10 What to Know When Managing Your Patients’ Lp(a) Risk z In patients already on statin therapy, high Lp(a) is associated with residual CVD risk. z In primary prevention for adults ages 40-75 with a 10-year CVD risk of 7.5% to 19.9%, risk-enhancing factors favor initiation of statin therapy. If measured, an Lp(a) ≥50 mg/dL or ≥125 nmol/L may be considered a risk-enhancing factor. z In high-risk or very-high-risk patients with LDL-C ≥70 mg/dL (non–HDL-C ≥100 mg/dL) and a Lp(a) ≥50 mg/dL or ≥100 nmol/L on maximally tolerated statin treatment, it’s reasonable to consider more intensive therapies (such as ezetimibe and/or PCSK9 inhibitors) to lower LDL-C (and non–HDL-C) to better reduce CVD risk.6 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 NLA scientific statement.6 z Maximize treatment of modifiable risk factors. z Good adherence to various LDLlowering diets will reduce LDL-C levels by 10% to >15%. Moderateintensity statins can be expected to reduce LDL-C levels by an additional 30% to 49%, and highintensity statins by ≥50%. Adding ezetimibe or bile acid sequestrants to statin therapy typically provides an additional 13% to 30% reduction in LDL-C. Much greater additive reductions occur by adding a PCSK9 inhibitor to statin plus ezetimibe, providing a 43% to 64% reduction.3
RkJQdWJsaXNoZXIy MjI2NjI=