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Personalized hyperlipidemia care strategies
Finding a New Rhythm in Hyperlipidemia Care: Personalized ASCVD Risk Reduction Strategies for Key Populations

Released: April 27, 2026

Pam R. Taub
Pam R. Taub, MD, FACC, FASPC
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Key Takeaways
  • In patients with dyslipidemia and discordant biomarkers and imaging findings, ASCVD risk should be managed according to the highest-risk parameter identified rather than a normal finding in one domain.
  • A CAC score of zero does not eliminate future ASCVD risk in patients with elevated LDL-C, elevated Lp(a), strong family history, or suspected noncalcified plaque, particularly in younger patients.
  • In patients with persistent residual ASCVD risk despite maximally tolerated statin therapy, healthcare professionals should identify the factors driving ongoing risk and personalize treatment accordingly, using coronary CT angiography—not serial CAC scoring—when repeat imaging is needed to assess plaque burden and treatment response.

In this commentary, Pam R. Taub, MD, FACC, FASPC, answers questions posed by healthcare professionals (HCPs) during a live symposium titled “Grooving Through Lipid Management: A New Rhythm in ASCVD Risk Reduction.” Learn about specific considerations for managing atherosclerotic cardiovascular disease risk (ASCVD) in patients with hyperlipidemia, including best practices for addressing discordant labs vs imaging results, personalizing treatment for key populations, and aligning your practice with current guideline recommendations.

How do you approach ASCVD risk assessment and management when patients’ imaging and biomarkers appear discordant? For example, lab results show elevated lipoprotein (a) (Lp[a]) levels, but there is little to no plaque on imaging.

The evidence base for managing discordant labs and imaging remains limited, which makes your clinical judgment particularly important. My general approach is to manage patients’ ASCVD risk based on the highest parameter identified. This is a safer approach than being falsely reassured by a normal finding in one domain.

For example, in patients with a coronary artery calcium (CAC) score of zero and significantly elevated Lp(a), I do not interpret the absence of calcified plaque as low risk. Lp(a) is an independent, genetically determined risk factor that operates through distinct pathophysiologic mechanisms, including the promotion of oxidized phospholipids, inflammation, and thrombosis, which may not be reflected in CAC scoring. This is particularly true among younger patients. Therefore, I would manage their elevated Lp(a) aggressively in accordance with current guidelines and emerging evidence.

Conversely, in patients with a high CAC score despite normal Lp(a), I would treat the burden of established atherosclerosis as the primary driver of risk and intensify preventive therapy accordingly. Regardless, larger prospective studies are needed to guide ASCVD risk management in precisely these patient case scenarios.

How should HCPs think about elevated low-density lipoprotein-cholesterol (LDL-C) in the setting of a CAC score of zero or minimal plaque burden on imaging, particularly among younger patients and those with a strong family history of premature ASCVD?

A CAC score of zero should not provide HCPs false reassurance in the setting of elevated LDL-C. CAC scoring only detects calcified plaque, whereas younger patients and those with a strong family history of premature ASCVD may harbor significant noncalcified and potentially vulnerable plaque that goes undetected. My approach in these patients is to manage their ASCVD risk based on the highest parameter present.

In patients where coronary CT angiography confirms the absence of both calcified and noncalcified plaque, I monitor them closely and consider repeat imaging in 3-5 years. Meanwhile, I will continue to aggressively address their modifiable risk factors. The key message: An absence of plaque today does not eliminate a future ASCVD risk in those with persistently elevated LDL-C and/or a compelling family history.

In asymptomatic patients with subclinical ASCVD identified via CAC or coronary CT angiography, when is repeat imaging appropriate and how should these findings influence ongoing risk management?

The approach to repeat imaging depends on the modality used and clinical question being asked. For CAC scoring, repeat imaging is generally not appropriate in patients who have already been evaluated. Lipid-lowering therapy like statins can paradoxically increase CAC scores through the calcification and stabilization of previously soft plaque. This makes serial CAC scoring an unreliable measure of treatment response in hyperlipidemia. A rising CAC score in treated patients does not necessarily indicate disease progression and should not be misinterpreted as therapeutic failure.

Coronary CT angiography, by contrast, is well-suited for monitoring treatment response because it characterizes both calcified and noncalcified plaque burden and composition. Emerging artificial intelligence (AI)–guided platforms provide sophisticated tools for quantifying and tracking plaque progression vs regression over time, offering a more granular and clinically actionable picture than CAC alone.

In practice, I use these imaging tools to guide the intensity of risk factor modification needed and reinforce the importance of adherence to lipid-lowering therapies and lifestyle modifications. Then, where available, I incorporate AI-assisted analysis to objectively assess whether patients’ treatment is achieving the desired effect on their atherosclerotic burden.

In patients with persistent residual ASCVD risk despite receiving maximally tolerated statin therapy, how do you prioritize add-on therapies, especially when cost, access, and adherence may limit their options?

Managing residual ASCVD risk in patients beyond using maximally tolerated statin therapy requires a personalized approach. That means HCPs should identify which risk factors are most likely driving the ongoing ASCVD risk and prioritize treatment accordingly.

Where possible, I favor therapies with pleiotropic benefits that address multiple risk factors simultaneously, as this approach is clinically efficient and cost-effective. For example, when obesity is a primary driver of residual ASCVD risk, incretin-based therapies offer substantial value beyond weight reduction alone. These therapies also improve lipids, glycemic control, systemic inflammation, and renal function via a single therapeutic strategy.

What are your strategies for individualizing lipid-lowering and ASCVD risk-reduction therapy for special populations (ie, older adults, young adults with severe disease and/or a family history, and those with established cerebrovascular disease at intermediate risk per traditional scores)?

Individualizing lipid-lowering strategies across special populations requires HCPs to move beyond traditional risk calculators by applying their clinical judgment and using more advanced tools. The recently published 2026 lipid guidelines provide an excellent framework for intermediate-risk patients. It emphasizes the role of imaging-based risk reclassification with CAC scoring and coronary CT angiography to guide decision-making when treatment thresholds are uncertain. These tools are particularly valuable when patients’ benefit-to-risk calculus is less straightforward, including among older adults, younger adults with severe hyperlipidemia, and those with cerebrovascular disease at intermediate risk.

In older adults, I weigh the absolute risk reduction achievable with lipid-lowering therapy against their frailty, polypharmacy, and life expectancy. I favor the simpler, well-tolerated regimens and prioritize quality of life alongside ASCVD risk reduction for these patients. Then, in young adults with severe hyperlipidemia or a compelling family history of premature ASCVD, I take a more aggressive and early intervention approach, recognizing that cumulative lifetime LDL-C exposure is a critical determinant of long-term risk. I also pursue genetic testing for familial hypercholesterolemia when appropriate in these patients.

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Do you feel confident in determining ASCVD risk and management plans in patients with discordant imaging and biomarkers? You can get involved in the conversation by answering the poll question and posting a comment below.

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