The cholesterol story

Cholesterol is used by the body to maintain cell structure. It is manufactured by the liver (although some additional cholesterol finds its way into the body from the food we eat). Cholesterol circulates in the blood via a process of cholesterol influx and efflux.1


Any imbalance between cholesterol influx and efflux can cause excess cholesterol to build up in the artery walls, leading to the development of plaque.2

What is cholesterol efflux?

As cholesterol cannot be broken down by the body, it relies on cholesterol efflux to remove cholesterol accumulated in arterial plaque. It is an essential process in which apolipoprotein A-I (ApoA-I) plays a crucial role.1,3-6

ApoA-I mediated

Cholesterol efflux occurs when cholesterol is transferred from macrophages within the arterial plaque to ApoA-I, the key functional component of high-density lipoproteins (HDL).3–7


ApoA-I is produced in the liver and intestines and secreted into plasma in lipid-poor form.4,5

High-density lipoproteins

Cholesterol efflux may help encourage plaque regression as excess cholesterol from macrophages within arterial plaque is transferred to ApoA-I in HDL.4,5


These cholesterol-enriched HDL particles then transport the cholesterol to the liver where it may be excreted either as free cholesterol or after conversion to bile acids.1

Low-density lipoproteins

Cholesterol influx works in the opposite direction and may promote plaque formation, with low-density lipoprotein (LDL) moving cholesterol from the liver and intestines to the heart.3,7

cholestrolStory 

Adapted from Pepine et al. 19988

Discover the importance of cholesterol efflux

This video provides a visual overview of the important role of cholesterol efflux in the prevention of plaque development.

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What is cholesterol efflux?

ApoA-I mediated

High-density lipoproteins

Low-density lipoproteins

Discover the importance of cholesterol efflux

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Impact of low cholesterol efflux

Understand why a continued reduction in already impaired cholesterol efflux directly after an AMI increases the risk of a recurrent CV event4,9–13

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What happens to cholesterol efflux after an AMI?

Learn about why patients are at a disproportionately high risk in the 90-day period post AMI13–17

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Current standard of care post AMI

Current standard of care and newer therapies have lowered the long-term risk of recurrent CV events; however, data show that patients are still at risk during the 90-day high-risk period after an AMI18–25

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Abbreviations

AMI, acute myocardial infarction; ApoA-I, apolipoprotein A-I; CV, cardiovascular; HDL, high-density lipoprotein; LDL, low-density lipoprotein

References

1. Angelin B et al. Atheroscler Suppl 2002; 3:23–30.

2. Bentzon JF et al. Circ Res 2014; 114:1852–1866.

3. Kingwell BA, Chapman MJ. Circulation 2013; 128:1112–1121.

4. Rader DJ et al. J Lipid Res 2009; 50 Suppl:S189–S194.

5. Rader DJ, Hovingh GK. Lancet 2014; 384:618–625.

6. Rosenson RS et al. Circulation 2012; 125:1905–1919.

7. Estrada-Luna D et al. Molecules 2018; 23:2730.

8. Pepine CJ. Am J Cardiol 1998; 82:23S–27S.

9. Ray KK et al. Eur Heart J 2014; 35:1792–1800.

10. Soares AAS et al. Clin Chim Acta 2018; 478:51–56.

11. Ross R. N Engl J Med 1999; 340:115–126.

12. Saleheen D et al. Lancet Diabetes Endocrinol 2015; 3:507–513.

13. Rohatgi A et al. N Engl J Med 2014; 371:2383–2393.

14. Piepoli MF et al. Eur J Prev Cardiol 2016; 23:1994–2006.

15. Chi G et al. Clin Cardiol 2022; 45:299–307.

16. Guerin M et al. J Am Coll Cardiol 2018; 72:3259–3269.

17. Zhang J et al. Am J Cardiol 2016; 117:508–514.

18. Schwartz GG et al. N Engl J Med 2018; 379:2097–2107.

19. Cannon CP et al. N Engl J Med 2015; 372:2387–2397.

20. Schwartz GG et al. JAMA 2001; 285:1711–1718.

21. Bhatt DL et al. N Engl J Med 2019; 380:11–22.

22. Bhatt DL et al. J Am Coll Cardiol 2019; 73:2791–2802.

23. Mehta SR et al. N Engl J Med 2019; 381:1411–1421.

24. Wallentin L et al. N Engl J Med 2009; 361:1045–1057.

25. Nair R et al. J Am Heart Assoc 2021; 10:e019270.

 

USA-GEN-0051 | August 2023