🩸 Atherosclerosis is a chronic disease of large and medium-sized arteries. It involves endothelial dysfunction, vascular inflammation, and accumulation of lipids, cholesterol, calcium and cellular debris within the intima of vessel walls [1].
⚠️ It leads to the formation of atherosclerotic plaques which may disrupt blood flow either by progressive fixed stenosis or by rupture → acute vessel occlusion.
❤️ Can cause myocardial infarction (coronary arteries), 🧠 stroke or TIA (carotid/cerebral vessels), 🚶‍♂️ peripheral vascular disease (limbs), and renal dysfunction (renal artery stenosis).

🧬 Aetiology & Pathophysiology

Earliest visible abnormality = fatty streak (lipid deposition in intima).
Lipid accumulation → triggers inflammation → monocyte recruitment → foam cells → cytokine release → endothelial injury → ↓ nitric oxide vasodilation.
Smoking 🚬 increases reactive oxygen species (ROS), further damaging endothelium.
Matrix metalloproteinases (MMPs) break down collagen → thins fibrous cap → makes plaque prone to rupture [2].
Stable plaques → gradual stenosis → angina. Unstable plaques → rupture → thrombosis → MI, stroke, limb ischaemia.
Atherosclerosis tends to occur at arterial branch points / curves → low shear stress & turbulent flow. 📉

📊 Epidemiology

Still a leading cause of death and disability in the Western world.
🌍 Global burden rising in low- and middle-income countries with lifestyle change.
Risk factors: hypercholesterolaemia, modified lipoproteins, hypertension, diabetes, smoking, infections, obesity.

🫀 Carotid Plaque

📈 Infographics

⚡ Risks

Modifiable risk factors
🧪 Dyslipidaemia (↑ LDL, ↓ HDL)	LDL accumulates in intima, becomes oxidised → foam cells. HDL is protective and promotes cholesterol efflux.
🚬 Tobacco smoking	Enhances LDL oxidation, ↑ endothelial dysfunction, ↑ adhesion molecules.
📈 Hypertension	Increases permeability of intima to lipoproteins, ↑ smooth muscle proteoglycans binding LDL.
🍬 Diabetes mellitus	Glycation of LDL + chronic endothelial dysfunction.
⚖️ Obesity / inactivity	Promotes insulin resistance, hypertension and dyslipidaemia.
Non-modifiable risk factors
👴 Age	Risk rises steeply with age.
👨 Male sex	Lack of oestrogen’s protective effects (↑ HDL, ↓ LDL).
🧬 Family history	Premature CAD in 1st-degree relatives (<55M, <65F).
Biological markers
🔬 Homocysteine	Pro-inflammatory, promotes platelet adhesiveness.
🧪 Lp(a)	Competes with plasminogen → inhibits fibrinolysis.
🔥 CRP and other inflammatory markers	Linked to plaque instability & rupture [3].

🩺 Clinical Features

❤️ Angina (exertional chest pain, fixed stenosis).
💔 Myocardial infarction (plaque rupture + thrombosis).
⚡ Arrhythmias or sudden cardiac death.
🧠 Ischaemic stroke or TIA (carotid, intracranial vessels).
🚶‍♂️ Peripheral vascular disease → intermittent claudication, critical limb ischaemia.
🧪 Renal artery stenosis → renovascular hypertension, CKD.

🔍 Investigations

Bloods: FBC, U&E, glucose, LFTs, lipids, TFT, CRP.
ECG, CXR.
🧠 Stroke: CT ± CTA head; carotid Doppler USS for stenosis.
❤️ MI: Troponin, coronary angiography (STEMI → urgent PCI).

🔎 Differentials

Takayasu’s arteritis → large vessel inflammation.
Carotid dissection → vessel narrowing/occlusion without plaque.

💊 Management

ABC resuscitation as needed; acute cases → CCU/Stroke unit.
STEMI → PCI; NSTEMI → medical stabilisation + early invasive strategy.
Ischaemic stroke → consider thrombolysis or thrombectomy in eligible patients.
🛑 Smoking cessation immediately.
High-dose statin therapy.
Optimise BP and diabetes control.
Antiplatelet therapy for secondary prevention.
🏃 Lifestyle: weight reduction, exercise, Mediterranean diet.

📚 References

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Atherosclerosis ❤️

🌍 Introduction