction or stroke. The National Heart, Lung, and Blood Institute's research on atherosclerosis emphasizes that plaque stability, rather than stenosis severity alone, determines acute event risk. Inflammatory activity within the plaque, driven by macrophage accumulation and protease release, is the principal determinant of cap integrity.

Diagnosis and Biomedical Imaging

Clinical diagnosis relies on a combination of risk factor assessment and non-invasive imaging. Coronary computed tomography angiography (CCTA) and calcium scoring quantify arterial calcification, providing a measure of plaque burden. Intravascular ultrasound and optical coherence tomography allow direct visualization of plaque morphology and cap thickness during catheterization. Magnetic resonance imaging is used to characterize plaque composition, distinguishing lipid-rich from fibrous lesions. Diagnostics of atherosclerosis reviewed in PMC catalogs the sensitivity and specificity of these approaches. Emerging approaches include artificial intelligence-assisted image analysis to identify high-risk plaques from standard CT datasets without additional radiation exposure.

Applications

Atherosclerosis research has applications across a wide range of fields, including:

• Cardiovascular device development: stents, angioplasty catheters, and flow diverters designed to restore vessel patency
• Computational fluid dynamics: patient-specific arterial models used to predict wall shear stress and plaque-prone regions
• Pharmacology: development and evaluation of statins, PCSK9 inhibitors, and anti-inflammatory agents targeting plaque progression
• Medical imaging systems: CT, MRI, and ultrasound hardware and algorithms for plaque characterization and risk stratification
• Wearable and remote monitoring: continuous blood pressure and lipid monitoring for high-risk patient populations