The development of atherosclerosis and cardiovascular disease, the roles of cholesterol, lipoproteins and blood pressure as risk factors, and how diet, lifestyle and treatments reduce risk.

What this dot point is asking

Edexcel wants you to describe how atherosclerosis develops and leads to cardiovascular disease (CVD), explain the roles of cholesterol, lipoproteins and blood pressure as risk factors, and evaluate how diet, lifestyle and treatments reduce risk. Questions often include data on risk factors, so be ready to interpret correlation versus causation.

How atherosclerosis develops

The process starts with damage to the endothelium (for example from high blood pressure or toxins in cigarette smoke). White blood cells and lipids accumulate at the site, forming a plaque that contains cholesterol. The plaque narrows the lumen, so blood pressure rises further (a positive feedback effect). If a plaque ruptures, a blood clot (thrombus) can form and block the artery.

Risk factors

• Blood cholesterol and lipoproteins: cholesterol is carried in the blood by lipoproteins. LDL (low-density lipoprotein) carries cholesterol to cells and is linked to plaque formation, while HDL (high-density lipoprotein) carries cholesterol to the liver for removal and is protective.
• High blood pressure (hypertension): increases the risk of endothelial damage.
• Smoking: carbon monoxide reduces oxygen carriage and chemicals damage the endothelium.
• Diet, obesity and inactivity: a diet high in saturated fat raises LDL cholesterol; high salt raises blood pressure; obesity and inactivity worsen both.
• Non-modifiable factors: age, being male and a family history of CVD also raise risk and cannot be changed.

The LDL to HDL balance is central. LDL deposits cholesterol in artery walls, feeding plaque growth, while HDL removes cholesterol back to the liver, so a high HDL fraction is protective even if total cholesterol is moderate.

Reducing the risk

Lifestyle changes lower risk: reducing saturated fat and salt intake, eating more fibre and unsaturated fats (which raise HDL), losing weight, exercising and stopping smoking. Treatments include statins (which inhibit the liver enzyme that makes cholesterol, lowering LDL), antihypertensives (which lower blood pressure and so reduce endothelial damage) and anticoagulants or antiplatelet drugs such as aspirin (which reduce clot formation). Evaluating treatments means weighing benefits against side effects, for example statins can cause muscle pain and anticoagulants increase bleeding risk.

Examples in context

Example 1. The statin trials. Large randomised controlled trials showed statins reduce LDL cholesterol and cut the rate of heart attacks and strokes by roughly a quarter in high-risk patients. Because they were randomised trials, they provide evidence of cause, not just correlation, which is exactly the distinction examiners test. Statins are now prescribed widely, balanced against side effects such as muscle aches.

Example 2. Salt reduction and blood pressure. Population studies link high salt intake to raised blood pressure, which damages the endothelium and promotes atherosclerosis. When the UK reduced salt in processed foods, average population blood pressure and stroke deaths fell. This is a population-level intervention and a good example of reducing a modifiable risk factor, though confounding lifestyle changes mean the effect is an association rather than absolute proof.

Try this

Q1. Explain how high blood pressure can increase the risk of atherosclerosis. [2 marks]

• Cue. It damages the endothelium, triggering inflammation and plaque formation.

Q2. Suggest why a diet high in HDL-raising unsaturated fats may reduce CVD risk. [2 marks]

• Cue. HDL carries cholesterol to the liver for removal, reducing plaque build-up in arteries.