Today, I review, link to, and excerpt from The Curbsiders‘ “518: Cardiology Meets Longevity”.*

*Wurtz PJ, Katz G, Williams PN, Watto MF.  “Cardiology Meets Longevity.” The Curbsiders Internal Medicine Podcast. thecurbsiders.com/category/curbsiders-podcast March 23, 2026.

All that follows is from the above resource.

Transcript available via YouTube

Metabolic Health, Advanced Lipidology, and Preventing ASCVD

Level up your primary prevention game. Learn when ApoB, Lp(a), and CAC actually change management, how to spot cardiometabolic risk before diabetes declares itself, and how to make smarter lipid decisions beyond the standard panel. We’re joined by Dr. Greg Katz, cardiologist and prevention expert at NYU Langone Health.

Show Segments

• Intro
• Primary Prevention & Metabolic Syndrome (Case 1)
• Beyond the Standard Lipid Panel
• When to Order ApoB
• How Lp(a) Changes Management (Case 2)
• Using CAC/CCTA in the Gray Zone
• Recognizing Early Cardiometabolic Risk
• CGMs, Wearables, and Signal vs Noise (Case 3)
• How to Talk to Patients About Risk
• Take-Home Points

Dr. Katz reports no relevant financial disclosures. The Curbsiders report no relevant financial disclosures.

Cardiology Meets Longevity Pearls

1. ApoB is most useful when the standard lipid panel may be lying to you. In patients with high triglycerides, insulin resistance, central adiposity, or metabolic syndrome, LDL-C can underestimate atherogenic particle burden; when LDL-C and ApoB are discordant, risk generally tracks more closely with ApoB.
2. Lp(a) is not a niche test anymore. A one-time Lp(a) level is worth ordering in all adults, especially those with premature ASCVD, strong family history, unexpectedly severe disease, or risk that seems out of proportion to traditional markers.
3. An elevated Lp(a) usually changes management indirectly, not directly. You usually are not treating the Lp(a) itself yet; you are using it to justify more aggressive treatment of the modifiable parts of risk such as LDL-C, blood pressure, weight, and lifestyle, among others.
4. Coronary artery calcium (CAC) is a decision tool. CAC is most helpful when you are on the fence about starting or intensifying lipid-lowering therapy in primary prevention.
5. Do not order CAC unless you know how the result will change management. The test is most valuable in common gray-zone patients, not when the answer is already obvious from the clinical picture.
6. Coronary CTA and CAC are not interchangeable. CAC is generally the better tool for asymptomatic risk refinement in primary prevention, whereas coronary CTA is more useful when you are evaluating symptoms or need more detailed anatomic plaque information.
7. A normal A1c does not rule out important cardiometabolic risk. Rising triglycerides, low HDL, abdominal adiposity, MASLD, hypertension, sleep apnea, and creeping glucose can all signal insulin resistance *and elevated future risk before diabetes is formally present. *Google Search
8. The triglyceride-HDL pattern can be a practical clue to metabolic dysfunction. It should not be overinterpreted as a stand-alone diagnosis, but it can help identify patients whose risk is being underestimated by a routine lab review. Clinical validation for these markers is not uniform across all racial and ethnic groups. Clinicians should remain cognizant of these limitations, as the predictive accuracy of specific tools can fluctuate significantly depending on a patient’s background.
9. Statins are still the anchor of primary prevention, even in the era of advanced biomarkers and GLP-1 therapy. Adjunctive medications (ezetimibe, PCSK9 inhibitors) can be added as necessary for statin intolerance, or if further risk lowering is warranted / desired.
10. Risk calculators are starting points, not final answers. Younger patients with strong family history, elevated Lp(a), metabolic dysfunction, or other risk-enhancing features may be higher risk than a pooled calculator suggests, so prevention decisions still require judgment.

Cardiology Meets Longevity 

Primary Prevention for Cardiovascular Disease

Dr. Katz discusses that the trajectory toward a major cardiovascular event often begins decades before the first symptom of angina or the sudden onset of a myocardial infarction. Many patients present with overt signs of metabolic dysfunction, such as abdominal obesity, borderline hypertension, or impaired fasting glucose, that serve as precursors to atherosclerotic cardiovascular disease (ASCVD). The primary goal of prevention is to intervene during this prolonged subclinical phase to alter the patient’s lifetime risk trajectory. Metabolic syndrome, abdominal obesity, hypertension, insulin resistance, dyslipidemia, MASLD, obstructive sleep apnea, and chronic kidney disease often travel together and compound risk over time. The clinical task is not only to estimate risk, but to identify which risk drivers are modifiable and which tools a given patient is actually willing to use. A central tenet of the modern preventive approach is focusing on modifiable risk factors (expert opinion). While a patient cannot control their genetic heritage or the health of their parents, they can exert significant control over the “compound effect” of multiple risk factors over time. Dr. Katz mentions that a reasonable approach to these modifiable risk factors is trying to figure out exactly how “medicalized” a patient wants to be. There are lots of “tools in the toolbelt,” so to speak, but some patients may prefer lifestyle modification first, some may prefer medications up front, and some may prefer some combination of both. Shared decision making and learning about the patient’s goals is an essential first step when partnering together towards a common goal. Remember the human side of medicine, because that’s what matters here. Patients may not have many traditional “medical conditions” at this stage, so the primary focus of the visit can be about understanding dietary patterns, exercise barriers, understanding their sleep and stress patterns, etc. (expert opinion).

Metabolic Syndrome and Cardiometabolic Risk

What is Metabolic Syndrome?

Metabolic syndrome refers to a cluster of cardiometabolic abnormalities that tend to occur together and raise risk for cardiovascular disease, diabetes, and other downstream complications. Common components include elevated waist circumference, high triglycerides, low high-density lipoprotein (HDL) cholesterol, elevated blood pressure, and elevated glucose (Swarup 2024).

Metabolic dysfunction is better understood as a spectrum than a strict binary state. Patients may show early warning signs such as rising triglycerides, lower HDL, rising fasting insulin/glucose, metabolic associated fatty liver disease, or increasing waist size years before formal diabetes develops (Mechanick 2020, expert opinion).

The traditional diagnosis of metabolic syndrome requires the presence of 3 or more metabolic abnormalities (Swarup 2024):

• A waist circumference of more than 40 inches in men and 35 inches in women
• Serum triglycerides level of 150 mg/dL or greater
• Reduced HDL cholesterol, less than 40 mg/dL in men or less than 50 mg/dL in women
• Elevated fasting glucose of l00 mg/dL or greater
• Blood pressure values of systolic 130 mm Hg or higher or diastolic 85 mm Hg or higher

However, it is more helpful to think about any of these factors as red flags towards an increased cardiometabolic risk rather than a binary state of either having metabolic syndrome or not (expert opinion).

Lifestyle Matters

Advanced biomarkers never replace the foundation of lifestyle. Nutritional quality, physical activity, weight management, restorative sleep, and blood pressure control—including the treatment of sleep apnea—remain the bedrock of cardiovascular prevention. Guidelines explicitly emphasize a healthy lifestyle across the lifespan, reinforcing exercise and consistent activity as core therapy (Arnett 2019).

Lifestyle modification can dramatically improve modifiable risk, but it does not erase inherited risk. Patients with a striking family history or markedly elevated Lp(a) may still warrant aggressive preventive measures even when they appear clinically “healthy” (Reyes-Soffer 2022).

Lipids, Atherogenesis, and Metabolic Health

Atherosclerosis starts when cholesterol-carrying particles get into the walls of blood vessels, trigger inflammation, and gradually build plaque. The key idea is that cholesterol cannot move through the bloodstream on its own, so it has to be carried by lipoprotein particles (Nurmohamed 2021).

That is where ApoB comes in. ApoB is the main protein attached to every major atherogenic particle,  including LDL, VLDL, IDL, and Lp(a), so it gives you a direct sense of how many plaque-forming particles are actually circulating (Ference 2018, Sniderman 2019).

Dr. Katz gives us a helpful framework. If you think about traffic: LDL-C tells you how many passengers are traveling, while ApoB tells you how many cars are on the road. And if traffic is what causes the damage, the number of cars is often a much better way to estimate risk.