STEPTRACKERCARDIOVASCULAR | PATHOLOGY | HIGH-YIELD REVIEW

Atherosclerosis

Intimal plaques of lipid, foam cells and fibrous tissue in large and medium arteries — the root of most heart attacks and strokes.

FOCUS ON
Learn the build sequence: endothelial injury → LDL oxidized → foam cells (fatty streak) → smooth muscle migrates via PDGF → fibrous cap. Stable plaques narrow vessels (angina, claudication). Vulnerable plaques rupture (MI, stroke). Know the sites in order and each vascular bed's symptoms.
TOPIC
DETAIL
MECHANISM
CLUE
Definition
Intimal plaque: fibrous cap over a necrotic lipid core (cholesterol clefts, foam cells, debris).
Large elastic and medium muscular arteries
Cholesterol clefts = dissolved crystals in the core
Risk factors
Modifiable: smoking, HTN, ↑ LDL, diabetes, obesity, inactivity. Fixed: age, male sex, family history of premature disease.
Each injures endothelium or raises LDL entry
Premature = men < 55, women < 65
Fatty streak
earliest lesion
Flat yellow streaks of lipid-laden macrophages.
Oxidized LDL taken up by scavenger receptors → foam cells
Seen even in teenagers; not clinically significant
Mature atheroma
Smooth muscle cells migrate from media to intima and lay down collagen → fibrous cap.
PDGF, FGF, TGF-β from macrophages, platelets, endothelium
Plaques often calcify
Sites
Abdominal aorta > coronary arteries > popliteal > internal carotid > circle of Willis.
Branch points and turbulent flow
Abdominal aorta below the renals is #1
Stable plaque
Thick cap, small core; slowly narrows the lumen.
> 70% stenosis → ischemia on demand
Stable angina, claudication, mesenteric angina
Vulnerable plaque
Thin cap, large lipid core, many inflammatory cells.
Macrophage MMPs weaken cap → rupture → thrombosis
Acute coronary syndrome, stroke — often from < 70% lesions
Complications
Stenosis, rupture with thrombosis, atheroembolism, aneurysm (media weakened).
Ischemia, infarct, emboli, dilation
AAA is the classic aneurysm of atherosclerosis
Familial hypercholesterolemia
LDL receptor (or ApoB, PCSK9) defect · autosomal dominant.
LDL cannot be cleared from blood
Tendon xanthomas, corneal arcus, MI in 20s–40s
Prevention & treatment
Statins, antiplatelets, BP and glucose control, smoking cessation; stents or bypass.
Statins also stabilize plaques
ABI < 0.9 confirms peripheral artery disease

Mechanism — how a plaque is built

Endothelial injurySmoking, HTN, glucose, shear
→
LDL enters intimaOxidized
→
Foam cellsFatty streak
→
SMC migrationPDGF → collagen cap
→
AtheromaStenosis or rupture

Clinical picture by vascular bed

BED
PRESENTATION
Coronary
Angina, MI, sudden death, ischemic cardiomyopathy
Carotid / cerebral
TIA, stroke, amaurosis fugax (Hollenhorst plaques)
Peripheral
Claudication → rest pain → ulcers, gangrene
Mesenteric
Postprandial pain, fear of eating, weight loss
Renal
Renovascular hypertension, ischemic nephropathy
Aorta
Abdominal aortic aneurysm

How it's tested

COMMON CONFUSIONMost MIs come from rupture of plaques that were not severely stenotic. Stable angina comes from fixed, severe stenosis.
THE TRAP"Which growth factor drives smooth muscle migration into the intima?" The answer is PDGF, not VEGF or TGF-β.
YOUR APPROACHRisk factors → endothelial injury → plaque stage → complication → the vascular bed that explains the symptoms.

If you see… think…

Earliest visible lesion, even in a teenager → fatty streak (foam cells)
Smooth muscle migrating into the intima → PDGF
Most common site of atherosclerosis → abdominal aorta
Calf pain on walking, relieved by rest, ABI 0.6 → peripheral artery disease
Pain 30 minutes after meals + weight loss → chronic mesenteric ischemia
Transient "curtain" over one eye → carotid atheroembolism (amaurosis fugax)
MI at 32 with Achilles tendon xanthomas → familial hypercholesterolemia
Thin cap, large lipid pool, many macrophages → vulnerable plaque
Needle-shaped spaces in a plaque core → cholesterol clefts