Pathogenesis and Development of Liposclerosis
The disease is triggered by endothelial damage and cell activation under the action of risk factors. Endotheliocytes begin to produce adhesion molecules, attracting mononuclear cells and platelets.
The process develops in two key directions:
- Lipid pathway: transport of lipoproteins into the subendothelium and their modification under the influence of free-radical oxidation.
- Cellular pathway: penetration of macrophages, which actively uptake modified lipids and transform into foam cells.
Growth factors stimulate the proliferation of smooth muscle cells. As a result, modified lipoproteins and connective tissue accumulate in the intima, forming liposclerotic changes.
Forms of Arteriosclerosis and Risk Factors
Atherosclerosis is the most clinically significant atheromatous form of arteriosclerosis. In addition, focal calcification of muscular-type arteries and arteriolosclerosis affecting small vessels and arterioles are distinguished.
Medicine recognizes more than 250 risk factors, among which the main ones are:
- Smoking and physical inactivity.
- Diabetes mellitus and arterial hypertension.
- Obesity and burdened heredity.
- Lipid profile disorders: hypercholesterolemia with a high atherogenic index and hypertriglyceridemia.
Complications and Mechanisms of Ischemia
At the complication stage, fibroatheromas undergo critical changes. These include calcification (atherocalcinosis), destruction and ulceration of the fibrous cap, as well as thrombus formation.
Tissue and organ ischemia develops due to a combination of two pathogenetic factors:
- Mechanical narrowing of the arterial lumen by a plaque, thrombus, or embolus.
- Vascular spasm caused by the contraction of smooth myocytes under the influence of vasoconstrictors (endothelin, thromboxane A2, leukotrienes).
Clinical consequences include organ infarctions, ischemic lesions, hemorrhages, and aneurysm formation.
Briefly: answers to topical questions
Which classes of lipoproteins possess the highest atherogenicity?
Atherogenic lipoproteins that contribute to the development of atherosclerosis include:
- Low-density lipoproteins (LDL) — their concentration directly correlates with the probability of developing atherosclerosis; at very high LDL cholesterol levels, coronary artery disease (CAD) can develop even in young people.
- Very low-density lipoproteins (VLDL) — possess atherogenic effects and contribute to the development of atherosclerosis.
- Intermediate-density lipoproteins (IDL) — also classified as atherogenic lipoproteins.
High-density lipoproteins (HDL) are antiatherogenic.
What are the stages of atherosclerotic plaque morphogenesis?
The patho- and morphogenesis of atherosclerosis involve four consecutive stages reflecting the dynamics of processes within the plaque.
- Pre-lipid stage — intimal damage is caused by changes in blood composition and is visible only under an electron microscope.
- Lipoidosis stage — focal infiltration of the intima by lipids with the formation of foam cells, macroscopically manifesting as fatty spots and streaks.
- Liposclerosis stage — proliferation of connective tissue and formation of a fibrous plaque that narrows the vascular lumen.
- Complicated lesions stage — includes breakdown of the central part of the plaque (atheromatosis), ulceration of its cap, and deposition of calcium salts (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 lies in their proliferation, participation in plaque formation, lipid accumulation, and induction of ischemia.
- Fibrous plaque formation — under the action of released growth factors, SMC proliferation increases, contributing to the transformation of fatty streaks into fibrous plaques (liposclerosis).
- Cholesterol accumulation — when the clearance system is deficient, excess lipids can accumulate directly within the SMCs of the vascular wall.
- Development of ischemia — in the lesion zone, under the action of local vasoconstrictors, spastic contraction of arteriolar SMCs occurs, exacerbating the mechanical narrowing of the vessel.
Lipids infiltrate the intima, macrophages ingest them until they become foam cells, and the plaque undergoes surface calcification, posing a thrombotic threat.
Class and exam questions
What are foam cells and how do they form?
These are macrophages with cytoplasm overloaded with modified lipids. They form in the subendothelial space after the active uptake of oxidized lipoproteins.
Why do lipoproteins actively oxidize in the vessel wall?
Lipoxygenases are present in the arterial wall and free radicals accumulate (free-radical lipid oxidation), while plasma antioxidants are absent there.
What factors cause vascular spasm in atherosclerosis?
Spasm develops under the action of vasoconstrictors released by cells in the lesion area: thromboxane A2, endothelin, leukotrienes, and vasoconstrictor prostaglandins.
What else to study on this topic
- Etiotropic Principle of Therapy and the Role of Statins
- Pathogenetic Treatment and Thrombosis Prevention
- Symptomatic Principle of Relieving Ischemic Pain
- Molecular Mechanisms of Adhesion and Selectin Expression
- The Role of the Atherogenic Index in Diagnostics
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