ACC / AHA 2026 Clinical Practice Guideline

ACC/AHA 2026 Dyslipidemia Guidelines: Key Updates & Clinical Summary

A practical clinician summary of risk assessment, LDL-C targets, Lp(a), CAC and modern lipid management.

Reviewed by Dr Reza Moazzeni, MD FRACP · Consultant Cardiologist · Published 20 March 2026 · Updated June 2026

What changed in 2026

LDL-C treatment goals return and guide therapy
PREVENT replaces PCE within the ACC/AHA framework
Lp(a) recommended at least once in all adults
CAC used to reclassify risk and guide decisions

Treatment targets Risk assessment Full guideline ↗

Australian context

This page summarises the 2026 ACC/AHA dyslipidaemia guideline. Australian prescribing, PBS eligibility and local practice may differ — access to PCSK9 inhibitors, inclisiran and bempedoic acid depends on PBS criteria, private prescribing, specialist review and individual patient context.

Most useful for: GPs, cardiologists, endocrinologists and clinicians wanting a practical summary of the 2026 ACC/AHA guideline.

How to read the labels

COR (Class of Recommendation) appears throughout this page: 1 is recommended · 2a is reasonable · 2b may be reasonable · 3 no benefit or harm. Full COR and Level of Evidence detail in Evidence & Methodology.

In 30 Seconds — What Changed?

The 2026 update reframes lipid management around lifetime cardiovascular risk rather than a single LDL-C number.

Risk assessment

PREVENT

Replaces the PCE within the 2026 ACC/AHA framework and improves individualised risk estimation.

Treatment strategy

Earlier & lower

Earlier, lower and longer LDL-C reduction across the risk spectrum.

Targets

Goals return

Clear LDL-C and non-HDL-C goals return, especially in higher-risk patients.

Biomarkers

Lp(a) & ApoB

Lp(a) measured at least once in all adults; ApoB used selectively for residual risk.

Imaging

CAC

Coronary calcium reclassifies risk when the treatment decision is uncertain.

Scope

Beyond LDL-C

Broader focus including triglycerides and lifetime cardiovascular risk.

Key shift in 2026

From risk estimation → risk personalisation

From statins only → multi-pathway lipid management

From an LDL focus → a global dyslipidaemia strategy

A shift from treating numbers to treating lifetime cardiovascular risk.

What Changed in 2026

Key practice updates from the guideline — what every clinician needs to know.

10 Top Take-Home Messages

Practice priorities

Treat earlier. Lifestyle counselling from youth; pharmacotherapy in youth with FH and young adults with LDL-C ≥160 mg/dL (4.1 mmol/L) or a strong family history of premature ASCVD.
PREVENT replaces the PCE for 10- and 30-year risk. Apply the CPR model: Calculate → Personalise → Reclassify with CAC.
Borderline risk starts at 3%. Lipid-lowering therapy can be considered at PREVENT 3–<5% and should be considered at 5–<10%.
Treatment goals are back. Absolute LDL-C and non-HDL-C targets now guide therapy alongside percentage LDL-C reduction.
ApoB for residual risk. Useful once LDL-C / non-HDL-C goals are met, especially with elevated TG, diabetes or achieved LDL-C <70.
Lp(a) at least once (COR 1) in all adults. ≥125 nmol/L / 50 mg/dL (~1.4× risk); ≥250 nmol/L / 100 mg/dL (≥2× risk). If elevated, intensify LDL-C lowering and manage other modifiable risk factors.
CAC for reclassification (COR 1). Men ≥40, women ≥45. CAC >0 → initiate LLT; ≥100 or ≥75th percentile → high-intensity; CAC 0 → may defer.
LLT for diabetes, CKD 3–4 and HIV (COR 1) regardless of LDL-C in adults 40–75. After 75, consider with shared decision-making.
Very-high-risk ASCVD: LDL-C <55 mg/dL (1.4 mmol/L), non-HDL-C <85 mg/dL (2.2 mmol/L). Ezetimibe no longer required before a PCSK9 mAb; bempedoic acid added.
Hypertriglyceridaemia: statin first-line for ASCVD risk; TG-lowering for pancreatitis prevention, especially TG ≥1000.

Key Recommendation Changes (Table 1)

Tap any row to expand the 2018 vs 2026 comparison.

Revised — LDL-C estimation method

2018 (COR 2a): direct LDL-C or a modified estimate reasonable when LDL-C <70.

2026 (COR 1): Martin/Hopkins or Sampson/NIH preferred over Friedewald in all adults and children.

New (COR 2a) — ApoB measurement

2026 (COR 2a): in adults on LLT with ASCVD, CKM, T2DM and/or elevated TG, ApoB is reasonable to guide intensification once LDL-C / non-HDL-C goals are achieved.

New (COR 1) — Lp(a) measurement

2026 (COR 1): Lp(a) at least once in all adults. ≥125 nmol/L = risk enhancer; ≥250 nmol/L = ≥2× risk. Fasting not required.

New (COR 1) — PREVENT-ASCVD equations

2026 (COR 1): adults 30–79 y use PREVENT-ASCVD. Low <3%, borderline 3–<5%, intermediate 5–<10%, high ≥10%. Estimates run 40–50% lower than the PCE.

New — CAC score → treatment decisions

COR 1: CAC >0 → initiate LLT, particularly if ≥100 AU or ≥75th percentile. Incidental CAC on non-cardiac CT (visual or AI) should trigger LLT.

COR 2a: CAC 0 with no high-risk conditions → defer LLT, repeat in 3–7 y.

New — reproductive risk & supplements

COR 2a: reproductive risk markers (menopause <45, pre-eclampsia, gestational diabetes/hypertension, preterm delivery) personalise risk.

COR 3 (no benefit): dietary supplements are not recommended for LDL-C or TG lowering.

Risk Assessment Framework

The CPR model replaces the old PCE-driven approach: start with PREVENT, then personalise, then reclassify where the decision is uncertain.

Step 1 · Calculate

PREVENT-ASCVD

10-year risk in adults 30–79 y without ASCVD.

Low <3% · Borderline 3–<5% · Intermediate 5–<10% · High ≥10%

Step 2 · Personalise

Risk enhancers

Consider factors not captured by PREVENT: Lp(a) ≥125 nmol/L, hsCRP ≥2 mg/L, family history of premature ASCVD, South Asian / Filipino ancestry, reproductive risk markers, chronic inflammatory disease.

Step 3 · Reclassify

CAC scoring

Use when the LLT decision is uncertain. CAC 0 → defer, repeat 3–7 y; 1–99 → LDL <100 (2.6); ≥100 → LDL <70 (1.8); ≥1000 → ≥50% ↓, LDL <55 (1.4).

PREVENT vs PCE

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 LLT. Inputs: age, sex, BP, total cholesterol, HDL-C, diabetes, tobacco, eGFR, statin use, antihypertensive use. Optional: HbA1c, urine ACR, area deprivation index.

Biomarkers & Testing

What to measure, when, and what each test adds.

Baseline test

Standard lipid profile

Total cholesterol, LDL-C, HDL-C, TG and non-HDL-C. Screen from age 19 y; children 9–11 y. LDL-C by Martin/Hopkins or Sampson/NIH. Report non-HDL-C routinely. Fasting not required unless hypertriglyceridaemia is known.

Add-on · COR 2a

ApoB

Atherogenic particle number; superior when LDL-C and ApoB are discordant. Use in ASCVD, CKM, diabetes, TG >200 or LDL <70. Very-high-risk goal <55 mg/dL. Unaffected by fasting.

New · COR 1

Lp(a)

Genetically determined; measure once. ≥125 nmol/L (50 mg/dL) ~1.4× risk; ≥250 nmol/L (100 mg/dL) ≥2× risk. If elevated, intensify LDL-C lowering and manage other modifiable risk factors. Lp(a) comprehensive review →

Reclassification · COR 1

CAC score

Men ≥40, women ≥45; absolute score and percentile both prognostic. CAC 0 = very low near-term risk; ≥100 or ≥75th percentile → high-intensity LLT. Incidental CAC on non-cardiac CT should trigger LLT. Calcium score explained →

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 ≈ LDL-C goal + 30 mg/dL (0.8 mmol/L).

Patient category	% LDL-C ↓	LDL-C goal	Non-HDL-C goal	ApoB
ASCVD — very high risk	≥50%	<55 (1.4)	<85 (2.2)	<55
ASCVD — not very high risk	≥50%	<70 (1.8)	<100 (2.6)	Consider
Severe hypercholesterolaemia + HeFH / risk / 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)	Consider
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 100–999 or ≥75th percentile	≥50%	<70 (1.8)	<100 (2.6)	—
CAC 1–99 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%	Individualise	Individualise	—
Primary prevention — borderline (3–<5%)	≥30–49%	Individualise	Individualise	—

Quick reference — statin intensity (Table 6)

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/moderate statin can achieve ≥50% LDL-C reduction. East Asian ancestry may need lower starting doses.

Management Pathways

Select a patient profile for a concise decision pathway.

Primary prevention30–79 y · LDL-C 70–189 Severe hypercholesterolaemiaLDL-C ≥190 (4.9) DiabetesNo established ASCVD Clinical ASCVDSecondary prevention Subclinical / CACCAC-based HypertriglyceridaemiaBy TG range

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. If LDL-C 160–189 (4.1–4.9) or 30-y risk ≥10%, consider a moderate statin.
Borderline (3–<5%): personalise with enhancers. Moderate statin → ≥30–49% ↓.
Intermediate (5–<10%): at least a moderate statin (COR 1). Upper range → high-intensity ≥50% ↓.
High (≥10%): high-intensity statin. Goal LDL-C <70 (1.8), non-HDL-C <100 (2.6). Add a nonstatin if needed.
Uncertain? CAC to reclassify. CAC 0 → may defer; CAC >0 → initiate LLT.

Severe hypercholesterolaemia

LDL-C ≥190 mg/dL (4.9 mmol/L)

Exclude secondary causes (hypothyroidism, nephrotic syndrome, ketogenic diet, medications).
Max tolerated statin for all patients (COR 1).
No FH / risk factors / CAC: add ezetimibe, a PCSK9 mAb and/or bempedoic acid. Goal LDL-C <100 (2.6), non-HDL-C <130 (3.4).
With HeFH / risk factors / CAC: aggressive combination. 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). Consider ApoB <55.
Cascade screening + genetic testing for FH. FH guide →

Diabetes — without established ASCVD

Adults with diabetes, no clinical ASCVD

40–75 y: moderate statin (COR 1) → ≥30–49% ↓. Goal LDL-C <100 (2.6), non-HDL-C <130 (3.4).
Multiple risk factors: high-intensity → ≥50% ↓. Goal LDL-C <70 (1.8), non-HDL-C <100 (2.6).
10-y risk ≥10%: add ezetimibe or a PCSK9 mAb to reach LDL-C <70 (1.8).
TG 150–499 (1.7–5.6) on statin, LDL-C <100: consider adding icosapent ethyl.
>75 y: a moderate statin may be reasonable (life expectancy ≥2.5 y, shared decision-making).

Clinical ASCVD — secondary prevention

Established atherosclerotic disease

Very high risk (majority)

≥2 major ASCVD events, or 1 major event + ≥2 high-risk conditions.

First: high-intensity statin → ≥50% ↓. Goal: LDL-C <55 (1.4), non-HDL-C <85 (2.2).

Add-on: ezetimibe and/or a PCSK9 mAb (no longer sequential — choose by LDL-C lowering needed). Bempedoic acid an option; inclisiran second-line if a mAb is not tolerated or accessible.

Not very high risk

First: high-intensity statin → ≥50% ↓. Goal: LDL-C <70 (1.8), non-HDL-C <100 (2.6).

Consider treating to <55 / <85 in younger patients (COR 2a). Safety data to median LDL-C 30 (0.8); no de-escalation signal at very low LDL-C.

Subclinical atherosclerosis — CAC-based

Management by coronary artery calcium score

≥1000High-intensity → ≥50% ↓. Goal <55 (1.4) / <85 (2.2) (COR 1). Treat like very-high-risk ASCVD.
300–999High-intensity → ≥50% ↓. Goal <70 (1.8) / <100 (2.6). Consider intensifying to <55 / <85.
100–299High-intensity → ≥50% ↓. Goal <70 (1.8) / <100 (2.6). Also if ≥75th percentile.
1–99Moderate → ≥30–49% ↓. Goal <100 (2.6) / <130 (3.4) (COR 2a).
0Low near-term risk. May defer LLT if no high-risk conditions. Repeat CAC in 3–7 y.

Hypertriglyceridaemia

Statin foundation; TG-lowering for pancreatitis risk

Foundation: statin remains first-line for ASCVD risk and lowers TG 10–30%. Non-HDL-C and ApoB are better targets than TG alone.
TG 150–499 (1.7–5.6): lifestyle + statin. If on a statin with LDL-C <100, consider icosapent ethyl.
TG ≥500 (5.7): pancreatitis prevention — prescription omega-3 ± fenofibrate (do not combine gemfibrozil with a statin). Refer to an accredited dietitian.
TG ≥1000 (11.3): urgent TG-lowering, strict dietary fat limitation, mandatory dietitian referral (COR 1).

Lifestyle Foundation

Built on AHA Life's Essential 8 and applied lifelong from youth — capable of roughly 50% relative risk reduction even with genetic predisposition.

LDL-C lowering lifestyle

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)

How to prevent a heart attack →

Triglyceride lowering (by range)

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): add 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.

Special Populations

When standard pathways need tailoring. Tap to expand.

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

Statins, PCSK9 mAbs, bempedoic acid and ezetimibe are contraindicated; colesevelam is the safest option. Reproductive risk markers are ASCVD risk enhancers.

CKD stage 3+

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.

HIV (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. Lovastatin and simvastatin are contraindicated with protease inhibitors.

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. Lp(a) overview →

Older adults (>75 y)

Primary prevention: LLT 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 mAbs are options. CoQ10 is not recommended (COR 3); routine CK is not useful (COR 3); routine LFTs are no longer required.

Cancer survivors & chronic inflammatory disease

Cancer: continue LLT — 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.

Baseline

Before therapy

Fasting or non-fasting lipid profile, ASCVD risk assessment, lifestyle ± pharmacotherapy. Measure Lp(a) once.

COR 1

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.

Ongoing

Every 6–12 months

Individualise frequency; stable patients annually. Monitoring improves adherence and reduces therapeutic inertia.

Safety

Ongoing safety

Routine CK not useful (COR 3); routine LFTs not required; CoQ10 not recommended (COR 3); screen drug interactions (COR 1), especially CYP3A4 statins. Statin-related T2DM risk: do not discontinue.

Safety — CYP3A4 statin drug interactions

Interaction	Statins	Action
Protease inhibitors (ritonavir, cobicistat)	Lovastatin, simvastatin	Contraindicated
Protease inhibitors	Atorvastatin	Max 20 mg/day
Azole antifungals (itraconazole, ketoconazole)	Lovastatin, simvastatin	Contraindicated
Cyclosporine	Lovastatin, simvastatin, pitavastatin	Contraindicated
Amiodarone, dronedarone	Simvastatin	Max 20 mg/day
Verapamil, diltiazem	Lovastatin, simvastatin	Max 20 mg/day
Ticagrelor	Simvastatin	Max 40 mg/day
Gemfibrozil	All statins	Avoid; use fenofibrate

Pravastatin avoids CYP450; pitavastatin (preferred in HIV) avoids CYP3A4; rosuvastatin and fluvastatin use CYP2C9.

Evidence & Methodology

How the guideline was built and how to interpret its recommendations.

Class of recommendation

COR

1 — benefit ≫ risk; is recommended.
2a — benefit ≫ risk; is reasonable.
2b — benefit ≥ risk; may be reasonable.
3 — no benefit or harm.

Level of evidence

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: FOURIER, ODYSSEY OUTCOMES, CLEAR OUTCOMES, REDUCE-IT and REPRIEVE. Chair: Roger S. Blumenthal, MD; Vice Chair: Pamela B. Morris, MD. Read the full guideline (Circulation 2026) →

Frequently Asked Questions

What is the PREVENT risk calculator and why does it replace the PCE?

The AHA PREVENT-ASCVD equations are a more contemporary tool that replaces 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 it is LDL-C <70 mg/dL (1.8 mmol/L). For primary prevention with diabetes or multiple risk factors the goal may be <70 or <100 mg/dL (2.6 mmol/L) depending on risk. In all cases a percentage LDL-C reduction of ≥30–50% is also a treatment objective. 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 →

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; CAC >0, particularly ≥100 AU or ≥75th percentile, should prompt therapy. Learn about calcium scoring →

What role does ApoB play in the 2026 guideline?

ApoB is not recommended universally but has been elevated in importance (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. It helps identify residual risk after LDL-C and non-HDL-C goals are met and guides further intensification. It is unaffected by fasting and especially valuable when LDL-C and ApoB are discordant. Learn more about ApoB →

Are dietary supplements effective for lowering cholesterol?

No. The guideline gives a Class 3 (no benefit) recommendation for dietary supplements for LDL-C or triglyceride lowering, citing limited and inconsistent data — including fish-oil supplements, red yeast rice and plant sterols as routine ASCVD risk-reduction strategies. Evidence-based pharmacotherapy (statins, ezetimibe, PCSK9 mAbs, bempedoic acid) remains the standard of care when lifestyle alone is insufficient.

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.

Cardiovascular risk assessment

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 appointment →

About the author

Dr 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.

Full biography →

Clinical disclaimer

This page summarises the 2026 ACC/AHA dyslipidaemia guideline for educational purposes. It does not replace clinical judgement, and treatment decisions must be individualised.

Blumenthal RS et al. Circulation. 2026;153:e00–e00. DOI: 10.1161/CIR.0000000000001423. Updated June 2026.