RT Book, Section A1 Dixon, Dave L. A1 Riche, Daniel M. A1 Kelly, Michael S. A2 DiPiro, Joseph T. A2 Yee, Gary C. A2 Michael Posey, L. A2 Haines, Stuart T. A2 Nolin, Thomas D. A2 Ellingrod, Vicki L. SR Print(0) ID 1191226499 T1 Dyslipidemia T2 DiPiro: Pharmacotherapy A Pathophysiologic Approach, 12e YR 2021 FD 2021 PB McGraw Hill PP New York, NY SN 9781260116564 LK accesspharmacy.mhmedical.com/content.aspx?aid=1191226499 RD 2022/07/01 AB KEY CONCEPTS Lipid abnormalities increase the risk of atherosclerotic cardiovascular disease (ASCVD) which includes ischemic coronary heart disease, ischemic stroke, and peripheral arterial disease. Low-density-lipoprotein cholesterol (LDL-C) is the primary target to reduce the risk of ASCVD events. Genetic abnormalities and environmental factors are involved in the development of dyslipidemia. Therapeutic lifestyle change is the first-line therapy for any lipoprotein disorder. If therapeutic lifestyle changes are insufficient, lipid-lowering agents should be chosen based on which lipid is at an undesirable level and the degree to which it is expected to increase the risk of ASCVD. Statins are the drug of choice for dyslipidemia because they significantly lower LDL-C and the risk of ASCVD events, and are generally well tolerated. If statin monotherapy is insufficient, patients may be treated with evidence-based combination therapy but should be monitored closely for drug-drug interactions. Reducing total cholesterol and LDL-C reduces CHD and total mortality. Lipid-lowering therapies that reduce ASCVD event rates are cost-effective. Several novel medications including antisense oligonucleotide inhibitors of apoB, microsomal triglyceride transport protein inhibitors, adenosine triphosphate-citrate lyase (ACL) inhibitors, and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors can be used as add-on therapy or in lieu of statin therapy in select high-risk populations.