2026 ACC/AHA Dyslipidemia Guidelines
Algorithms and tables for deciding on treatment plans.
2026 ACC/AHA DYSLIPIDEMIA GUIDELINE
Primary prevention statin decision algorithm
Adults 30–79 without established clinical ASCVD. Step through each gate using the CPR (Calculate, Personalize, Reclassify) framework.
LDL-C = LDL cholesterol · ASCVD = atherosclerotic cardiovascular disease · CAC = coronary artery calcium · hsCRP = high-sensitivity C-reactive protein · HeFH = heterozygous familial hypercholesterolemia · Lp(a) = lipoprotein(a) · apoB = apolipoprotein B · CKM = cardiovascular-kidney-metabolic · All goals refer to on-treatment LDL-C targets
2026 ACC/AHA Dyslipidemia Guideline
Statin-associated muscle symptoms (SAMS) management
For patients experiencing muscle symptoms (myalgia, weakness, cramping) on statin therapy. Evaluate cause, assess severity, then adjust therapy based on ASCVD risk profile to maintain cardiovascular protection.
SAMS = statin-associated muscle symptoms · CK = creatine kinase · ULN = upper limit of normal · LDL-C = LDL cholesterol · non-HDL-C = non-HDL cholesterol · CAC = coronary artery calcium · PCSK9 mAb = PCSK9 monoclonal antibody
2026 ACC/AHA Dyslipidemia Guideline
Statin intensity dosing reference
Daily doses categorized by expected LDL-C reduction. Prescribe the highest tolerated intensity appropriate to the patient's risk profile.
| Statin | High intensity | Moderate intensity | Low intensity |
|---|---|---|---|
| Atorvastatin | 40–80 mg | 10–20 mg | — |
| Rosuvastatin | 20–40 mg | 5–10 mg | — |
| Simvastatin | — | 20–40 mg | 10 mg |
| Pravastatin | — | 40–80 mg | 10–20 mg |
| Lovastatin | — | 40–80 mg | 20 mg |
| Fluvastatin | — | 40 mg BID or 80 mg XL | 20–40 mg |
| Pitavastatin | — | 2–4 mg | 1 mg |
HIGH INTENSITY
≥50% LDL-C reduction
MODERATE INTENSITY
30–49% LDL-C reduction
LOW INTENSITY
<30% LDL-C reduction
BID = twice daily · XL = extended release · Only atorvastatin and rosuvastatin are available in high-intensity doses · Pitavastatin is preferred in patients on certain antiretroviral regimens (fewer CYP3A4 interactions) · Simvastatin 80 mg is restricted to patients already tolerating it for ≥12 months due to myopathy risk
AHA 2023 · Cardiovascular-Kidney-Metabolic Syndrome
CKM syndrome staging framework
A staging system introduced by the American Heart Association in 2023 to classify individuals across the CKM disease continuum, emphasizing early identification and prevention before end-organ damage occurs.
STAGE 0No CKM risk factors
No metabolic risk factors, CKD, or CVD present.
BMI <25 kg/m² (<23 for Asians)
Normal waist circumference
Women <88 cm, men <102 cm (Asian women <80 cm, Asian men <90 cm)
No metabolic abnormalities
[3, 4]
STAGE 1Excess or dysfunctional adiposity
Adiposity or dysglycemia present, without other CKM risk factors.
BMI ≥25 kg/m² (≥23 for Asians)
Waist ≥88 cm women, ≥102 cm men
Asian thresholds: ≥80 cm women, ≥90 cm men
Dysglycemia / prediabetes: fasting glucose 100–124 mg/dL or HbA1c 5.7–6.4%
History of gestational diabetes
[3, 4, 5]
STAGE 2Metabolic risk factors or CKD
Metabolic disease or moderate-to-high-risk chronic kidney disease present.
Triglycerides ≥135 mg/dL
Hypertension
Diabetes mellitus
Moderate-to-high-risk CKD (KDIGO)
Metabolic syndrome (≥3 of the following):
Increased waist circumference
HDL-C <40 mg/dL (men) or <50 mg/dL (women)
Triglycerides ≥150 mg/dL
Blood pressure ≥130/80 mm Hg
Prediabetes (fasting glucose 100–124 mg/dL or HbA1c 5.7–6.4%)
[3, 4, 5]
STAGE 3Subclinical CVD or high CVD risk
Subclinical cardiovascular disease or predicted high risk, without clinical CVD events.
Very-high-risk CKD per KDIGO criteria
10-year CVD risk ≥20% using AHA PREVENT equations
[3, 4]
STAGE 4Clinical CVD
Established cardiovascular disease, particularly with persistent metabolic dysfunction or CKD.
Coronary heart disease
Myocardial infarction
Heart failure
Stroke
Angina
Occurring with persistent metabolic dysfunction and/or CKD
[3, 6]
Pathophysiology: CKM most commonly originates from excess or dysfunctional adipose tissue, which secretes proinflammatory and prooxidative products that damage arterial, cardiac, and kidney tissues — creating multidirectional relationships among metabolic risk factors, CKD, and the cardiovascular system. [1]
References
[1] Ndumele CE, Neeland IJ, Tuttle KR, et al. A Synopsis of the Evidence for the Science and Clinical Management of CKM Syndrome. Circulation. 2023;148(20):1636-1664.
[2] Ndumele CE, Rangaswami J, Chow SL, et al. Cardiovascular-Kidney-Metabolic Health: A Presidential Advisory From the AHA. Circulation. 2023;148(20):1606-1635.
[3] Zhu R, Wang R, He J, et al. Prevalence of CKM Syndrome Stages by Social Determinants of Health. JAMA Netw Open. 2024;7(11):e2445309.
[4] Chen Y, Wu X, Long T, et al. Prevalence and Mortality Association of Different Stages of CKM Syndrome. JACC Advances. 2025;4(6 Pt 2):101843.
[5] Khan SS, Berwanger O, Fiuzat M, et al. Prioritising the Primary Prevention of Heart Failure. Lancet. 2025;406(10508):1138-1153.
[6] Gunnarsson S, Vito O, Unwin RJ. CKM Syndrome: Prevalence, Risks, Disease Trajectories, and Early-Stage Management. Am J Physiol Cell Physiol. 2025.