How cholesterol affects your arteries: an interactive walk-through

Follow cholesterol from the bloodstream into the artery wall in six short steps. Swipe or tap Next.

1. Cholesterol travels in packages

Cholesterol is carried in the blood inside particles called lipoproteins.[4] LDL particles carry cholesterol out to the body’s cells; HDL particles carry cholesterol back to the liver.[1,4]

Both kinds are part of normal body function. Too much LDL is the part that can harm the arteries, as the next steps show.[1,4]

2. A healthy artery wall

An artery wall is made of several layers. The inner lining, the endothelium, is normally smooth and unbroken.[2]

Blood flows through the open channel in the middle, called the lumen.

3. When LDL builds up in the wall

Atherosclerosis begins when the lining is injured or diseased.[2] With too much LDL cholesterol, fatty deposits called plaque form in the artery wall.[1]

A European Atherosclerosis Society consensus statement concluded that LDL particles cause atherosclerotic cardiovascular disease.[3]

The picture shows direction only. It is not a level, and not a threshold for any person.

4. Plaque builds up slowly

White blood cells move into the wall and swell into foam cells as they collect cholesterol and other fats. Foam cells accumulate into patchy deposits, called plaque, covered by a fibrous cap.[2]

This happens gradually. Over time the plaque narrows and hardens the artery (atherosclerosis).[1] The animation is a time-lapse of a slow process.

5. When a plaque cracks

Some plaques narrow or block the artery. Others split open, which can trigger a blood clot that suddenly blocks it.[2]

If a clot blocks an artery supplying the heart, the heart’s blood supply is cut off (a heart attack). In the brain, blood supply can be severely reduced or cut off (a stroke).[1] A partly narrowed artery can also reduce blood flow and oxygen to the heart, which can cause angina.[1]

6. Why some people have high LDL from birth

Normally, LDL is moved from the blood into the liver by LDL receptors, which can be pictured as “doors”.[4]

Familial hypercholesterolaemia (FH) is an inherited condition, present from birth, that markedly raises LDL cholesterol.[5] In its most common form about half of these doors don’t work properly, so LDL builds up in the blood.[4]

FH is usually due to a variant in the LDL receptor gene (LDLR), and occasionally APOB or PCSK9.[6] Clinicians can use the Dutch Lipid Clinic Network score, built from factors such as family history and untreated LDL cholesterol, to estimate how likely FH is.[6]

See the Dutch Lipid Score calculator →
Sources
  1. healthdirect Australia. Cholesterol (last reviewed April 2026). healthdirect.gov.au
  2. Merck Manual Consumer Version. Atherosclerosis. merckmanuals.com
  3. Borén J, Chapman MJ, Krauss RM, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights. A consensus statement from the European Atherosclerosis Society. Eur Heart J 2020;41(24):2313–2330. doi:10.1093/eurheartj/ehz962
  4. FH Australia / Australian Atherosclerosis Society. What is familial hypercholesterolaemia? athero.org.au/fh
  5. Watts GF, et al. Integrated guidance for enhancing the care of familial hypercholesterolaemia in Australia. Heart Lung Circ 2021;30(3):324–349. doi:10.1016/j.hlc.2020.09.943
  6. Pathology Tests Explained (RCPA). What you should know about testing for familial hypercholesterolaemia. pathologytestsexplained.org.au

Sources reviewed November 2026. The diagram is a simplified schematic and is not to scale.

General information only, not medical advice. This does not assess your own cholesterol, family history or heart risk. For questions about your results, speak with your GP.

Related on AskMyGP

This page explains general mechanisms and is not medical advice. It does not assess your own cholesterol, family history or heart risk. Your GP or specialist can interpret your results in the context of your individual circumstances.

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