Etymology

Atherosclerosis
Hardening of arteries

Atheroma
Latin: Tumour full of matter resembling gruel

Sclerosis

Athera
Greek: gruel

-oma
tumor

Skleros
hard

-osis

denoting process/action

Atherosclerosis plaques
Focal elevated lesion of tunica intima Protrude into vessel lumen Soft lipid core Fibrous cap Starts forming in early stages of life especially if high dietary fat intake Bifurcations; arterial branches where high turbulent flow

Early lesion
Fatty streak yellow linear elevation on intima Lipid-rich macrophages No clinical significance disappears from intima In high risk pts accumulation w/o removal plaques

Fully developed lesion

Central lipid core

Endogenous and exogenous

lipids, cell debris Soft; thrombogenic Border of foam cells

Cap of fibrous tissue covered by endothelium

Connective tissue; collagen

(SMC-derived) Inflammatory cells (recruited by arterial endothelium or microvessels)

Advanced stages

Dystrophic calcification of plaque

Development

Endothelial injury (dysfunction)

Tissue response to injurious agent

Formation of plaque after chronic/episodic exposure

Injury to endothelium
Injured endothelial cells undergo functional alteration, increasing: expression of cell-adhesion molecules
ICAM-1; E-selectin

Permeability for macromolecules e.g. LDL Thrombogenicity (ability to form clots)

Lipid accumulation
Accumulation of LDL/oxidised LDL at site and in macrophages

Migration
Inflammatory cells enter intima Monocyte adhesion macrophages; foam cells

Plaque formation
Accumulation of T-cells, macrophages, foam cells, lipids. Foam cells die by apoptosis

Tissue repair
Growth factors e.g. PDGF from platelets, endothelium, macrophages, SMC Induce proliferation of SMC (myointimal cells) Synthesis of collagen, elastin, mucopolysaccharide (SMC) In cycles of endothelial loss increase plaque volume

Clinical manifestations and complications