What’s Your ApoB?

Written By Ian Riddock

Case Presentations: Lipid Phenotypes

Patient A: Cheating Death: The Heart Attack Survivor

Cardiologist: “Your LDL-C isn’t too bad at 92 mg/dL and after your heart attack we put you on the highest dose of atorvastatin 80 mg which is what is recommended in the guidelines.


CardiAdvocate.com: Not true. Those were older controversial guidelines (2018 ACC/AHA Cholesterol Guidelines) which de-emphasized LDL-C goals and set the preventive community back a decade! Newer guidelines recommend additional non-statin therapies in such high risk patients. Newer international guidelines emphasize even lower LDL-C goals. See Follow the Leader - A Statement About Lipid Guidelines.


Advocating for Change:

  1. Remember who we consider our highest risk patients

  2. Have a patient-centered discussion focusing on risk, benefit, cost of therapy balanced against cost of another ASCVD event. 

  3. Remember, it’s a person, not a population.

  4. Use multiple guidelines

  5. Use expert consensus documents

  6. Consider expert white papers and “calls to action”

Patient B: Atherogenic Triad:

Provider: “Your LDL-C is very low - this is fantastic!”

Patient: “But my triglycerides (TG) are high, what do you recommend?”

Provider: “We really only treat the LDL-C, which is low in you. But you can work on diet and exercise if you want to get your triglycerides down”


The CardiAwareness.com Advocate: Not true. 

When TG’s are elevated (> 150 mg/dL), we need to be focusing on non-HDL-C, or better yet, Apo B. This has been in the guidelines for decades, but rarely performed. 


Advocating for Change: 

  1. Pay attention to triglycerides when scanning the lipid profile.

  2. Use the proper lipid biomarkers: non-HDL-C, Apo B. 

  3. TG’s and HDL-C are not targets, per se, but the presence of high TG’s and low HDL-C should alert us to use the preferred biomarkers of non-HDL-C and Apo B.

Patient C: Hiding in Plain Site - Familial Hypercholesterolemia

Patient: “I’ve had high cholesterol since I was 20 and nothing ever works. It runs in my family”

Cardiologist: “Well, you’re 40 now and we’ve tried a couple of statins over the years and they don’t seem to be doing much, so let’s just stop and focus on diet and exercise”

Patient: “What about those newer drugs.”

Cardiologist: “They’re expensive and if the statins didn’t work, it’s probably just your genetics.”


The CardiAwareness.com Advocate: Yikes. Run. Familial Hypercholesterolemia (FH) is caused by a genetic defect that most commonly impacts the LDL receptor (LDLR gene). Most lipid lowering drugs like statins, ezetimibe, PCSK9 inhibitors and bempedoic acid ultimately work by upregulating LDL receptors, which then clear LDL from plasma. Patients with high LDL-C who do not respond as expected to therapies that increase LDL receptors should raise suspicion for an underlying genetic condition affecting LDL receptors, such as FH. It’s not that uncommon, 1 in 250 people.


Advocating for Change: 

  1. It’s not ok to dismiss high LDL-C in the family as “well, that’s just you.”

  2. It’s not ok to identify someone with high LDL-C at a young age and allow them to drift through the decades untreated.

  3. It’s not ok to declare a less than desired response to statins as futile and give up on the patient. Especially in the modern era of robust non-statin therapies.

  4. The opportunity was not only missed on this patient, but their family members, by failing to perform cascade screening. 


Patient D:  Too Much of a GOOD Thing - Dysfunctional HDL


Lousy Cholesterol (LDL-C) is high, but so is your Healthy Cholesterol (HDL-C), so your RATIO is perfect!”

Patient: “So my GOOD cholesterol makes up for my BAD cholesterol?

Provider: “That’s right, let’s just keep an eye on it for now”


The CardiAwareness.com Advocate: Not true. 

Levels of HDL-C tell us nothing about HDL functionality. Higher levels of LDL-C increase the risk of atherosclerosis, even if HDL-C is high.


Advocating for Change: 

  1. Stop using terms like Healthy or Good cholesterol to describe HDL-C. There is no such thing. It is not only erroneous, but dangerous. The truth is, we don’t know how HDL is performing based upon HDL-C levels. High levels could be a bad thing. Low levels could be a good thing. 

  2. Stop using ratios. It’s lazy, misleading and wrong, particularly when including HDL-C (see above).

  3. Until we get a functional assay for HDL, we just don’t know what a particular HDL-C concentration means.




Flying Under the Radar


The above lipid “phenotypes” are all examples of patients who are routinely missed everyday in the clinic. 


If the frontline provider (PCP) doesn’t understand the lipid panel, the screening process for ASCVD risk falls apart. But if the PCP does their part and appropriately recognizes the problem and then refers the patient to a specialist, such as a cardiologist, who doesn’t understand lipids, we’re in real trouble. At that point, the patient may feel they have nowhere left to go, or are never the wiser that they remain at heightened risk for the #1 killer amongst us. They may feel reassured by the specialist, never questioning their advice and spend many years undertreated.



CardiAdvocate.com Checklist:

  • Obtain a lipid panel

  • Which lipid biomarkers matter most for ASCVD risk assessment?

    • We evaluate NonHDL-C (Total Cholesterol minus HDL-C), LDL-C, ApoB, Lp(a), TG and HDL-C (kinda in that order)

      • It’s prioritized based upon the biomarker’s significance to the pathogenesis of atherosclerosis, availability, superiority in accurately reflecting atherogenic particles, pragmatism, cost and insurance requirements

      • Non-HDL-C and ApoB best reflect causal atherogenic particles and can always be done nonfasting!

      • LDL-C when compared to non-HDL-C (the delta) gives us a clue about the existence of “discordance”

        • Non-HDL-C should not deviate by > 30 mg/dL from LDL-C

          • Some say 15-20 mg/dL, particularly with lower values

          • The higher the delta the greater the discordance to LDL particles (ApoB)

            • The greater the likelihood of high amounts of sdLDL-P (small dense LDL particles)

              • But ALL LDL-P sizes are still bad

              • It’s just high sdLDL-P are less likely to be recognized by LDL-C/non-HDL-C  measurements

    • Non-HDL-C

      • NLA Classification: 

        • ≥ 220 mg/dL - Very High 

        • Lab should flag as “Severe hypercholesterolemia” in all

          • Rule out genetic disorders, particularly Familial Hypercholesterolemia (link to FH topic)

        • 190-219 mg/dL - High

        • Lab should flag as “Severe hypercholesterolemia” in children

        • 160-189 mg/dL - Borderline High 

        • 130-159 mg/dL - Above Desirable

        • < 129 - Desirable


  • NLA declares this a superior biomarker to LDL-C

  • More predictive of ASCVD events than LDL-C

  • When LDL-C and NonHDL-C don’t agree (discordance), risk better follows non-HDL-C 

  • Has been recommended over LDL-C when TG > 200 mg/dL (now we say 150 mg/dL) as far back as 2001 NCEP/ATP III Report on High Blood Cholesterol issued by NHLBI (NIH)

    • Seldom followed in clinical practice

  • Reflects LDL-C + other atherogenic cholesterol, mainly VLDL-C

  • Despite recommendations, many labs don’t list Non-HDL-C in report

  • If not listed, can be manually calculated (TC - HDL-C), but nobody likes to do math in a busy clinic

    • If your lab doesn’t list NonHDL-C, request that they do - it’s not hard

  • Comes “free” in standard Lipid panel - but this isn’t helpful if the lab doesn’t list it, or the provider doesn’t calculate it or know what it means

  • No fasting required. Let’s repeat that again – No fasting required

  • So why do we continue to use LDL-C? Great question. Mostly because it’s cheap, available, standardized (?), and let’s face it - would probably cause mass hysteria if we replaced it overnight. LDL-C works pretty well. But we do have better tools. Only YOU can advocate for better.

  • LDL-C

    • NLA Classification:

      • ≥ 190 mg/dL - Very high

      • Lab should flag as “Severe hypercholesterolemia”

      • 160-189 mg/dL - High

        • ASCVD Risk Enhancer in adults - may consider initiation of statin therapy

        • Lab should flag as “Severe hypercholesterolemia” in children

        • Rule out genetic disorders, particularly Familial Hypercholesterolemia in children

      • 130-159 mg/dL - Borderline high 

      • 100-129 mg/dL - Above desirable 

      • < 100 mg/dL - Desirable 

    • LDL-C: most commonly used biomarker due to availability, familiarity and legacy. Calculated metric. Usually not directly measured.

      • A surrogate for LDL particles

      • Friedewald equation no longer the preferred way to calculate LDL-C but remains most common

      • Hopkins-Martin or NIH are the preferred equations

        • If LDL-C not being calculated using above, ask your lab to change

      • Less accurate if TGs > 150 mg/dL

      • The higher the TGs, the worse LDL-C performs (discordance)

    • The more LDL-C is lowered (< 70 mg/dL), the less accurately it reflects LDL particles and ApoB

  • ApoB (Apolipoprotein B)

    • > 130 mg/dL - ASCVD Risk Enhancer 

    • May be used as the preferred biomarker for all patients with high TG, diabetes, obesity, metabolic syndrome or “very low LDL-C” for screening, diagnosis, risk management (Ia ESC/EAS) 

    • No fasting required

    • NLA declares ApoB an “optional secondary target” for all

      • More predictive than LDL-C

      • Didn’t feel ApoB consistently outperformed Non-HDL-C

      • May account for residual risk when LDL-C and nonHDL-C goals attained yet ApoB remains elevated 

    • Many lipidologists and preventive cardiologists feel ApoB is the superior biomarker for risk assessment and treatment 

  • Lp(a): Lipoprotein a, or “Lp(a)” (pronounced Lp “little a”) 

    • Another lipoprotein that is causal to atherosclerosis

      • 85-90% genetically imparted

      • 1 in 5 have levels > 125 nmol/L or > 50 mg/dL, which impart greater risk of ASCVD

        • Makes this the most common genetic lipid disorder increasing ASCVD risk

      • We want to know who these carriers are

    • Lp(a) levels in mg/dL or nmol/L (preferred)

      • < 30 mg/dL or 75 nmol/L = low risk

      • 30-50 mg/dL or 75-125 nmol/L = gray area

      • > 50 mg/dL or 125 nmol/L = high risk

    • When elevated, may opt for more intense treatment of LDL-C and stricter adherence to optimal lifestyle measures

    • When to check Lipoprotein a, or “Lp(a)” (pronounced Lp “little a”): 

      • Every adult at least once in their lifetime - ESC/EAS, Canadian Cardiovascular Society (2021 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in Adults)

        • To screen for severely elevated Lp(a)

          • > 180 mg/dL or 430 nmol/L = severely elevated risk 

            • Represents similar risk to those with Heterozygous Familial Hypercholesterolemia (25 x higher risk of ASCVD event). IIa recommendation by ESC/EAS to screen everyone at least once for this risk. 

            • Recent paper suggests ~325-350 nmol/L may actually impart this risk

      • Other Recommendations (AACE/ACE)

        • Family History of premature ASCVD or elevated Lp(a)

        • Patients with premature ASCVD or recurrent events despite LDL-C lowering

  • If Lp(a) is elevated, patients are encouraged to inform first degree family members so they may be screened and begin preventive measures as early in life as possible. 

  • LDL-P

    • ApoB is preferred over LDL-P

    • If already obtained or patient requests it, we will utilized this biomarker

    • LDL-P goals: 

      • Multiple LDL-C x 10 and that’s the goal (i.e. LDL-C goal < 70 mg/dL = LDL-P < 700 nmol/L)

    • In general, can be used in place of ApoB to account for discordance or inaccuracies with LDL-C (residual risk) 

    • Should reflect and be concordant with ApoB, but not always the case

      • In our experience, LDL-P is not as well standardized as ApoB. We have observed not too infrequent cases of discordance between ApoB and LDL-P. 

    • ApoB/LDL-P discordance is a much more advanced and nuanced discussion with many gaps in knowledge. Use clinical judgment.

      • If ApoB > LDL-P, treat ApoB

      • If LDL-P > ApoB

        • Look for other cardiometabolic comorbidities (DM and dysglycemia, high TG, fatty liver, obesity) and treat

          • It may be prudent to consider more aggressive treatment of LDL-P

      • If no other cardiometabolic features present, consider LDL-P a false positive

    • Small dense LDL-P vs Large buoyant LDL-P (Hint: they’re all bad)

      • “Size Doesn’t Matter” - when it comes to LDL particles. They are all atherogenic.

      • No convincing data exists demonstrating increased atherogenicity to small dense LDL-P, once total LDL-particle number is accounted for

      • Measuring sub-particle fractions does not appear to provide additional clinical value apart from measuring ApoB, or total LDL-particle count

      • *Caveat - there may be some value in measuring advanced lipid subfractions in the individual with insulin resistance who has the “Pattern B” (old nomenclature for sdLDL-P) phenotype and is transitioning to a “Pattern A” (large buoyant LDL-P) through optimal treatment pathways and therefore providing some bit of “proof” of progress. 

  • Triglycerides (TG)

  • Not themselves known to be directly causal to atherosclerosis, though this continues to be investigated

    • NLA Classification

    • Look for and address associated comorbidities:

      • Obesity/Visceral adiposity

      • Dysglycemia

        • Diabetes

        • Prediabetes

      • NAFLD

      • CKD

      • Hypothyroidism

    • Evaluate for medications

      • Hydrochlorothiazide

      • Beta blockers (nonselective)

      • Corticosteroid

    • Lifestyle

      • Alcohol

      • Smoking

  • “Atherogenic triad”: High TG’s, low HDL-C, high sdLDL-P

    • Elevated TG’s should alert you to the high likelihood of elevated ApoB and discordance to LDL-C (lower LDL-C may be misleading)

      • Underestimates risk

      • Don’t use LDL-C

      • Use non-HDL-C

      • Use Apo B

  • If > 135 mg/dL and DM or ASCVD present, patient may benefit from icosapent ethyl (Vascepa)

    • Cost may be prohibitive

  • HDL-C

    • Never has been a target or goal of therapy in any cholesterol guideline

    • NLA Classification:

      • < 40 mg/dL (Men) - Low

      • < 50 mg/dL (Women) - Low

    • Used in many risk calculators (for better or worse)

    • If low, < 50 mg/dL female, < 40 mg/dL male

      • It’s a visual reminder (particularly if TG high), that one should think about metabolic syndrome and – once again, discordance

      • Consider other cardiometabolic diseases

        • Obesity

        • Dysglycemia

          • Diabetes

          • Prediabetes

        • NAFLD

        • CKD

        • Hypothyroidism

      • Consider lifestyle issues

        • Smoking

      • HDL-C tells us nothing about the functionality of HDL particles. For example:

        • Low HDL-C has been seen with highly efficient HDL, where HDL is so efficient at offloading cholesterol that the HDL-C concentration is low. 

          • Apo A-1 Milano. Founder effect genetic variant with very low HDL-C and associated with higher lifespan

        • Conversely, very high HDL-C may suggest dysfunctional HDL

          • HDL cannot offload cholesterol and hence the concentration (mg/dL) goes up

          • But that’s just a possibility, usually high HDL-C is a good thing

        • Until an HDL functional assay is developed, HDL-C or HDL-P will not be particularly helpful in lipid management

    • Stop saying “Good cholesterol”. It’s erroneous and potentially dangerous.

      • Giving out “points” for high HDL-C may underestimate risk

      • Women typically have high HDL-C than men - another example of missing the mark in assessing CV risk in women

      • Years (decades) of inaccurate public health messaging on this topic has lead to this. We’re trying to undo this.

  • Other Lipid metrics:

    • TC/HDL-C Ratios: Does not matter. Again, high HDL-C is not necessarily protective

      • Focus on LDL-C, Non-HDL-C and ApoB. That’s all you really need

        • In fact, if you just focused on Non-HDL-C or ApoB, you’d be doing great

Deeper Dive:


Far too many clinicians continue to struggle with the basic lipid panel. When the providers don’t understand it, it’s no surprise when patients are confused. In hindsight this is in large part due to poor teaching and public messaging over several decades. Unfortunately, medicine evolves this way sometimes. We learn from our mistakes and try to correct them. But when so entrenched in common practice, overcoming that clinical inertia requires widespread campaigning and advocacy. 


LDL-C is calculated, in most places using a Friedewald equation, which includes TGs.

There are better calculators such as “Martin-Hopkins” or “NIH”

Even a “direct” LDL-C is inaccurate when TGs are significantly elevated. You need to be looking at non-HDL-C when TG > 150 mg/dL. Perhaps even better, check an ApoB


What about small dense LDL vs big and fluffy LDL?

Short answer: they’re all atherogenic. Size doesn’t matter after accounting for the number of Apo B particles. “It’s the particles, stupid.”

How do various lipid drugs work?


Statins:

  • Inhibits HMG-CoA Reductase

  • Reduces hepatic synthesis of cholesterol

  • Depletes cholesterol pool in liver

  • Upregulates LDLR (LDL receptor) leading to increased clearance of LDL from plasma

  • May cause hyperabsorption of cholesterol through intestines 


Ezetimibe: 

  • NPC1-Like 1 protein inhibition

  • Reduces intestinal absorption of cholesterol

  • Reduces delivery of cholesterol to liver thereby depleting cholesterol pool

  • Upregulates LDLR leading to increased clearance of LDL from plasma


PCSK9i 

  • mAb binds with PCSK9

  • PCSK9 binds to LDL receptors, signaling degradation of the entire complex of Apo B particle and LDLR in the lysosome

  • Therefore PCSK9 inhibitors, reduces degradation of LDLR by preventing PCSK9 from attaching to LDLR and delivering it to the lysosome


Inclisiran (Leqvio) 

  • Small interfering messenger RNA (simRNA)

  • Prevents the manufacturing of the protein PCSK9i by inhibiting translation of mRNA in the cytoplasm

  • Select to the liver

  • Lack of PCSK9 in the liver allows for more LDLR to clear atherogenic particles (LDL)

  • No impact on DNA


Bempedoic Acid

  • Inhibits adenosine triphosphate-citrate lyase (ACL) which inhibits cholesterol synthesis

  • Reduces cholesterol pool in liver

  • Upregulates LDLR leading to increased clearance of LDL from plasma


EPA/DHA

  • Reduces hepatic production of VLDL

  • Increases postprandial activity of LPL


Lipid Blood Testing

  • Age of initial lipid testing

    • Beginning age 20 years old (ACC/AHA Class I)

    • Lipid panel by age 2

      • In children or adolescents with family history of early CVD or significant hypercholesterolemia, to rule out FH or other rare forms

      • Many experts argue that everyone should have a lipid panel by age 2

        • Little downside

        • Huge potential to miss devastating disease; leading to a shortened lifespan fraught with multiple preventable ASCVD events

    • Children/adolescents with obesity or other metabolic risk factors to rule out lipid disorders or metabolic syndrome

  • Repeat Testing

    • At least every 5 years

      • Or with any change in risk factors (NLA recommendation)

        • Weight gain

        • Co-morbidities

        • Secondary causes of dyslipidemia

        • Premature ASCVD events in 1st degree relatives

        • Other changes - clinical judgement

    • Lipid testing should be performed at 4-6 week intervals after each adjustment

  • 4 weeks is all it takes to see the maximal response to adjustments in therapyFasting is preferred (NLA recommendation) but not required

    • If non-fasting, use NonHDL-C -> not impacted by fasting state

      • ApoB also not impacted by fasting state

    • If non-fasting TG > 400 mg/dL, repeat lipid panel in fasting state (ACC/AHA Class I)

  • Nonfasting has many advantages

    • Patients traveling long ways

    • Already in the office and due for testing

      • Improves compliance with lab testing

      • Saves the patient another trip, gas expense etc



Lipid Goals:


It depends on risk. Below are examples of lipid goals based upon risk categories defined by various guidelines.  Please note, these guidelines are created by different organizations and they sometimes use different terms to classify risk. Other times they may use the same terms but define the risk differently. It’s confusing, but we attempt to break it down a bit.


Also, see Follow the Leader - A Statement About Lipid Guidelines


Extreme Risk: This is the terminology used by the joint Consensus Statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the Management of Dyslipidemia and Prevention of Cardiovascular Disease Algorithm – 2020 Executive Summary - ScienceDirect 

  • Progressive ASCVD including unstable angina

  • Established clinical ASCVD plus DM, CKD3 or HeFH


Very High Risk: This is the terminology used by the 2019 Joint European Society of Cardiology/European Atherosclerosis Society Dyslipidemia Guidelines (2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk | European Heart Journal | Oxford Academic) 

  • Recurrent events (more than 1)

  • Extensive atherosclerotic cardiovascular disease

  • Higher global cardiovascular risk scores.


  • LDL-C < 55 mg/dL and > 50% reduction from baseline 

    • (This is important: for example, if your LDL-C is 72 mg/dL at baseline, the goal would be < 36 mg/dL! 

    • It is not 69 mg/dL! Far too many clinicians mistakenly practice this way - based upon false beliefs that < 70 mg/dL is a goal, as recommended by ACC/AHA guidelines. It is not a goal, but rather a threshold to treat with high intensity (> 50% reduction of LDL-C). That's a huge difference!

    • It is the absolute LDL-C reduction determines the relative risk reduction

  • LDL-C < 40 mg/dL

    • Patients with ASCVD with another vascular event within 2 years (not necessarily the same type of event)


  • NonHDL-C < 80 mg/dL 

  • Apolipoprotein B (ApoB) < 70 (AACE/ACE)

    • < 50 mg/dL (Expert Opinion)

  • Triglycerides < 150 mg/dL


The 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

states that in Adults With Clinical ASCVD at Very High Risk on StatinTherapy for Secondary Prevention: 

“In view of the favorable net clinical benefit of the addition of nonstatin therapies in patients with clinical ASCVD at very high risk on high-intensity statin therapy and lifestyle management and the very low levels of LDL-C achieved in RCTs of nonstatin therapies, a lower LDL-C threshold of LDL-C ≥55 mg/dL (or non–HDL-C ≥85 mg/dL) is recommended by the writing committee. There is evidence from clinical trials that individuals who achieve LDL-C<55 mg/dL experience lower event rates than those with higher LDL-C”


Advanced Atherosclerosis (Expert Opinion): 


Very High Risk:

AACE/ACE 2020 Consensus Statement (Consensus Statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the Management of Dyslipidemia and Prevention of Cardiovascular Disease Algorithm – 2020 Executive Summary - ScienceDirect) 

  • Established clinical ASCVD or recent hospitalization for ACS, carotid, peripheral arterial disease, or 10 year risk > 20%

  • Diabetes with ≥ 1 risk factor

  • CKD ≥ 3 with albuminuria

  • HeFH

Or,

High Risk: 

2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk | European Heart Journal | Oxford Academic



High Risk: (AACE/ACE)

  • ≥ 2 Risk factors and 10 year risk 10-20%

  • DM or CKD ≥ 3 with no other risk factors


Lipid Goals

  • LDL-C < 100 mg/dL

  • nonHDL < 130 mg/dL 

  • ApoB < 90 mg/dL

  • TG < 150 mg/dL


Moderate Risk (AACE/ACE)

  • < 2 Risk Factors

  • 10 year risk < 10%


Lipid Goals 

  • LDL-C < 100 mg/dL

  • nonHDL < 130 mg/dL 

  • ApoB < 90 mg/dL

  • TG < 150 mg/dL


Low Risk (AACE/ACE)

  • No risk factors


Lipid Goals 

  • LDL-C < 130 mg/dL

  • nonHDL < 160 mg/dL 

  • TG < 150 mg/dL


All Patients:

  • Check Lipoprotein a, or “Lp(a)” (pronounced Lp “little a”) 

    • See Little Napoleon Complex - Lipoprotein (a)

    • If > 50 mg/dL or 125 nmol/L (2 different assays - nmol/L preferred), may opt for more intense treatment of  LDL-C and stricter adherence to optimal lifestyle measures

  • If Lp(a) is elevated, patients are encouraged to inform first degree family members so they may be screened and begin preventive measures as early in life as possible. 



Lipid Lowering Drug Therapy:

  • Acute Coronary Syndrome (presenting with) and LDL-C not at goal despite max statin and ezetimibe

    • PCSK9i initiated early, ideally while in hospital (Class IIa ESC/EAS)

    • Repeat lipids at 4-6 weeks after max statin + ezetimibe. If not at goal, add PCSK9i (Class I ESC/EAS)

Ian Riddock
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