Impact of low cholesterol efflux

Cholesterol efflux is the first step in removing excess cholesterol from plaque in the arterial wall. An alternative approach is to consider the role of efflux in protecting against increasing plaque build up in the arteries.1,2

Atherosclerotic plaque build up over time

Atherosclerosis causes clinical disease through luminal narrowing, affecting blood flow to the heart, brain or lower extremities.3


Atherosclerotic plaque may occur at multiple sites in the arterial tree, which increases the risk of recurrent CV events in the first year after an AMI.3–7


Atherosclerosis begins as a fatty streak within the arterial wall which develops due to an imbalance between cholesterol influx and efflux.3–7


This fatty streak gradually thickens to form an atherosclerotic plaque.7


Some of the common reasons for an AMI include plaque rupture, blood clot formation at the site, or block of blood flow through the coronary artery.7

impact-1

Adapted from Pepine et al. 19988 and Rader and Daugherty 20087

 

Plaque rupture

Compromised efflux causes cholesterol build up

Any imbalance between cholesterol influx and efflux will allow atherosclerotic plaque to become engorged with excess cholesterol, making them vulnerable to rupture.2,8–12


The integrity of the fibrous cap overlying the lipid-rich core determines the stability of an atherosclerotic plaque, and reducing the lipid core may improve stability.13,14

plaque-rupture

Adapted from Libby 199513

 

Recurrent CV events are just as likely to originate from an existing non-culprit lesion as they are from the initial culprit lesion.3,15–17

Low cholesterol efflux is associated with greater CV risk

low-cholestrol

Clinically, a strong association exists between low cholesterol efflux and greater risk of a fatal CV event or a non-fatal AMI or stroke independent of HDL-cholesterol.18–24


The Dallas Heart Study, a population-based cohort of 2,924 adults free from cardiovascular disease at baseline, showed those with low cholesterol efflux are about six times more likely to die due to incidence of CV events compared with those with high cholesterol efflux (median follow-up of 9.4 years).19

High cholesterol efflux is associated with lower CV risk

In a meta-analysis of 20 clinical trials, high cholesterol efflux was associated with a 37% lower risk of adverse cardiovascular events compared with low cholesterol efflux.24 


In the pivotal ePARIS registry, a prospective study of 1,609 consecutive patients treated for an AMI, patients with high cholesterol efflux had a 68% lower risk of mortality compared with patients with low cholesterol efflux.22

 

Page content

Atherosclerotic plaque builds up over time

Plaque rupture

Low cholesterol efflux may be associated with greater CV risk

High cholesterol efflux may be associated with lower CV risk

Continue to

What happens to cholesterol efflux after an AMI?

Learn about why patients are at a disproportionately high risk in the 90-day period post AMI19,20,22,25,26

Get more info

Burden of recurrent CV events

Find out about the significant healthcare costs associated with recurrent CV events post AMI27–30

See more

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 AMI31–38

Discover More

Get the latest news

Sign up to receive news alerts and information about educational resources to help your patients through the 90-day high-risk period post AMI

By submitting this form, you are consenting to disclose any information provided, including your name, email address, telephone number, and any other information (collectively “Personal Information”) to CSL Behring and its representatives, agents, and contractors, including CSL Behring’s support program(s) (collectively “CSL Behring Entities”) and to receive communications with relevant information from CSL Behring Entities. You may be contacted by mail, email, telephone, and/or SMS/text message in relation to our business, products, services, and educational programs intended to benefit patients using or eligible to use CSL Behring therapies. You will have the ability to opt-out from receiving communications from CSL Behring Entities at any time. CSL Behring and CSL Behring Entities will not sell your personal information. CSL Behring respects your privacy. For an explanation of how CSL Behring will use the information you are submitting, please view our Privacy Policy

Abbreviations

AMI, acute myocardial infarction; CV, cardiovascular; HDL, high-density lipoprotein; LDL, low-density lipoprotein

References

1. Silvain J et al. Curr Opin Cardiol 2019; 34:714–720.

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

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

4. Allison MA et al. Arterioscler Thromb Vasc Biol 2004; 24:331–336.

5. Bhatt DL et al. JAMA 2010; 304:1350–1357.

6. Steg PG et al. JAMA 2007; 297:1197–1206.

7. Rader DJ, Daugherty A. Nature 2008; 451:904–913.

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

9. Wentzel JJ et al. Cardiovasc Res 2012; 96:234–243.

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

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

12. Rached F et al. Biochim Biophys Acta 2015; 1851:1254–1261.

13. Libby P. Circulation 1995; 91:2844–2850.

14. Libby P. N Engl J Med 2013; 368:2004–2013.

15. Stone GW et al. N Engl J Med 2011; 364:226–235.

16. Varenhorst C et al. J Am Heart Assoc 2018; 7:e007174.

17. Brener SJ et al. JACC Cardiovasc Imaging 2012; 5:S86–S94.

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

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

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

21. Liu C et al. Atherosclerosis 2016; 249:116–124.

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

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

24. Lee J et al. Front Cardiovasc Med 2021; 8:774418.

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

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

27. Bakhai A et al. J Interv Cardiol 2012; 25:19–27.

28. Punekar RS et al. Clin Cardiol 2015; 38:483–491.

29. Zhao Z, Winget M. BMC Health Serv Res 2011; 11:35.

30. Chapman RH et al. BMC Cardiovasc Disord 2011; 11:11.

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

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

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

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

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

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

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

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

USA-GEN-0051 | August 2023