A practical clinician summary of the 2026 ACC/AHA cholesterol and dyslipidemia guideline, covering PREVENT-ASCVD risk assessment, LDL-C and non-HDL-C goals, Lp(a), ApoB, CAC, triglycerides and modern lipid-lowering therapy. Australian practice notes are included where availability or terminology differs.
Risk Assessment Framework
The calculate–personalise–reclassify model replaces the old PCE-driven approach: start with PREVENT, then personalise with risk enhancers, then reclassify where the decision remains uncertain.
PREVENT-ASCVD
10-year risk in adults 30–79 y without ASCVD. Low <3% · Borderline 3–<5% · Intermediate 5–<10% · High ≥10%. PREVENT calculator →
Risk enhancers
Examples include Lp(a) ≥125 nmol/L or ≥50 mg/dL, hsCRP ≥2 mg/L, family history of premature ASCVD, South Asian or Filipino ancestry, reproductive risk markers, chronic inflammatory disease, CKM syndrome, persistently elevated triglycerides, and LDL-C 160–189 mg/dL, non-HDL-C 190–219 mg/dL or ApoB ≥120 mg/dL.
CAC scoring
Use when the therapy decision remains uncertain in intermediate-risk and selected borderline-risk adults. CAC 0 → deferral reasonable, repeat in 3–7 y; CAC >0 in that setting supports initiating therapy, with intensity set by score. MESA CAC tool →
PREVENT-ASCVD estimates run 40–50% lower than the PCE for the same profile. The new borderline threshold (≥3%) identifies a similar number of adults eligible for lipid-lowering therapy. Inputs: age, sex, BP, total cholesterol, HDL-C, diabetes, tobacco, eGFR, statin use, antihypertensive use. Optional: HbA1c, urine ACR, area deprivation index.
Screening, Biomarkers & Testing
Lipid screening is recommended in adults from age 19 years and at least every five years thereafter, with more frequent testing where risk factors are present or a treatment decision is pending. Children are screened at 9–11 years, with cascade screening from age 2 where there is a family history.
Standard lipid profile
Total cholesterol, LDL-C, HDL-C, TG and non-HDL-C. LDL-C by Martin/Hopkins or Sampson/NIH rather than Friedewald. Report non-HDL-C routinely. Fasting not required unless hypertriglyceridaemia is known. Estimate untreated LDL-C before therapy →
ApoB
Selective, not universal. Most useful in ASCVD, CKM syndrome, diabetes, TG >200 mg/dL or LDL-C <70 mg/dL, and once LDL-C and non-HDL-C goals are met, to identify residual atherogenic particle burden. In severe hypercholesterolaemia with established ASCVD, an ApoB goal <55 mg/dL may be reasonable. Unaffected by fasting. ApoB calculator →
Lp(a)
Genetically determined; measure at least once in all adults. ≥125 nmol/L or ≥50 mg/dL confers roughly 1.4× risk; ≥250 nmol/L or ≥100 mg/dL roughly 2×. If elevated, intensify LDL-C lowering and manage other modifiable risk factors. Lp(a) comprehensive review →
CAC score
Men ≥40, women ≥45; absolute score and percentile both prognostic. CAC 0 indicates very low near-term risk. Treatment intensity follows the score rather than a single cut-point. Incidental CAC on non-cardiac CT should prompt therapy — moderate-intensity for mild calcification, with high-intensity reasonable for moderate–severe. Calcium score explained →
Advanced Lipoprotein Subclass Testing — Class 3, No Benefit
The 2026 guideline is explicit: routine advanced lipoprotein subclass testing — including NMR-derived LDL subclasses and LDL particle size — is not recommended for estimating ASCVD risk or for deciding whether to initiate lipid-lowering therapy. It is graded Class 3 (no benefit). This matters clinically because a large volume of social media content promotes the opposite view, and patients — particularly younger adults on ketogenic or carbohydrate-restricted diets — frequently arrive having self-funded an NMR panel and expecting a “pattern A” result to override an elevated LDL-C or ApoB.
Why size adds nothing once particle number is known
Small dense LDL and large buoyant LDL were compared as independent predictors in cohorts such as MESA, the Framingham Offspring Study and the Quebec Cardiovascular Study. In each, the apparent association between small dense LDL and events attenuated substantially — usually to null — after adjustment for total atherogenic particle number (ApoB or LDL-P) and triglycerides. Small dense particles travel with insulin resistance, high triglycerides and low HDL-C; they are a marker of that metabolic phenotype rather than an independent driver. Mendelian randomisation and the accumulated LDL-lowering trial data point the same way: the causal exposure is the number of ApoB-containing particles crossing the endothelium and their cumulative time-integral, not their buoyancy.
Two patients with the same ApoB carry broadly the same risk regardless of whether their particles are large or small. A patient with a high ApoB made up of large buoyant particles is not protected — there are more particles, and each one is atherogenic. “Large and fluffy” describes the cargo, not the exposure.
Common claims and what the evidence actually shows
| Claim | Evidence position |
|---|---|
| “Pattern A / large fluffy LDL is benign” | No outcome data show that particle size confers protection at a given ApoB. Size loses independent predictive value after adjustment for particle number. |
| “LDL-C is misleading, I need NMR” | Where discordance is the concern, the guideline answer is ApoB (COR 2a) or non-HDL-C — both standardised, inexpensive and interpretable. NMR subclass panels add cost, not decision value. |
| “High HDL and low TG cancel out a high LDL-C” | HDL-C is not a treatment target and HDL-raising has failed in outcome trials. A favourable TG/HDL ratio does not neutralise a high ApoB. |
| “Metabolically healthy people are exempt” | Absence of metabolic syndrome lowers absolute risk but does not abolish the effect of a markedly elevated ApoB sustained over years. |
The ketogenic diet and the lean mass hyper-responder phenotype
A subset of lean, insulin-sensitive people develop a striking rise in LDL-C and ApoB on carbohydrate restriction, alongside high HDL-C and low triglycerides — the lean mass hyper-responder (LMHR) pattern. This phenotype is the usual reason a young, athletic patient presents asking for NMR fractionation.
The KETO-CTA study followed 100 such individuals with serial coronary CT angiography over one year. The original report concluded that baseline plaque, rather than ApoB, predicted progression — a finding widely circulated as reassurance. That paper has since been retracted by the authors and editors over methodological concerns affecting data reliability, and a revised primary-outcome analysis has been posted as a preprint. Two points survive intact for the consultation room:
- A one-year study of 100 people, all with uniformly very high ApoB, has no low-ApoB comparator. Failing to find a dose–response within a high-exposure cohort over 12 months does not demonstrate that the exposure is safe.
- Non-calcified plaque volume increased over the year from a near-zero baseline. Progression, not stability, was the observed direction of travel.
Read LDL-P as a rough surrogate for particle number and disregard the subclass and size columns. Do not let a “pattern A” result defer therapy in a patient who otherwise meets an indication. If discordance is genuinely suspected, order a standardised ApoB. Where the decision remains finely balanced in primary prevention, CAC is the reclassification test with guideline support — not lipoprotein fractionation.
Treatment Goals by Risk Category
Both absolute goals and percentage LDL-C reduction guide therapy. All values mg/dL with mmol/L in parentheses; non-HDL-C goal ≈ LDL-C goal + 30 mg/dL (0.8 mmol/L). One of the major changes in this edition is that explicit goals are now stated for borderline- and intermediate-risk primary prevention once treatment is started.
| Patient category | % LDL-C ↓ | LDL-C goal | Non-HDL-C goal |
|---|---|---|---|
| ASCVD — very high risk | ≥50% | <55 (1.4) | <85 (2.2) |
| ASCVD — not very high risk | ≥50% | <70 (1.8) | <100 (2.6) |
| Severe hypercholesterolaemia + HeFH, risk factors or CAC | ≥50% | <70 (1.8) | <100 (2.6) |
| Severe hypercholesterolaemia (no additional risk) | Max tolerated | <100 (2.6) | <130 (3.4) |
| Diabetes + multiple risk factors | ≥50% | <70 (1.8) | <100 (2.6) |
| Diabetes (40–75 y, no ASCVD) | ≥30–49% | <100 (2.6) | <130 (3.4) |
| CAC ≥1000 AU | ≥50% | <55 (1.4) | <85 (2.2) |
| CAC 300–999 AU | ≥50% | <70 (1.8) | <100 (2.6) |
| CAC 100–299 AU or ≥75th percentile | Individualised intensity | <70 (1.8) | <100 (2.6) |
| CAC 1–99 AU and <75th percentile | ≥30–49% | <100 (2.6) | <130 (3.4) |
| Primary prevention — high (≥10%) | ≥50% | <70 (1.8) | <100 (2.6) |
| Primary prevention — intermediate (5–<10%) | ≥30–49% | <100 (2.6) | <130 (3.4) |
| Primary prevention — borderline (3–<5%) | ≥30–49% | <100 (2.6) | <130 (3.4) |
ApoB is not a universal goal. Where it is measured, an ApoB <55 mg/dL may be reasonable in severe hypercholesterolaemia with established ASCVD, and ApoB generally tracks the non-HDL-C goal in other categories.
Statin Intensity Reference
Grouped by expected LDL-C reduction.
| High-intensity (≥50% ↓) | Moderate (30–49% ↓) | Low (<30% ↓) |
|---|---|---|
| Atorvastatin 40–80 mg Rosuvastatin 20–40 mg |
Atorvastatin 10–20 mg Rosuvastatin 5–10 mg Simvastatin 20–40 mg Pravastatin 40–80 mg Lovastatin 40 mg Fluvastatin XL 80 mg Pitavastatin 1–4 mg |
Simvastatin 10 mg Pravastatin 10–20 mg Lovastatin 20 mg Fluvastatin 20–40 mg |
Nonstatins added to a low or moderate statin can achieve ≥50% LDL-C reduction. East Asian ancestry may warrant lower starting doses. Lovastatin, fluvastatin and pitavastatin are not available in Australia; atorvastatin, rosuvastatin, simvastatin and pravastatin are the practical options.
Management Pathways
Six common profiles, condensed to the decision sequence.
Primary prevention — adults 30–79 y, LDL-C 70–189 mg/dL (1.8–4.9 mmol/L)
- Calculate 10-year risk with PREVENT-ASCVD.
- Low (<3%): lifestyle. In adults aged 30–59 years with low 10-year risk, a moderate-intensity statin is reasonable when LDL-C is 160–189 mg/dL (4.1–4.9 mmol/L) or 30-year ASCVD risk is ≥10%.
- Borderline (3–<5%): personalise with risk enhancers. If treatment is chosen, moderate-intensity statin, 30–49% reduction. Goal LDL-C <100 (2.6), non-HDL-C <130 (3.4).
- Intermediate (5–<10%): at least moderate intensity (COR 1); consider high intensity at the upper end of the range. Goal LDL-C <100 (2.6), non-HDL-C <130 (3.4).
- High (≥10%): high-intensity statin, ≥50% reduction. Goal LDL-C <70 (1.8), non-HDL-C <100 (2.6). Add a nonstatin if the goal is not met.
- Decision uncertain in intermediate-risk or selected borderline-risk adults: use CAC to reclassify. CAC 0 → deferral reasonable, repeat in 3–7 y; CAC >0 → initiate therapy, with intensity set by the score (see the CAC pathway below).
Severe hypercholesterolaemia — LDL-C ≥190 mg/dL (4.9 mmol/L)
- Exclude secondary causes — hypothyroidism, nephrotic syndrome, cholestasis, ketogenic or very low-carbohydrate diet, medications. See our stepwise assessment of severe hypercholesterolaemia.
- Maximally tolerated statin for all patients (COR 1).
- No FH, risk factors or CAC: add ezetimibe, a PCSK9 monoclonal antibody and/or bempedoic acid. Goal LDL-C <100 (2.6), non-HDL-C <130 (3.4).
- With HeFH, risk factors or CAC: aggressive combination therapy. Goal LDL-C <70 (1.8), non-HDL-C <100 (2.6).
- With clinical ASCVD: most aggressive combination. Goal LDL-C <55 (1.4), non-HDL-C <85 (2.2); an ApoB goal <55 mg/dL may be reasonable.
- Cascade screening plus genetic testing for FH. FH guide → · Dutch Lipid Clinic Network FH calculator →
For the nonstatin options in detail, see PCSK9 inhibitors and inclisiran.
Diabetes without established ASCVD
- 40–75 y: moderate statin (COR 1) targeting ≥30–49% reduction. Goal LDL-C <100 (2.6), non-HDL-C <130 (3.4).
- Multiple risk factors: high-intensity statin, ≥50% reduction. Goal LDL-C <70 (1.8), non-HDL-C <100 (2.6).
- 10-year risk ≥10%: add ezetimibe or a PCSK9 monoclonal antibody to reach LDL-C <70 (1.8).
- Icosapent ethyl (COR 2b): may be reasonable in adults aged ≥50 y with diabetes plus at least one additional ASCVD risk factor, where TG remain 150–499 mg/dL (1.7–5.6 mmol/L) and LDL-C is <100 mg/dL despite maximally tolerated statin therapy.
- Age >75 y: a moderate statin may be reasonable where life expectancy is ≥2.5 y, with shared decision-making.
Clinical ASCVD — secondary prevention
Defined by ≥2 major ASCVD events, or 1 major event plus ≥2 high-risk conditions.
First line: high-intensity statin, ≥50% reduction. Goal: LDL-C <55 (1.4), non-HDL-C <85 (2.2).
Add-on: ezetimibe and/or a PCSK9 monoclonal antibody — no longer sequential; choose by the magnitude of LDL-C lowering required. Bempedoic acid is an option; inclisiran is second-line where a monoclonal antibody is not tolerated or accessible.
Class 1 goals: LDL-C <70 (1.8), non-HDL-C <100 (2.6), on a high-intensity statin targeting ≥50% reduction.
On maximally tolerated statin therapy, adding ezetimibe, a PCSK9 monoclonal antibody or bempedoic acid to reach <55 / <85 may also be reasonable, based on the additional reduction required and patient preference. Safety data extend to a median LDL-C of 30 mg/dL (0.8 mmol/L), with no de-escalation signal at very low levels.
Subclinical atherosclerosis — CAC-directed
Intensity follows the score. CAC is a reclassification tool applied after a clinician–patient discussion in intermediate-risk and selected borderline-risk adults, not a universal trigger.
| CAC score (AU) | Management |
|---|---|
| ≥1000 | High-intensity statin, ≥50% reduction. Goal <55 (1.4) / <85 (2.2). Manage as very-high-risk ASCVD. |
| 300–999 | ≥50% reduction. Goal <70 (1.8) / <100 (2.6). Intensifying toward <55 / <85 is reasonable. |
| 100–299, or any score ≥75th percentile | Initiate lipid-lowering therapy, statin first-line. Goal <70 (1.8) / <100 (2.6). A ≥50% reduction is not mandated for every patient in this group — set intensity individually. |
| 1–99 and <75th percentile | Moderate-intensity statin, 30–49% reduction. Goal <100 (2.6) / <130 (3.4). |
| 0 | Low near-term risk. Deferral is reasonable if no high-risk conditions. Repeat CAC in 3–7 years. |
Incidental coronary calcification on a non-cardiac CT should prompt lipid-lowering therapy: moderate-intensity for mild calcification, with high-intensity reasonable where calcification is moderate to severe.
Hypertriglyceridaemia
A statin remains the foundation for ASCVD risk reduction and lowers triglycerides by approximately 20–40% on average; non-HDL-C and ApoB are better therapeutic targets than triglycerides alone. Dedicated TG-lowering is driven mainly by pancreatitis risk. See practical triglyceride-lowering strategies.
| TG mg/dL (mmol/L) | Action |
|---|---|
| 150–499 (1.7–5.6) | Lifestyle plus statin. Icosapent ethyl may be reasonable (COR 2b) in adults aged ≥50 y with established ASCVD, or with diabetes plus at least one additional ASCVD risk factor, where TG remain in this range and LDL-C is <100 mg/dL despite maximally tolerated statin therapy. |
| ≥500 (5.7) | Pancreatitis prevention: prescription omega-3 ± fenofibrate. Avoid combining gemfibrozil with a statin. Refer to an accredited practising dietitian. |
| ≥1000 (11.3) | Urgent TG-lowering, strict dietary fat restriction, mandatory dietitian referral (COR 1). Exclude familial chylomicronaemia syndrome. |
In confirmed FCS with TG ≥1000 mg/dL (11.3 mmol/L), the guideline recommends olezarsen as an adjunct to dietary fat restriction. Olezarsen is not currently available in Australia; management here rests on strict dietary fat restriction, alcohol avoidance, dietitian involvement and specialist lipid clinic referral.
Lifestyle Foundation
Built on AHA Life's Essential 8 and applied lifelong from youth. Sustained adherence substantially reduces lifetime ASCVD risk, including in those with genetic predisposition.
- Mediterranean, DASH or vegetarian patterns — fruit, vegetables, nuts, legumes, whole grains and fibre
- Replace saturated and trans fats with mono- and polyunsaturated fats
- ≥150 min/week moderate–vigorous activity plus resistance training ≥2 days/week
- Healthy weight and tobacco cessation
- Dietary supplements are not recommended for LDL-C lowering (COR 3)
- TG 150–499 mg/dL (1.7–5.6 mmol/L): reduce sugar, refined carbohydrate and saturated fat; minimise alcohol; physical activity.
- TG 500–999 mg/dL (5.7–11.3 mmol/L): no alcohol and individualised fat limitation; refer to a dietitian (COR 2a).
- TG ≥1000 mg/dL (11.3 mmol/L): mandatory dietitian referral (COR 1), strict fat restriction, exclude familial chylomicronaemia syndrome.
Triggers: alcohol, sugar and refined carbohydrate, uncontrolled diabetes, hypothyroidism, obesity, corticosteroids, oestrogens, retinoids and antiretrovirals. Alcohol and heart health →
Special Populations
When standard pathways need tailoring.
Children & adolescents
Screen 9–11 y (COR 1); cascade from ≥2 y if family history. About 20% of adolescents have lipid abnormalities and roughly 1 in 250 have HeFH; family history alone misses about half. Early pharmacotherapy for FH.
Pregnancy & lactation
Most patients planning pregnancy should stop statin therapy 1–2 months before conception, or when pregnancy is recognised. Bile-acid sequestrants may be used during pregnancy and lactation. In selected pregnant patients with familial hypercholesterolaemia or established ASCVD, continuing a statin — typically a hydrophilic agent such as pravastatin — may be reasonable after an individualised benefit–risk discussion. Ezetimibe, PCSK9 monoclonal antibodies, bempedoic acid and inclisiran should generally be avoided because of insufficient pregnancy safety data. Statins should be avoided during lactation. Reproductive risk markers are ASCVD risk enhancers.
CKD stage 3 and above
Moderate statin ± ezetimibe for CKD 3+ with LDL-C 70–189 mg/dL (1.8–4.9 mmol/L) (COR 1, SHARP). With ASCVD: high-intensity statin to LDL-C <55 (1.4), non-HDL-C <85 (2.2). On dialysis, initiating a statin is not beneficial though continuing may be reasonable. Atorvastatin preferred; rosuvastatin ≤10 mg in severe CKD.
Heart failure
Lipid-lowering therapy should not be initiated solely to improve outcomes in HFrEF in the absence of ASCVD or another established indication (COR 3, no benefit). Where an indication exists, continue therapy as usual.
People living with HIV
Pitavastatin 4 mg for adults 40–75 y on stable ART (COR 1; REPRIEVE showed a 35% MACE reduction). Not metabolised by CYP3A4. Pitavastatin is not marketed in Australia — rosuvastatin or pravastatin are the practical alternatives. Statin choice and dose must be checked against the specific antiretroviral regimen.
Elevated Lp(a)
A risk enhancer rather than a direct treatment target with current therapies. If elevated, intensify LDL-C lowering and manage all other modifiable risk factors aggressively. Novel Lp(a)-lowering agents (pelacarsen, olpasiran, lepodisiran) are in phase 3 trials but not yet available.
Older adults over 75 years
Primary prevention: lipid-lowering therapy may be considered where life expectancy is ≥2.5 y. Continue an existing statin — discontinuation increases heart-failure hospitalisation and cardiovascular events.
Statin-associated muscle symptoms (SAMS)
About 10% are intolerant. Try an alternative statin or reduce the dose; bempedoic acid (COR 1), ezetimibe and PCSK9 monoclonal antibodies are options. CoQ10 is not recommended (COR 3); routine CK is not useful (COR 3).
Cancer survivors & chronic inflammatory disease
Cancer: continue lipid-lowering therapy — statins may protect against anthracycline cardiotoxicity. Chronic inflammatory disease: standard calculators underestimate risk, so it is treated as a risk enhancer; monitor lipids on anti-inflammatory therapy.
Monitoring & Follow-Up
Assess response, adherence and safety at defined intervals.
Before therapy
Fasting or non-fasting lipid profile, ASCVD risk assessment, lifestyle ± pharmacotherapy. Measure Lp(a) once. A baseline ALT is suggested.
4–12 weeks post-initiation
Repeat lipid profile; assess percentage LDL-C reduction, absolute goals and adherence. Non-fasting adequate unless hypertriglyceridaemia. Inadequate response → intensify.
Every 6–12 months
Individualise frequency; stable patients annually. Monitoring improves adherence and reduces therapeutic inertia.
Ongoing safety
Routine CK not useful (COR 3); routine ongoing liver-function testing is unnecessary in the absence of symptoms; CoQ10 not recommended (COR 3); screen drug interactions (COR 1). Statin-related type 2 diabetes risk is not a reason to discontinue.
Simvastatin and lovastatin carry the greatest interaction burden. Review the complete medication list and current prescribing information before selecting the statin and dose, particularly with antiarrhythmics (amiodarone, dronedarone), calcium-channel blockers (verapamil, diltiazem), antiretrovirals, azole antifungals, ciclosporin and fibrates. Pravastatin avoids CYP450 metabolism; rosuvastatin and fluvastatin use CYP2C9. Gemfibrozil should generally be avoided in combination with a statin — use fenofibrate.
Evidence & Methodology
How the guideline was built and how to interpret its recommendations.
COR
1 — benefit far outweighs risk; is recommended.
2a — benefit outweighs risk; is reasonable.
2b — benefit ≥ risk; may be reasonable.
3 — no benefit, or harm.
LOE
A — high quality, multiple RCTs.
B-R — moderate, one or more RCTs.
B-NR — non-randomised studies.
C-LD — limited data.
C-EO — expert opinion.
Literature search October–December 2024. Key cardiovascular outcomes trials informing the document include FOURIER, ODYSSEY OUTCOMES, CLEAR OUTCOMES, REDUCE-IT and REPRIEVE. Chair: Roger S. Blumenthal, MD; Vice Chair: Pamela B. Morris, MD.
- PREVENT replaces the Pooled Cohort Equations; estimates run 40–50% lower, and the treatment thresholds have moved down to match.
- Explicit LDL-C and non-HDL-C goals now apply to borderline and intermediate primary prevention once therapy is started — <100 and <130 mg/dL respectively.
- Lp(a) is a Class 1 once-in-a-lifetime measurement; ApoB is a selective Class 2a add-on rather than a universal goal.
- CAC-directed intensity is graded: 1–99 moderate; 100–299 or ≥75th percentile initiate therapy to <70; 300–999 ≥50% reduction; ≥1000 treated as very-high-risk ASCVD.
- NMR lipoprotein subclass and LDL particle size testing is Class 3, no benefit. Particle number, not particle size, carries the risk.
- In secondary prevention, ezetimibe and PCSK9 inhibition are no longer sequential — select by the LDL-C reduction required to reach goal.
Frequently Asked Questions
What is the PREVENT risk calculator and why does it replace the PCE?
The AHA PREVENT-ASCVD equations replace the older Pooled Cohort Equations for 10- and 30-year cardiovascular risk in adults 30–79 y. PREVENT estimates run 40–50% lower than the PCE for the same profile, but the lower thresholds (borderline from ≥3%) identify a similar number of adults who may benefit from therapy. It adds inputs such as eGFR and statin use, with optional HbA1c, urine albumin-to-creatinine ratio and a social deprivation index. Try our PREVENT calculator →
What LDL-C level should I aim for?
Targets depend on risk category. For established ASCVD at very high risk the goal is LDL-C <55 mg/dL (1.4 mmol/L) and non-HDL-C <85 mg/dL (2.2 mmol/L); for ASCVD not at very high risk, <70 mg/dL (1.8 mmol/L) and <100 mg/dL (2.6 mmol/L). In primary prevention, high risk carries a goal of <70 mg/dL, while borderline and intermediate risk carry <100 mg/dL (2.6 mmol/L) with non-HDL-C <130 mg/dL (3.4 mmol/L). A percentage LDL-C reduction of 30–50% or more is a treatment objective alongside the absolute goal. Cholesterol unit converter →
Should everyone have their Lp(a) tested?
The guideline gives a Class 1 recommendation for Lp(a) measurement at least once in all adults. Lp(a) is largely genetically determined and is not meaningfully lowered by lifestyle or standard therapy. If elevated (≥125 nmol/L or ≥50 mg/dL) it is a risk-enhancing factor that should prompt more aggressive LDL-C lowering and management of other modifiable risk factors. It is not a direct treatment target with currently available therapies, though novel agents are in late-stage trials. Read our Lp(a) overview →
Is NMR lipoprotein particle testing worth doing? Is “large fluffy” LDL safe?
The guideline grades routine advanced lipoprotein subclass testing — NMR subfractions and LDL particle size — as Class 3, no benefit, for estimating risk or deciding on therapy. Once total atherogenic particle number is accounted for, particle size carries no independent predictive value; small dense LDL is a marker of insulin resistance and high triglycerides rather than an independent driver. A high ApoB made up of large buoyant particles is still a high ApoB. If discordance between LDL-C and particle burden is suspected, order a standardised ApoB rather than a subclass panel. ApoB explained →
When should a coronary artery calcium (CAC) score be used?
CAC scoring is recommended (COR 1) in adults at intermediate risk (5–<10%) and selected adults at borderline risk (3–<5%) when the decision about therapy remains uncertain after a clinician–patient discussion. It is a selective reclassification tool, not a universal test. CAC 0 with no other high-risk conditions may allow deferral with repeat testing in 3–7 y. Where CAC is greater than zero, treatment intensity is graded by the score rather than by a single cut-point. Learn about calcium scoring →
What role does ApoB play in the 2026 guideline?
ApoB is recommended selectively rather than universally (COR 2a). It is most useful in adults already on therapy — particularly with ASCVD, CKM syndrome, type 2 diabetes or elevated triglycerides — where LDL-C may underestimate the true atherogenic particle burden, and once LDL-C and non-HDL-C goals have been met, to identify residual risk. In severe hypercholesterolaemia with established ASCVD, an ApoB goal below 55 mg/dL may be reasonable. It is unaffected by fasting.
Are dietary supplements effective for lowering cholesterol?
The guideline does not recommend dietary supplements for LDL-C or triglyceride management. Some products can produce modest lipid changes, but variable formulation and the lack of convincing cardiovascular-outcome evidence mean they should not replace evidence-based lifestyle measures or pharmacotherapy.
How often should lipids be checked on treatment?
A lipid profile should be repeated 4–12 weeks after starting or adjusting therapy and every 6–12 months thereafter (COR 1). Non-fasting testing is adequate in most cases unless hypertriglyceridaemia is known. Regular monitoring assesses both percentage LDL-C reduction and achievement of absolute goals, improves adherence and reduces therapeutic inertia.
Primary Sources
- Blumenthal RS, Morris PB, Gaudino M, et al. 2026 ACC/AHA Guideline on the Management of Dyslipidemia. J Am Coll Cardiol. 2026;87(19):2624–2757. doi:10.1016/j.jacc.2025.11.016
- American Heart Association — professional guideline hub and PREVENT calculator resources. professional.heart.org
- American College of Cardiology — guideline hub, slide sets and clinician summaries. acc.org/Guidelines
Personalised cardiovascular risk assessment
For a comprehensive assessment — including Lp(a), ApoB, coronary calcium scoring and individualised lipid management — book an appointment with Dr Reza Moazzeni at Heartcare Sydney.
Book an appointmentDr Reza Moazzeni, MD FRACP — consultant cardiologist specialising in preventive cardiology and advanced cardiac imaging. Consultations in English and Persian (Farsi) at Westmead and St Leonards, Sydney.
This page summarises the 2026 ACC/AHA dyslipidaemia guideline for educational purposes. Dosing, availability and reimbursement differ in Australia. It does not replace clinical judgement, and treatment decisions must be individualised.