SUN-060 Statin-Resistant Hyperlipidemia: Role of Lipoprotein (a)

BACKGROUND: Statin resistance is a term used to describe failure to reach LDL-cholesterol target values despite high dose statin therapy. Common causes for this is nonadherence to therapy and polymorphisms in mechanisms that involve lipid absorption and metablism. We report a case of a patient with resistance to high statin therapy found to have elevated lipoprotein a [Lp(a)]. CLINICAL CASE: A 30 year old Caucasian male presented with hyperlipidemia. He was diagnosed since age of 16 and reports failure to “multiple cholesterol medications”. He had a normal EKG and stress test in the past. Denies prior history of coronary events, peripheral vascular disease or stroke. Currently only medication is atorvastatin 40 mg daily which was recently started when establishing care with new PCP. Otherwise, he was not on any lipid lowering medication for the past 6 months. He adheres to low fat diet. The patient’s body mass index is 25.6. Physical exam is benign including no xanthomas, intact pulses bilaterally, and extremities warm to touch. Labs reveal normal liver function tests, TSH 1.979, HbA1c 5.2% and Lp(a) 169 nmol/L (reference < 75 nmol/L). Lipid profile without statin therapy: total cholesterol 490, triglyceride 146, HDL 52, LDL 409. After 2 months of statin therapy: total cholesterol 448, triglyceride 127, HDL 58, LDL 370. A CT coronary calcium study revealed moderate plaque on left anterior descending artery with CAC score 104.15 suggesting atherosclerotic process. DISCUSSION: The metabolism and function of Lp(a) is still not completely understood but it is known to be a risk factor for coronary heart disease, stroke, and peripheral artery disease. Lp(a) closely resembles an LDL particle with the addition of the very large apolipoprotein (a) linked onto apolipoprotein B100 by a disulfide bond. There is structural similarity between apo(a) and plasminogen and is proposed as the missing link between atherosclerosis and thrombosis. Reduced caloric intake can decrease Lp(a) but low fat diet does affect Lp(a) levels. Aspirin reduces Lp(a) by up to 80% and itself is reduces the risk of ASCVD events. Niacin has been shown to reduce Lp(a) and adverse effects can be better tolerated with aspirin but risk reduction has not been proven. PSCK9 inhibitors are newer drugs that markedly lower LDL and can modestly lower Lp(a). CONCLUSION: Statin therapy remains the foundation treatment in patients with hyperlipidemia and elevated Lp(a) despite little effect of Lp(a) due to its ability to lower ASCVD risk. Additional pharmacological agents including aspirin & PSCK9 inhibitors can be a useful adjuncts to reduce ASCVD risk despite modest Lp(a) reduction. Lipoprotein apheresis may be used in refractory cases.