The pathology of cardiovascular disease, including atherosclerosis, the formation of atheromas, thrombosis and embolism, the consequences of heart attack and stroke, the role of cholesterol and LDL and HDL, and the genetic and lifestyle risk factors and their control.

What this dot point is asking

The SQA wants you to describe atherosclerosis and the formation of atheromas, explain thrombosis and embolism and how they cause heart attack and stroke, explain the roles of cholesterol, LDL and HDL and how cholesterol is regulated, and describe the genetic and lifestyle risk factors for cardiovascular disease and how they are controlled.

Atherosclerosis and atheroma

It begins when the inner lining (the endothelium) of an artery is damaged, for example by high blood pressure or smoking. Cholesterol and other fatty substances accumulate beneath the damaged lining, forming an atheroma. As the atheroma grows, it makes the artery wall thicker and less elastic and narrows the lumen, reducing blood flow. The narrowing also raises blood pressure, which causes further damage in a vicious cycle.

Thrombosis, heart attack and stroke

The consequences depend on which artery is affected:

• A thrombus that blocks a coronary artery (supplying the heart muscle) starves that muscle of oxygen, so it dies. This is a heart attack (myocardial infarction).
• A thrombus or a burst vessel in the brain cuts off the blood supply to part of the brain, causing a stroke.

In both cases, tissue dies because it is deprived of the oxygen and nutrients carried by the blood.

Cholesterol, LDL and HDL

Cholesterol is essential for making cell membranes and some hormones, but too much in the blood is harmful. Because it does not dissolve in water, cholesterol is carried by lipoproteins:

• LDL (low-density lipoprotein) transports cholesterol to the body cells, where excess can be deposited in artery walls. LDL is the so-called bad cholesterol.
• HDL (high-density lipoprotein) transports excess cholesterol from the cells back to the liver, where it is broken down and removed. HDL is the so-called good cholesterol.

A high ratio of LDL to HDL means more cholesterol is being deposited in the arteries than removed, promoting atherosclerosis. The liver regulates blood cholesterol: when dietary cholesterol is high, the liver makes less, and drugs called statins lower cholesterol by inhibiting an enzyme in its synthesis pathway.

Risk factors and their control

CVD risk comes from both genetic and lifestyle factors. Some people inherit a tendency to high cholesterol or high blood pressure. Lifestyle factors that raise risk include smoking, a diet high in saturated fat and salt, obesity, lack of exercise and excessive alcohol. Most lifestyle factors can be controlled: stopping smoking, eating a balanced diet, exercising and, where needed, taking medicines such as statins all lower the risk of cardiovascular disease.

Examples in context

Example 1. A coronary thrombosis. An atheroma in a coronary artery ruptures and a thrombus forms on it, blocking the artery. The heart muscle beyond the blockage is starved of oxygen and dies, producing the chest pain and damage of a heart attack.

Example 2. Statins lowering LDL. A patient with a high LDL to HDL ratio is prescribed a statin, which inhibits the liver enzyme that makes cholesterol. Their LDL falls, the ratio improves, and the rate at which atheromas build up is reduced, lowering their CVD risk.

Try this

Q1. Name the fatty deposit that forms in an artery wall in atherosclerosis. [1 mark]

• Cue. An atheroma (plaque).

Q2. Explain why a high LDL to HDL ratio increases the risk of cardiovascular disease. [1 mark]

• Cue. LDL deposits cholesterol in artery walls while HDL removes it, so a high ratio means more cholesterol builds up, promoting atherosclerosis.