Conditions · Systemic conditions
Atherosclerosis and dyslipidaemia !
Atherosclerosis is the slow build-up of fatty plaques in artery walls, driven mainly by high LDL cholesterol; plaques can cause heart attack and stroke.
Updated 2026-10-29
Structures involved
Tap one to see what it is and open it in 3D.
- Left main coronary artery
- Right coronary artery
- Internal carotid artery
- Femoral artery
- Carotid bifurcation
- Middle cerebral artery
- Aortic arch
- Popliteal artery
- Posterior tibial artery
- Dorsalis pedis artery
In biochemistry
- Cholesterol synthesis: Step 3 · HMG-CoA reductase
- Lipid chemistry
- LDL receptor
- Lipoprotein lipase (LPL)
- CETP (cholesteryl ester transfer protein)
- PCSK9
- Cholesterol 7α-hydroxylase (CYP7A1)
- Apolipoprotein B (ApoB-100 and ApoB-48)
- Apolipoprotein E (ApoE)
- Cholesterol
- Lipoprotein metabolism
- VLDL (very-low-density lipoprotein)
- LDL (low-density lipoprotein)
- HDL (high-density lipoprotein)
- C-reactive protein (CRP) as a lab test
- Palmitate (palmitic acid)
- Dietary fibre
- Balanced diet
- Fredrickson classification of hyperlipoproteinaemias
- Reactive oxygen species and antioxidants
- HMG-CoA reductase
- Niacin (vitamin B3)
In histology
In physiology
- Flow, pressure and resistance: Poiseuille and turbulent flow
- Coronary circulation and myocardial ischemia
Why it happens
- Chronic inflammation: causes, cells and features
- Intracellular accumulations: cholesterol, proteins, hyaline, glycogen
- Multifactorial (complex) disorders
- Tobacco: how smoking injures tissue
- Obesity: leptin, adipokines and its consequences
- Pathologic calcification: dystrophic vs metastatic
Show 1 more
What it is
Atherosclerosis is the slow build-up of fatty, inflamed plaques inside the walls of medium and large arteries. Dyslipidaemia, chiefly high LDL cholesterol, is its main driver; plaques narrow arteries or rupture and cause heart attack, stroke and limb ischaemia.
Who gets it
Atherosclerotic cardiovascular disease is a leading cause of death worldwide and in Colombia and Latin America, where obesity, diabetes and hypertension are common. Plaques start silently from early adulthood.
Causes
- Retention of LDL and other apolipoprotein B-containing lipoproteins in the artery wall
- Primary (genetic) dyslipidaemias such as familial hypercholesterolaemia
- Secondary dyslipidaemia: diabetes, obesity, hypothyroidism, kidney disease, certain drugs
- Endothelial injury from smoking, high blood pressure and high glucose
Risk factors
- High LDL cholesterol; low HDL; high triglycerides
- Smoking
- Arterial hypertension
- Diabetes mellitus
- Age, male sex, and family history of early cardiovascular disease
- Obesity, physical inactivity and an unhealthy diet
- Chronic kidney disease and chronic inflammatory diseases
Pathophysiology
LDL particles enter a damaged endothelium, become oxidised and attract monocytes that turn into lipid-laden foam cells (fatty streak). Smooth muscle cells migrate and form a fibrous cap over a lipid necrotic core. Stable plaques narrow the lumen and cause ischaemia on exertion; thin-capped plaques can rupture or erode and trigger an occluding thrombus.
Classification
- By territory: coronary, cerebrovascular (carotid and intracranial), aortic and peripheral artery disease
- Dyslipidaemia by phenotype: high LDL, high triglycerides, low HDL, or mixed
- Dyslipidaemia by cause: primary (genetic) or secondary
Symptoms and signs
- Usually silent for decades until a plaque limits flow or ruptures
- Chest pain on exertion (angina)
- Calf pain on walking that eases with rest (intermittent claudication)
- Transient weakness, numbness or speech or vision loss (transient ischaemic attack)
- Signs of lipid deposits: xanthomas on tendons, xanthelasma, corneal arcus at a young age
- Weak or absent pulses and arterial bruits
Diagnosis
- Clinical
- Clinicians estimate global cardiovascular risk with a validated risk score adapted to the population, ask about symptoms in each territory and examine pulses, bruits, blood pressure and lipid deposits.
- Tests
- Lipid profile (total, LDL, HDL and triglycerides; fasting not always required), glucose or HbA1c, kidney function, thyroid tests when secondary causes are suspected. ECG and stress testing for suspected coronary disease; ankle-brachial index for leg arteries.
- Imaging
- Carotid duplex ultrasound, coronary artery calcium score or CT coronary angiography, and invasive angiography when revascularisation is considered.
Differential diagnosis
- Vasculitis (for example giant cell or Takayasu arteritis)
- Arterial embolism from the heart
- Fibromuscular dysplasia
- Non-cardiac chest pain (musculoskeletal, oesophageal)
- Spinal stenosis (neurogenic claudication)
Goal of treatment
Lower LDL cholesterol and the other risk factors enough to slow or stabilise plaque, prevent heart attack, stroke and limb loss, and relieve ischaemic symptoms. Targets depend on each person's overall risk.
Treatment
- Lifestyle
- Stopping smoking, a heart-healthy diet low in saturated and trans fats, regular physical activity and weight control.
- Medical
- Statins are the first-line lipid-lowering class; ezetimibe and PCSK9 inhibitors are added when targets are not met. Fibrates or omega-3 preparations may be used for marked hypertriglyceridaemia.
- Medical
- Antiplatelet therapy for established atherosclerotic disease, plus control of blood pressure and diabetes.
- Procedure
- Angioplasty with stenting, or surgical bypass or carotid endarterectomy, for severe symptomatic narrowing.
- Follow-up
- Repeat lipid profile after starting or changing therapy, and checks of adherence, muscle symptoms and liver tests when indicated.
Drugs for this condition
- Atorvastatin
- Simvastatin
- Rosuvastatin
- Ezetimibe
- Pravastatin
- Fenofibrate
- Gemfibrozil
- Nicotinic acid (niacin)
- Colestyramine
- Evolocumab
- Fluvastatin
- Lovastatin
- Colesevelam
- Alirocumab
Complications
- Myocardial infarction and sudden cardiac death
- Ischaemic stroke and transient ischaemic attack
- Peripheral artery disease with ulcers or amputation
- Abdominal aortic aneurysm
- Ischaemic heart failure
- Mesenteric or renal artery ischaemia
- Acute pancreatitis with very high triglycerides
Prognosis
A chronic, progressive disease, but lowering LDL and controlling other risk factors clearly reduces cardiovascular events. Risk stays high after a first event, so secondary prevention is lifelong.
Prevention
- No smoking from youth onwards
- Healthy diet, physical activity and a healthy weight
- Screening of lipids, blood pressure and glucose according to local guidelines
- Family screening when familial hypercholesterolaemia is found
Test yourself
Think of the answer, then tap the question to see it.
Which lipoprotein is the main causal driver of atherosclerosis?
LDL cholesterol (apolipoprotein B-containing particles): it is retained and oxidised in the artery wall, and lowering it reduces cardiovascular events.
What is the first-line drug class to lower LDL cholesterol?
Statins (HMG-CoA reductase inhibitors), which reduce liver cholesterol synthesis and upregulate LDL receptors.
What cell defines the fatty streak, the earliest lesion of atherosclerosis?
The foam cell: a macrophage (from monocytes) filled with oxidised LDL in the intima.
Why does plaque rupture cause sudden events rather than slow narrowing?
A thin fibrous cap breaks and exposes the thrombogenic lipid core, so a thrombus forms within minutes and can occlude the artery (heart attack or stroke).
Which physical findings in a young person suggest familial hypercholesterolaemia?
Tendon xanthomas (for example on the Achilles tendon), xanthelasma and corneal arcus, with very high LDL and early heart disease in the family.
Related conditions
- Myocardial Infarction (Heart Attack)
- Acute mesenteric ischaemia
- Ischaemic stroke
- Hypothyroidism
- Transient ischaemic attack
- Age-related macular degeneration
- Carotid artery stenosis
- Acute limb ischaemia
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Atherosclerosis (StatPearls (NCBI Bookshelf), 2023).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.
