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Topic 1: Lifestyle, health and risk›Cardiovascular disease (1.6, 1.5, 1.7)

Cardiovascular disease (1.6, 1.5, 1.7)

An overview of cardiovascular disease (1.6, 1.5, 1.7) from Edexcel A level Biology including: atherosclerosis, thrombosis and risk factors
4 min

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Atherosclerosis is the buildup of fatty deposits (atheromas) that go on to form plaques within the arterial walls.

Plaque formation leads to narrowing and hardening of the arteries. This leads to elevated blood pressure, as well as blockages and/or ruptures in the arterial network.

When a blockage occurs in the coronary artery, it can lead to a heart attack.
When the blockage or rupture impacts the blood supply to the brain, it can result in a stroke.

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The image is titled 'Atherosclerosis is Progressive' and illustrates the process of atherosclerosis in a circular flow diagram. At the top, a section of a blood vessel is shown with leukocytes adhering to the endothelium, labeled 'Leukocyte,' 'Attachment,' and 'Exiting blood vessel,' indicating an inflammatory response. Below this, there are three circular stages connected by arrows in a clockwise direction. The first stage is 'Endothelial dysfunction,' showing a cross-section of a blood vessel with 'Damage to endothelium' labeled. The second stage is 'Plaque formation,' depicting a buildup inside the vessel. The third stage is 'Raised blood pressure,' showing a narrowed vessel with arrows indicating pressure. The diagram emphasizes the progressive nature of atherosclerosis, with each stage leading to the next.
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Atherosclerosis begins with endothelial dysfunction.

The endothelium is the thin, smooth inner lining of blood vessels.

Damage to the endothelium of the artery can be caused by:

  • high blood pressure (mechanical stress)
  • toxins from cigarette smoke
  • high blood cholesterol.

Veins are less vulnerable to endothelial dysfunction because of their lower blood pressure. Once damaged or overstretched, the endothelium becomes leaky, triggering an inflammatory response.

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When damage to the endothelium is detected by the immune system, an inflammatory response is triggered.

White blood cells (macrophages) move into the artery wall and accumulate fatty chemicals from the blood, such as cholesterol. The buildup of fatty deposits forms a fatty streak called an atheroma.

Calcium salts and fibrous tissue build up over the atheroma, forming a hard lump on the inner wall of the artery called a plaque.

Arterial plaques cause:

  • Narrowing (stenosis) of the artery lumen leading to reduced blood flow and increased blood pressure.
  • Loss of elasticity of the artery wall (arteriosclerosis).
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Blood clotting (also called coagulation) is a vital process that prevents excessive bleeding when a blood vessel is damaged. It also prevents the entry of pathogens and provides a scab, under which healing occurs.

Inappropriate or excessive clot formation inside arteries can contribute to cardiovascular disease (CVD), such as coronary heart disease and stroke.

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The image illustrates the clotting cascade with chemical and physical progression. At the top, the title 'THE CLOTTING CASCADE' is shown. Below, a diagonal arrow labeled 'Chemical cascade' points downward. The cascade starts with a box labeled 'Thromboplastin, vitamin K and Ca2+' leading to 'Prothrombin,' which is connected by an arrow to 'Thrombin.' Thrombin connects to 'Fibrinogen,' which further leads to 'Fibrin (insoluble).' The bottom sequence shows three stages: 'Damage to blood vessel' with a broken vessel and scattered blood cells, 'Platelets collect at damaged wall' with clustered platelets, and 'Formation of a clot' showing a fibrin mesh forming a clot. Another horizontal arrow labeled 'Physical progression' runs beneath these stages. Annotations include 'Broken vessel' and 'Fibrin mesh.'

During clotting:

  1. Thromboplastin (a protein) is released from damaged tissues and platelets.
  2. Thromboplastin, alongside ions, trigger the release of an enzyme converting the protein prothrombin to the enzyme thrombin.
  3. Thrombin catalyses the conversion of soluble fibrinogen (a plasma protein) into insoluble fibrin.
  4. Fibrin fibres form a mesh network across the wound.
  5. The fibrin mesh traps red blood cells and platelets, forming a stable blood clot (thrombus). The clot seals damaged vessels, preventing blood loss and entry of pathogens.
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Atherosclerosis increases the risk of excessive or inappropriate blood clotting.

Plaques (atheromas) can rupture, exposing the underlying collagen and tissue. This triggers the clotting cascade at the plaque site, even though there’s no external injury. A blood clot (thrombus) forms within the already narrowed artery.

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Consequences of inappropriate clotting include:

  • Narrowing or blockage of the artery causes restricted blood flow.
  • If the clot blocks a coronary artery it causes heart attack (myocardial infarction). The heart does not receive enough oxygen, so heart cells cannot respire and produce ATP. The force of a heart contraction is reduced, and heart cells die.
  • If the clot blocks a cerebral artery it causes stroke as blood flow to the brain is restricted, so brain cells cannot respire and produce ATP and therefore die. This type of stroke is known as an ischemic stroke.
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Risk factors are established by investigating the proportion of people within a given subset who go on to exhibit a specific response variable within a specific time.

The proportion is usually conveyed as “x in y” rather than as a percentage to give more meaning to the figure. The specific time can vary; it could be per dose, per year or per lifetime.

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There are many different risk factors associated with the likelihood of developing cardiovascular disease.

The image is titled 'Risk Factors for CVD' and shows various factors contributing to cardiovascular disease. Genetics section: A DNA helix with a label 'Genetics'. Text below states inherited genes affect: cholesterol metabolism leading to high LDL levels, blood pressure regulation increasing hypertension risk, and arterial structure with some having weaker or less elastic arteries. Diet section: Image of a burger and fries labeled 'Diet'. Text lists high saturated fat increasing cholesterol in artery walls, low unsaturated fat reducing cholesterol removal, high salt increasing blood pressure, and low fiber slowing cholesterol removal and blood sugar regulation. Age and gender section: Illustrations of different ages and genders labeled 'Age and gender'. Text states arteries become less elastic with age, men are at greater risk before menopause, and estrogen in pre-menopausal women is protective. Smoking section: Image of a cigarette labeled 'Smoking'. Text explains nicotine increases heart rate and blood pressure, carbon monoxide reduces oxygen transport, and free radicals in smoke oxidize LDLs. Inactivity section: Illustration of a person watching TV labeled 'Inactivity'. Text notes increased obesity risk and reduced vascular elasticity. High blood pressure section: Image of a blood pressure cuff showing 186/90 labeled 'High blood pressure'. Text mentions more endothelial stress leading to atherosclerosis.
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