10 z In patients already on statin therapy, high Lp(a) is still associated with residual CVD risk. z In primary prevention for adults ages 30 to 79 with an intermediate PREVENT-ASCVD 10-year risk and with LDL-C of 70 to 189 mg/dL, LDL-C–lowering therapy with a statin is recommended after a clinician–patient discussion.4 If measured, an Lp(a) ≥125 nmol/L (≥50 mg/dL) may be considered a risk-enhancing factor. z In all individuals with elevated Lp(a) (≥125 nmol/L or ≥50 mg/ dL), optimal early control of modifiable cardiovascular risk factors is recommended to reduce ASCVD risk.1–4 z In individuals with clinical ASCVD and elevated Lp(a) who have not achieved LDL-C and nonHDL-C treatment goals on maximally tolerated statin therapy, the addition of a PCSK9 mAb with proven cardiovascular benefit is recommended to achieve treatment goals and reduce ASCVD risk.4-7 z The presence of an elevated Lp(a) in patients with very-high-CVD risk and baseline LDL-C ≥70 mg/dL or non–HDL-C ≥100 mg/dL despite maximally tolerated statin and ezetimibe therapies may be used as a factor favoring a PCSK9 inhibitor. z Although niacin and hormone replacement therapy can reduce Lp(a) levels, these drugs are not recommended because they haven’t demonstrated benefit and may be harmful, according to the 2024 focused update to the 2019 NLA scientific statement on Lp(a).7 z Maximize treatment of modifiable risk factors. What to Know When Managing Your Patients’ Lp(a) Risk
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