How would you approach residual risk when LDL-C is at goal but patient remains high risk?

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Multiple Choice

How would you approach residual risk when LDL-C is at goal but patient remains high risk?

When LDL-C is already at goal, residual cardiovascular risk comes from other atherogenic lipoproteins and factors beyond LDL-C. The key idea is to address the overall atherogenic particle burden, not just the LDL part. Non-HDL-C represents the cholesterol content of all apoB-containing lipoproteins (including VLDL, IDL, chylomicron remnants, LDL, and Lp(a)). In high-risk patients, non-HDL-C is often a better predictor of ASCVD risk than LDL-C alone, and targets for non-HDL-C tend to be higher than LDL-C targets. So, if someone remains high risk, you reassess and aim to optimize non-HDL-C and triglycerides, ensuring the overall atherogenic lipid load is reduced. Elevated Lp(a) is another independent risk factor. If Lp(a) is elevated, consider strategies to lower it where available, recognizing that benefit may be incremental but meaningful in high-risk individuals. Adjunctive therapies such as PCSK9 inhibitors can lower LDL-C, non-HDL-C, and also reduce Lp(a), offering a way to further decrease residual risk when LDL-C is already at goal but risk remains high. In short, the best approach is to re-evaluate the lipid profile beyond LDL-C and actively optimize non-HDL-C and TG, evaluate Lp(a) if elevated, and discuss or initiate adjunctive therapies like PCSK9 inhibitors to tackle ongoing residual risk.

When LDL-C is already at goal, residual cardiovascular risk comes from other atherogenic lipoproteins and factors beyond LDL-C. The key idea is to address the overall atherogenic particle burden, not just the LDL part.

Non-HDL-C represents the cholesterol content of all apoB-containing lipoproteins (including VLDL, IDL, chylomicron remnants, LDL, and Lp(a)). In high-risk patients, non-HDL-C is often a better predictor of ASCVD risk than LDL-C alone, and targets for non-HDL-C tend to be higher than LDL-C targets. So, if someone remains high risk, you reassess and aim to optimize non-HDL-C and triglycerides, ensuring the overall atherogenic lipid load is reduced.

Elevated Lp(a) is another independent risk factor. If Lp(a) is elevated, consider strategies to lower it where available, recognizing that benefit may be incremental but meaningful in high-risk individuals. Adjunctive therapies such as PCSK9 inhibitors can lower LDL-C, non-HDL-C, and also reduce Lp(a), offering a way to further decrease residual risk when LDL-C is already at goal but risk remains high.

In short, the best approach is to re-evaluate the lipid profile beyond LDL-C and actively optimize non-HDL-C and TG, evaluate Lp(a) if elevated, and discuss or initiate adjunctive therapies like PCSK9 inhibitors to tackle ongoing residual risk.

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