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Atherosclerosis

Atherosclerosis

For medical students2 min readUpdated 2026-10-10

Atherosclerosis is a chronic systemic lipid metabolism disorder characterized by the accumulation of excess lipoproteins within the tunica intima of arteries. The process leads to atheroma formation, sclerosis, calcification, and narrowing of the vascular lumen.

LocalizationIntima of elastic and muscular-elastic type arteries
High-risk zonesCoronary arteries, aorta, cerebral and renal vessels
Main risk factorsHypercholesterolemia, smoking, diabetes, hypertension
Target cellsMacrophages (foam cells) and smooth muscle cells

Pathogenesis and Development of Liposclerosis

The disease is triggered by endothelial injury and cell activation under the influence of risk factors. Endothelial cells begin to express adhesion molecules, recruiting mononuclear cells and platelets.

The process develops along two key pathways:

Growth factors stimulate the proliferation of smooth muscle cells. As a result, modified lipoproteins and connective tissue accumulate in the intima, forming liposclerotic lesions.

Forms of Arteriosclerosis and Risk Factors

Atherosclerosis is the most clinically significant atheromatous form of arteriosclerosis. Other forms include Mönckeberg medial calcific sclerosis (local calcification of muscular-type arteries) and arteriolosclerosis, which affects small vessels and arterioles.

There are over 250 identified risk factors, the primary ones being:

Complications and Mechanisms of Ischemia

At the complicated stage, fibroatheromas undergo critical changes. These include calcification (atherocalcinosis), destruction and ulceration of the fibrous cap, and thrombus formation.

Tissue and organ ischemia develops due to a combination of two pathogenetic factors:

  1. Mechanical narrowing of the arterial lumen by a plaque, thrombus, or embolus.
  2. Vascular spasm caused by the contraction of smooth muscle cells under the influence of vasoconstrictors (endothelin, thromboxane A2, leukotrienes).

Clinical consequences include organ infarctions, ischemic lesions, hemorrhages, and aneurysm formation.

Mnemonic

Lipids enter the intima, macrophages eat them until they foam, and the plaque caps off with calcium, threatening thrombosis.

Frequently asked questions

Which classes of lipoproteins possess the highest atherogenicity?

Atherogenic lipoproteins that promote the development of atherosclerosis include:

  • Low-Density Lipoproteins (LDL) — their concentration directly correlates with the probability of developing atherosclerosis; with extremely high LDL cholesterol, coronary heart disease can develop even in young individuals.
  • Very Low-Density Lipoproteins (VLDL) — possess atherogenic effects and contribute to atherosclerosis progression.
  • Intermediate-Density Lipoproteins (IDL) — are also classified as atherogenic lipoproteins.

High-Density Lipoproteins (HDL) are anti-atherogenic.

What are the stages of atherosclerotic plaque morphogenesis?

The pathomorphogenesis of atherosclerosis involves four sequential stages reflecting the dynamics of plaque development:

  • Pre-lipid stage — intimal injury caused by blood composition changes, visible only via electron microscopy.
  • Lipidosis stage — focal lipid infiltration of the intima with foam cell formation, macroscopically visible as fatty streaks and spots.
  • Liposclerosis stage — connective tissue proliferation and formation of a fibrous plaque narrowing the vessel lumen.
  • Complicated lesion stage — includes breakdown of the plaque's central core (atheromatosis), ulceration of its cap, and calcium salt deposition (atherocalcinosis).
What is the role of smooth muscle cells in the pathogenesis of atherosclerosis?

The role of smooth muscle cells (SMCs) in the pathogenesis of atherosclerosis includes their proliferation, participation in plaque formation, lipid accumulation, and induction of ischemia.

  • Fibrous plaque formation — stimulated by local growth factors, SMC proliferation accelerates the transformation of fatty streaks into fibrous plaques (liposclerosis).
  • Cholesterol accumulation — when clearance mechanisms fail, excess lipids can accumulate directly within vascular wall SMCs.
  • Development of ischemia — in the affected zone, local vasoconstrictors induce spastic contraction of arteriolar SMCs, compounding mechanical vessel narrowing.
What are foam cells and how do they form?

These are macrophages with cytoplasm engorged with modified lipids. They form in the subendothelial space after actively phagocytosing oxidized lipoproteins.

Why do lipoproteins undergo active oxidation within the vessel wall?

The arterial wall contains lipoxygenases and accumulates free radicals (free radical lipid oxidation), while plasma antioxidants are absent in this space.

What factors cause vasospasm in atherosclerosis?

Spasm develops due to vasoconstrictors released by cells in the lesion area: thromboxane A2, endothelin, leukotrienes, and vasoconstrictor prostaglandins.

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