Stopping ASCVD starts with lowering LDL-C1
Lowering LDL-C sooner and longer improves outcomes1,2
High levels of low-density lipoprotein cholesterol (LDL-C) are the root cause of atherosclerosis, the process that leads to atherosclerotic cardiovascular disease (ASCVD).1
ASCVD remains the leading cause of cardiovascular morbidity and mortality globally, despite advanced treatments and patient lifestyle changes.2
Lower is better4
Lower earlier is even better2
Even slight delays in managing LDL-C following an ASCVD event can lead to adverse outcomes5,6
ACC 2022 expert consensus decision pathway recommendations
Stringent LDL-C thresholds have been set for the management of ASCVD risk.
LDL-C thresholds7,*
<100
mg/dL
for primary prevention
(FH, diabetes, or borderline/
intermediate ASCVD risk)
<70
mg/dL
for secondary prevention
(not at very high risk)
<55
mg/dL
for secondary prevention
(very high risk)
*≥50% LDL-C reduction from baseline also considered a threshold for intensifying therapy.
Defining very high risk of recurrent ASCVD events
The majority of patients (90%-94%) with recent acute coronary syndrome (ACS), myocardial infarction (MI), ischemic stroke, or symptomatic peripheral arterial disease (PAD) are considered “very high risk” and should be managed to LDL-C levels <55 mg/dL.8
Multiple major ASCVD events7,9
(within the past
12 months)
(other than recent
ACS event)
ischemic stroke
peripheral artery disease
One major ASCVD event + multiple high-risk conditions7,9
outside major
ASCVD event(s)
mellitus
smoking
elevated LDL-C
The addition of nonstatin therapy should be considered in adults not achieving their LDL-C goals7
*≥50% LDL-C reduction on maximally tolerated statin therapy.
Are patients reaching evidence-based LDL-C levels to reduce their CVD risk?
ACC, American College of Cardiology; CABG, coronary artery bypass graft; CKD, chronic kidney disease; FH, familial hypercholesterolemia; HeFH, heterozygous familial hypercholesterolemia; HF, heart failure; PCI, percutaneous coronary intervention.
References: 1. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017;38(32):2459-2472. 2. Ray KK, Ference BA, Séverin T, et al. World Heart Federation Cholesterol Roadmap 2022. Glob Heart. 2022;17(1):75. 3. Baigent C, Blackwell L, Emberson J, et al; Cholesterol Treatment Trialists’ (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670-1681. 4. Raymond C, Cho L, Rocco M, Hazen SL. New cholesterol guidelines: worth the wait? Cleve Clin J Med. 2014;81(1):11-19. 5. Kytö V, Saraste A, Tornio A. Early statin use and cardiovascular outcomes after myocardial infarction: a population-based case-control study. Atherosclerosis. 2022;354:8-14. 6. Åivo J, Ruuskanen JO, Tornio A, Rautava P, Kytö V. Lack of statin therapy and outcomes after ischemic stroke: a population-based study. Stroke. 2023;54(3):781-790. 7. Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2022 ACC expert consensus decision pathway on the role of nonstatin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022;80(14):1366-1418. 8. Muntner P, Orroth KK, Mues KE, et al. Evaluating a simple approach to identify adults meeting the 2018 AHA/ACC cholesterol guideline definition of very high risk for atherosclerotic cardiovascular disease. Cardiovasc Drugs Ther. 2022;36(3):475-481. 9. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: executive summary: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines. J Am Coll Cardiol. 2019;73(24):3168-3209.