CardioAdvocate
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“What’s Your ApoB?”

Dr. Ian Riddock, Brett Stoddard •
A Practical Approach to Lipid Management (Hint: “It’s the particles, stupid”)
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Case Presentations: Lipid Phenotypes

Patient A: The Repeat Offender (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.

CardiAwarness.com Advocate: 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 (true personal story): 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.

CardiAwareness.com Advocate Checklist:

Non-HDL-C

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