What is atherosclerosis?

Atherosclerosis is a chronic, systemic condition that results in the build-up of lipid-rich plaques in the arteries of the body.1 Depending on the arteries affected, this may manifest as:

  • Coronary artery disease (CAD)
  • Peripheral artery disease (PAD), e.g. of the lower extremities or the carotid arteries

The formation of these plaques occurs over several decades, starting from a non-pathological lesion in the intima (the surface layer of the artery exposed to the blood) and progressing to a fibroatheroma – an advanced lesion characterized by a fibrous cap and a necrotic core.2,3 This process occurs to some extent in many individuals throughout adulthood, but it may be accelerated by a range of risk factors including diabetes, smoking or high blood cholesterol.4

atherosclerotic lesion development
Pathological atherosclerotic lesions develop in the arterial wall over several decades.3,5,6
Model of the stages of development of atherosclerotic lesions.

The process of atherogenesis is initiated by disturbances in blood flow at so-called ‘predilection sites’, which lead to changes in the endothelial lining of the vascular system.2 These changes cause low-density lipoproteins (LDLs) to accumulate in the intima, where they become modified by oxidation and aggregation. Increasing retention of LDL triggers the recruitment of inflammatory macrophages to the intima, where they ingest the lipids to become foam cells – so-called because they are filled with cholesteryl ester droplets, giving them a foamy appearance.1,2,7,8 As the lesion progresses, these lipid-rich cells in the core of the plaque begin to die, releasing lipids and forming the necrotic core of the fibroatheroma.1 Meanwhile, smooth muscle cells migrate from the artery wall into the intima, where they proliferate to form a fibrous cap that covers the surface of the plaque.1 In some cases, over time, infiltrating macrophages and the release of active proteases can lead to thinning of this cap.3 While very large plaques may impede blood flow, causing ischaemic symptoms such as stable angina, these ‘thin-cap fibroatheromas’ are the most likely to cause an acute atherothrombotic event because they are most vulnerable to rupture, exposing the plaque contents to the blood and triggering the formation of a blood clot.1,9


Back to overview