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Summary Table

Category	Details
Risk Factors	Smoking, hypertension, diabetes mellitus, obesity (BMI ≥25 kg/m2 for Asian), family history of premature CHD (male <55, female <65), age (male ≥45, female ≥55), chronic kidney disease, chronic inflammatory conditions, metabolic syndrome
Etiology	Primary (genetic): familial hypercholesterolemia, familial combined dyslipidemia, primary hypertriglyceridemia. Secondary: hypothyroidism, nephrotic syndrome, DM type 2, chronic alcohol use, medications (thiazides, beta-blockers, corticosteroids, protease inhibitors, oral contraceptives)
Patient Presentation	Usually asymptomatic. Discovered incidentally on routine screening. Symptomatic presentations are complications: chest pain (CHD), focal neurological deficit (stroke), severe epigastric pain (pancreatitis from TG ≥500 mg/dL)
Classic Physical Exam	Xanthoma (tendon: Achilles, elbow, knee), xanthelasma (eyelid), arcus corneae (in young patients suggests familial hypercholesterolemia), lipemia retinalis (cream-colored retinal vessels in severe hypertriglyceridemia), hepatosplenomegaly
Key Diagnostic Results	Fasting lipid profile: Total cholesterol ≥240 mg/dL (high), LDL-C ≥190 mg/dL (very high), HDL-C <40 mg/dL (low), TG ≥200 mg/dL (high). Friedewald formula: $\text{LDL} = \text{Total Cholesterol} - \text{HDL} - \frac{\text{TG}}{5}$ (invalid if TG >400 mg/dL)
Management	Lifestyle modification (diet, exercise, smoking cessation) for all patients. Statins are first-line pharmacotherapy. Ezetimibe and PCSK9 inhibitors as add-on for high/very-high risk patients not reaching target. Fibrates for TG ≥500 mg/dL to prevent pancreatitis
Keywords	"Xanthoma on Achilles tendon," "arcus corneae in young adult," "milky plasma," "fasting lipid profile," "LDL target," "Framingham risk score," "statin intensity," "10-year cardiovascular risk"

1. Pathophysiology

Dyslipidemia is a disorder of lipid metabolism characterized by elevation or reduction of one or more plasma lipid fractions. The principal abnormalities are elevated total cholesterol, elevated LDL-C, elevated triglycerides, and/or decreased HDL-C.

To understand why LDL-C is the primary therapeutic target, you must understand lipoprotein metabolism. The liver releases nascent VLDL containing apo B-100, apo E, apo C1, cholesteryl esters, and triglycerides into circulation. HDL donates apo C-II to nascent VLDL, making it mature. Mature VLDL interacts with lipoprotein lipase (LPL) on capillary endothelium of adipose tissue, cardiac muscle, and skeletal muscle, where triglycerides are extracted for energy use or storage.

VLDL then exchanges triglycerides for cholesteryl esters with HDL via cholesteryl ester transfer protein (CETP). This process reduces VLDL triglyceride content, converting it into IDL. Approximately half of IDL undergoes hepatic endocytosis (recognized by apo B-100 and apo E). The remaining IDL, now enriched in cholesterol relative to triglycerides and lacking apo E, transforms into LDL.

LDL particles contain apo B-100, the ligand recognized by hepatic LDL receptors (LDLR). When circulating LDL is excessive or LDLR expression is reduced (as in familial hypercholesterolemia), LDL accumulates in the plasma and undergoes oxidative modification. Oxidized LDL penetrates the arterial intima, is engulfed by macrophages via scavenger receptors, and forms foam cells, which is the earliest hallmark of atherosclerotic plaque formation.

HDL, carrying apo A-I and apo A-II, mediates reverse cholesterol transport, removing cholesterol from peripheral tissues back to the liver. This is why low HDL-C is considered atherogenic and why HDL is often called the "protective" lipoprotein.

The atherosclerotic plaque is a lipid-rich, inflammatory lesion covered by a fibrous cap. When the cap erodes, ulcerates, or ruptures, the thrombogenic core is exposed, triggering acute thrombosis, which is the direct mechanism behind acute coronary syndrome and ischemic stroke.

Statins work by competitively inhibiting HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis. Reduced intracellular cholesterol upregulates LDLR expression on hepatocyte surfaces, increasing LDL clearance from blood. Beyond lipid lowering, statins exert pleiotropic effects: improving endothelial function, stabilizing plaque, reducing oxidative stress, and decreasing vascular inflammation.

2. Classification and Clinical Manifestation

Classification of Plasma Lipid Levels

Lipid Fraction	Category	Value (mg/dL)
Total Cholesterol	Desirable	<200
	Borderline high	200-239
	High	≥240
LDL-C	Optimal	<100
	Near optimal	100-129
	Borderline high	130-159
	High	160-189
	Very high	≥190
HDL-C	Low	<40
HDL-C	High (protective)	≥60
Triglycerides	Normal	<150
	Borderline high	150-199
	High	200-499
	Very high	≥500

Classification by Etiology

Type	Description	Key Features
Primary (Genetic)	Polygenic hypercholesterolemia, familial combined dyslipidemia, familial hypercholesterolemia, remnant dyslipidemia, primary hypertriglyceridemia	Suspect when severe dyslipidemia is found in a young patient with xanthoma, xanthelasma, or arcus corneae, especially with a family history of premature CHD
Secondary	Dyslipidemia caused by an underlying condition	Treat the primary disease first. Exceptions: DM patients always require statin therapy because DM is considered a CHD risk equivalent

Secondary Causes of Dyslipidemia

Lipid Abnormality	Causes
Elevated Total Cholesterol and LDL-C	Hypothyroidism, nephrotic syndrome, cholestatic liver disease, progestin/anabolic steroid therapy, protease inhibitor therapy (HIV), dysgammaglobulinemia
Elevated Triglycerides and VLDL	DM type 2, obesity, chronic kidney disease, high alcohol intake, hypothyroidism, thiazides, beta-blockers, corticosteroids, oral contraceptives/estrogen, pregnancy, protease inhibitors (HIV)

Clinical Manifestations

Feature	Clinical Significance
Xanthoma (tendon)	Achilles, elbow, knee. Strongly associated with familial hypercholesterolemia (very high LDL-C)
Xanthelasma	Yellowish plaques on eyelids. Can occur in normal lipid levels but raises suspicion for dyslipidemia
Arcus corneae	Lipid deposition at corneal periphery. In patients <45 years old, highly suggestive of familial hypercholesterolemia
Lipemia retinalis	Cream-colored retinal vessels. Indicates very high TG (≥500 mg/dL)
Eruptive xanthomas	Yellowish papules over trunk and extremities, associated with very high TG
Acute pancreatitis	Major complication of TG ≥500 mg/dL. The primary goal of treating severe hypertriglyceridemia is pancreatitis prevention, not cardiovascular prevention

3. Diagnostic Workup

Test	Role	Key Points
Fasting lipid profile (Total-C, LDL-C, HDL-C, TG)	Best initial test (Level I/C recommendation)	12-hour fast required for accurate TG and calculated LDL. Non-fasting Total-C and HDL-C are acceptable for initial screening
Friedewald formula	Calculates LDL-C	$\text{LDL-C} = \text{Total-C} - \text{HDL-C} - \frac{\text{TG}}{5}$ . Invalid when TG >400 mg/dL
Direct LDL-C measurement	Confirmatory when Friedewald is invalid	Order when non-fasting TG ≥400 mg/dL
Non-HDL Cholesterol	Secondary target (Level IIa/B)	$\text{Non-HDL-C} = \text{Total-C} - \text{HDL-C}$. Useful when TG 200-499 mg/dL, in DM, metabolic syndrome, CKD, or established CVD. Target = LDL target + 30 mg/dL
Apo B	Alternative marker (Level IIa/C)	Reflects total atherogenic particle concentration. Equivalent to non-HDL-C. More accurate with lower variability, especially with high TG
Lipoprotein(a)	Risk enhancer (Level IIa/C)	Consider in patients with family history of premature CVD or borderline risk between high and moderate
Framingham Risk Score	10-year CVD risk calculator	Uses age, sex, total cholesterol, HDL-C, systolic BP, treatment status, diabetes, smoking status. Classifies into low (<10%), intermediate (10-19%), high (≥20%)
Coronary Artery Calcium (CAC) Score	Risk reclassification tool	CAC = 0 indicates low risk (may defer statin). CAC ≥100 indicates >7.5% 10-year risk (supports statin initiation). Most useful in intermediate-risk patients where the decision to start statin is uncertain

The diagnostic approach begins with identifying who should be screened. Screening is indicated for all patients with cardiovascular disease manifestations or risk factors including: active smokers, diabetics, hypertensive patients, family history of premature CHD or hyperlipidemia, CKD, chronic inflammatory disease, central obesity (waist circumference >90 cm male / >80 cm female), obesity (BMI ≥25 for Asians), erectile dysfunction, evidence of atherosclerosis, males ≥40 years or postmenopausal females.

The fasting lipid profile (Total-C, LDL-C, HDL-C, TG) is the initial panel ordered in all patients. A 12-hour fast is required primarily because triglyceride levels are affected by recent food intake, and the Friedewald formula uses TG to calculate LDL-C.

A critical exam trap involves the Friedewald formula limitation: it cannot be used when TG exceeds 400 mg/dL, in Frederickson type III dyslipidemia, or in the presence of apo E2/E2 phenotype. When this formula is invalid, a direct LDL-C measurement must be ordered.

After the lipid profile is obtained, the next step is to calculate the patient's 10-year cardiovascular risk using tools such as the Framingham Risk Score, Pooled Cohort Equations, or SCORE. This risk stratification determines the patient's risk category and drives all subsequent treatment decisions, including LDL-C targets and statin intensity.

4. Management and Treatment

Non-Pharmacological Therapy

Intervention	Details
Physical activity	≥30 min moderate intensity, 4-6 times/week, ≥200 kcal/day expenditure. Brisk walking, cycling, swimming. Resistance training ≥2 days/week
Medical nutrition therapy	≥5 portions/day fruits and vegetables, ≥6 portions/day whole grains, limit saturated fat, trans fat, and dietary cholesterol. Plant stanols/sterols 2 g/day, soluble fiber 10-25 g/day
Smoking cessation	Cessation for ≥30 days significantly increases HDL-C
Weight reduction	Target BMI <25 kg/m2 (Asian criteria)
Reduce alcohol intake	Limit or eliminate alcohol consumption

Pharmacological Therapy Summary

Drug Class	LDL-C Effect	TG Effect	HDL-C Effect	Key Side Effects	Contraindications
Statin	↓ 18-55%	↓ 7-30%	↑ 5-15%	Myopathy, elevated liver enzymes	Absolute: acute/chronic liver disease. Relative: drug interactions
Ezetimibe	↓ 10-18%	Minimal	Minimal	Generally well tolerated	Liver disease, elevated liver enzymes
PCSK9 Inhibitor	↓ 48-71%	Minimal	Minimal	Injection site reaction, pharyngitis, myalgia	No long-term safety data beyond 3 years
Fibrate	↓ 5-20%	↓ 20-50%	↑ 10-20%	Dyspepsia, gallstones, myopathy	Severe renal or hepatic disease
Bile Acid Sequestrant	↓ 15-30%	No change / may increase	↑ 3-5%	GI disturbance, constipation, decreased absorption of other drugs	Dysbetalipoproteinemia, TG >400 mg/dL
Nicotinic Acid (Niacin)	↓ 5-25%	↓ 20-50%	↑ 15-35%	Flushing, hyperglycemia, hyperuricemia, hepatotoxicity	Chronic liver disease, severe gout
Omega-3 Fatty Acids	Minimal (may ↑ LDL)	↓ 27-45%	Minimal	Prolonged bleeding time, GI disturbance	Anticoagulant therapy, hepatic dysfunction

Statin Classification by Intensity

Intensity	Expected LDL-C Reduction	Examples
High	≥50%	Atorvastatin 40-80 mg, Rosuvastatin 20-40 mg
Moderate	30% to <50%	Atorvastatin 10-20 mg, Rosuvastatin 5-10 mg, Simvastatin 20-40 mg, Pravastatin 40-80 mg, Pitavastatin 1-4 mg
Low	<30%	Simvastatin 10 mg, Pravastatin 10-20 mg, Lovastatin 20 mg, Fluvastatin 20-40 mg

Risk Categories and LDL-C Targets (PERKENI 2021 / AACE 2017)

Risk Category	Criteria	LDL-C Target	Non-HDL-C Target	Apo B Target
Extreme	Progressive CVD despite LDL <70, clinical CVD + DM or CKD 3-4 or familial hypercholesterolemia, premature CVD (M<55, F<65)	<55 mg/dL	<80 mg/dL	<70 mg/dL
Very High	Clinical CAD/carotid disease/PAD, 10-yr risk >20%, DM or CKD 3-4 + ≥1 other risk factor, familial hypercholesterolemia	<70 mg/dL	<100 mg/dL	<80 mg/dL
High	≥2 risk factors + 10-yr risk 10-20%, DM or CKD 3-4 without other risk factors	<100 mg/dL	<130 mg/dL	<90 mg/dL
Moderate	≤2 risk factors + 10-yr risk <10%	<100 mg/dL	<130 mg/dL	<90 mg/dL
Low	0 risk factors	<130 mg/dL	<160 mg/dL	Not required

Treatment Algorithms: Alur 1 (ATP III) vs Alur 2 (ACC/AHA 2018)

These are the two clinical pathways recommended by PERKENI 2021 for managing dyslipidemia in Indonesia. Alur 1 adapts the NCEP-ATP III framework and remains relevant for resource-limited settings across the Indonesian archipelago. Alur 2 follows the ACC/AHA 2018 guideline and is considered an alternative for urban populations and patients with adequate access to advanced diagnostic and therapeutic modalities.

ALUR 1: NCEP-ATP III Pathway

This algorithm is target-driven: it assigns a numerical LDL-C goal based on the patient's risk category.

Risk Category	Criteria	LDL-C Target	Start Statin When
Very High Risk	CHD + multiple risk factors (especially diabetes) and/or inadequate risk factor control (e.g., still smoking) and/or metabolic syndrome features	<70 mg/dL	Immediately, regardless of LDL-C level
High Risk	CHD or CHD risk equivalent (carotid artery disease, PAD, abdominal aortic aneurysm) without additional high-risk multipliers	<100 mg/dL	LDL-C ≥130 mg/dL (optional at 100-129 mg/dL)
Moderately High Risk	No CHD/equivalent, >2 major risk factors, Framingham 10-year risk 10-20%	<130 mg/dL	LDL-C ≥130 mg/dL
Moderate Risk	No CHD/equivalent, 2 major risk factors, Framingham 10-year risk <10%	<130 mg/dL	LDL-C ≥160 mg/dL
Low Risk	No CHD/equivalent, 0-1 major risk factor	<160 mg/dL	LDL-C ≥190 mg/dL

CHD and CHD Risk Equivalents

Category	Conditions
CHD (Coronary Heart Disease)	Acute coronary syndrome, history of myocardial infarction, stable/unstable angina, coronary revascularization (PCI or CABG)
CHD Risk Equivalents	Symptomatic carotid artery disease, peripheral arterial disease (PAD), abdominal aortic aneurysm, diabetes mellitus

Table 2: Major Risk Factors (Other Than LDL-C)

Risk Factor	Definition
Smoking	Active smoker
Hypertension	BP ≥140/90 mmHg or currently on antihypertensive therapy
Low HDL-C	HDL-C <40 mg/dL
Family history of premature CHD	First-degree relative with CHD: male <55 years or female <65 years
Age	Male ≥45 years or female ≥55 years

ALUR 2: ACC/AHA 2018 Pathway

This algorithm is intensity-driven with a hybrid approach: it groups patients into four clinical categories, prescribes statin intensity accordingly, and introduces LDL-C thresholds (≥70 mg/dL) as triggers for adding non-statin agents in very high-risk patients. This represents a departure from ACC/AHA 2013, which had no numerical LDL-C targets at all.

Group 1: Clinical ASCVD (Secondary Prevention)

This includes patients with a history of ACS, MI, stable/unstable angina, coronary revascularization, stroke, TIA, or PAD (including aortic aneurysm).

For patients ≤75 years: start high-intensity statin aiming for ≥50% LDL-C reduction. If high-intensity statin is contraindicated or not tolerated, use moderate-intensity statin targeting 30-49% reduction.

Within this group, further stratify into very high ASCVD risk if the patient has: history of multiple major ASCVD events, or one major ASCVD event plus multiple high-risk conditions. For these very high-risk patients, if LDL-C remains ≥70 mg/dL on maximally tolerated statin, add ezetimibe. If LDL-C is still ≥70 mg/dL or non-HDL-C ≥100 mg/dL after statin + ezetimibe, consider adding a PCSK9 inhibitor after discussing the benefits, risks, and costs with the patient.

For patients >75 years: initiate or continue moderate-to-high intensity statin after evaluating benefits versus risks of side effects and drug interactions. If LDL-C ≥70 mg/dL on maximally tolerated statin, add ezetimibe.

For patients with heart failure and reduced ejection fraction due to ischemic heart disease, with a life expectancy of 3-5 years: consider moderate-intensity statin.

Group 2: Severe Hypercholesterolemia (LDL-C ≥190 mg/dL)

For patients aged 20-75 years: start maximally tolerated high-intensity statin. If LDL-C reduction is <50% or LDL-C remains ≥100 mg/dL, add ezetimibe. If still inadequate, add bile acid sequestrant (provided TG ≤300 mg/dL).

Consider PCSK9 inhibitor in two scenarios: (a) Heterozygous familial hypercholesterolemia, age 30-75, LDL-C remains ≥100 mg/dL despite maximally tolerated statin + ezetimibe. (b) Age 40-75, baseline LDL-C ≥220 mg/dL, and LDL-C remains ≥130 mg/dL despite maximally tolerated statin + ezetimibe.

Group 3: Diabetes Mellitus (Age 40-75 years)

Start moderate-intensity statin regardless of baseline lipid levels, without needing a 10-year risk calculation. If the patient has multiple risk factors, upgrade to high-intensity statin aiming for ≥50% LDL-C reduction. If 10-year ASCVD risk is ≥20%, add ezetimibe when LDL-C target is not met on maximally tolerated statin.

For DM patients aged 20-39: statin is not routinely recommended unless risk enhancers are present (DM duration ≥10 years for type 2 or ≥20 years for type 1, albuminuria ≥30 mcg/mg, GFR <60, retinopathy, neuropathy, ABI <0.9).

For DM patients with established CVD: target LDL-C <70 mg/dL. If not achieved with high-intensity statin, add ezetimibe or consider PCSK9 inhibitor.

For DM patients aged >75: continue statin if already on therapy.

Group 4: Primary Prevention (No ASCVD, No DM, LDL-C 70-189 mg/dL)

For patients aged 40-75: calculate 10-year ASCVD risk.

10-Year Risk	Category	Statin Recommendation
≥20%	High risk	High-intensity statin
7.5% to <20%	Intermediate risk	Moderate-intensity statin. Evaluate risk enhancers. Consider CAC scoring if decision remains uncertain
5% to <7.5%	Borderline risk	Evaluate risk enhancers. Consider moderate-intensity statin if risk enhancers are present
<5%	Low risk	Lifestyle modification. Periodic risk reassessment

The risk enhancers that favor statin initiation include: family history of premature ASCVD, primary hypercholesterolemia (LDL-C 160-189 mg/dL), metabolic syndrome, CKD, chronic inflammatory conditions (RA, psoriasis, HIV/AIDS), premature menopause (<40 years), preeclampsia history, persistent hypertriglyceridemia (≥175 mg/dL), hs-CRP ≥2 mg/dL, elevated Lp(a), apo B ≥130 mg/dL, and ABI <0.9.

The CAC score is used when the risk calculation places the patient in an ambiguous zone: if CAC = 0, statin can reasonably be deferred; if CAC ≥100, the 10-year risk exceeds 7.5% and statin initiation is appropriate.

For patients aged 20-39: prioritize lifestyle modification. Pharmacotherapy is selective, only for those with LDL-C ≥160 mg/dL (moderately high) or ≥190 mg/dL (very high).

For patients aged >75: evidence from RCTs is limited. The decision to initiate or continue statin is made through shared decision-making between patient and clinician.

Monitoring

Parameter	Timing	Action Threshold
Lipid profile	Before therapy, every 4-12 weeks until target is reached, then annually	Adjust statin dose or add agents based on LDL-C target achievement
SGPT (ALT)	Before therapy, then once at weeks 8-12	If <3x ULN: continue therapy, recheck at weeks 4-6. If >3x ULN: stop/reduce dose, recheck at weeks 4-6
CK	Before therapy only. Repeat only if myalgia is reported	Do not start if CK >4x ULN. If CK >10x ULN: stop statin, check renal function, recheck CK every 2 weeks
HbA1c	Regularly in patients at risk for diabetes	Long-term statin therapy increases diabetes risk, especially in patients with obesity, metabolic syndrome, elderly, or insulin resistance

5. Differential Diagnosis and Distractors

Diagnosis	Why It Is Similar	Key Discriminator
Hypothyroidism	Causes elevated total cholesterol and LDL-C, may present with fatigue and weight gain	Check TSH. Hypothyroidism is a secondary cause; treating it with levothyroxine corrects the dyslipidemia. Look for cold intolerance, constipation, delayed DTR relaxation phase
Nephrotic syndrome	Causes severe hypercholesterolemia (elevated total-C, LDL-C, and TG)	Look for proteinuria >3.5 g/day, hypoalbuminemia, peripheral edema. The dyslipidemia is secondary to increased hepatic lipoprotein synthesis driven by hypoalbuminemia
Metabolic syndrome	Overlapping features: central obesity, hypertriglyceridemia, low HDL-C, hypertension, hyperglycemia	Metabolic syndrome is a cluster of risk factors, not a single lipid diagnosis. Requires ≥3 of 5 criteria. Dyslipidemia is one component, not the entire picture
Familial hypercholesterolemia (FH)	Very high LDL-C (often ≥190 mg/dL), premature CVD	Tendon xanthoma (especially Achilles), arcus corneae at age <45, family history of premature CHD in first-degree relatives. Homozygous FH presents in childhood with LDL-C >500 mg/dL
Pancreatitis from hypertriglyceridemia	Presents with severe epigastric pain, may be confused with biliary or peptic disease	TG ≥500 mg/dL with lipemia retinalis or milky-appearing plasma. The pancreatitis is a direct consequence of severely elevated TG, and the primary treatment goal is lowering TG to prevent recurrence, not lowering LDL-C
Cholestatic liver disease (e.g., primary biliary cirrhosis)	Markedly elevated total cholesterol and LDL-C	Elevated alkaline phosphatase and GGT, jaundice, pruritus, positive antimitochondrial antibodies (AMA). Dyslipidemia resolves with treatment of underlying cholestasis

6. Traps and High-Yield Pearls

The most common way students lose points on dyslipidemia questions is by failing to connect the patient's risk category to the correct LDL-C target and statin intensity. Test-writers frequently construct vignettes where the lipid values alone appear borderline, but the presence of diabetes, CKD, or established CVD dramatically changes the management. For instance, a patient with LDL-C of 110 mg/dL would not need pharmacotherapy in the low-risk category (target <160), but the same value in a patient with diabetes and established CHD (extreme risk, target <55) demands aggressive statin therapy and potentially add-on ezetimibe or a PCSK9 inhibitor.

Another classic trap involves the Friedewald formula. Exam vignettes will deliberately present a patient with TG >400 mg/dL and then ask for the next step. The correct answer is to order a direct LDL-C measurement, not to apply the formula. Students who calculate LDL-C using Friedewald in this setting will get an inaccurate value and choose the wrong management.

Watch for vignettes presenting very high triglycerides (≥500 mg/dL) with epigastric pain. The primary concern is pancreatitis prevention, and the first-line drug is a fibrate, not a statin. However, if the question asks about long-term cardiovascular risk reduction in a patient with elevated TG and high cardiovascular risk, the answer shifts back to statin as first-line.

Remember that statin is contraindicated in pregnancy and breastfeeding. A question featuring a woman of reproductive age on statin therapy who is now planning pregnancy should prompt you to select discontinuation of statin 1-2 months before conception.

For the monitoring section, a frequently tested scenario is a patient on statin who develops myalgia with CK elevation. If CK is <4x ULN, continue therapy with monitoring. If CK is >10x ULN, stop statin immediately and evaluate for rhabdomyolysis (check renal function). Do not confuse routine CK monitoring (not recommended) with symptom-driven CK testing (only when the patient reports muscle complaints).

Finally, the distinction between Alur 1 and Alur 2 is itself testable in the Indonesian licensing exam context. Alur 1 (ATP III) is a target-driven model where each risk category has a defined LDL-C number to achieve. Alur 2 (ACC/AHA 2018) is an intensity-driven model that prioritizes statin potency classification (high vs. moderate vs. low intensity) and introduces the concept of add-on non-statin therapy (ezetimibe, then PCSK9 inhibitor) specifically for very high-risk patients who fail to reach LDL-C <70 mg/dL on maximally tolerated statin. When the exam presents a patient with ASCVD who remains at LDL-C 85 mg/dL on atorvastatin 80 mg, the next best step is to add ezetimibe, not to switch statins or increase the dose further.

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