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KEY CONCEPTS

KEY CONCEPTS

  • image Lipid abnormalities increase the risk of atherosclerotic cardiovascular disease (ASCVD) which includes ischemic coronary heart disease, ischemic stroke, and peripheral arterial disease.

  • image Low-density-lipoprotein cholesterol (LDL-C) is the primary target to reduce the risk of ASCVD events.

  • image Genetic abnormalities and environmental factors are involved in the development of dyslipidemia.

  • image Therapeutic lifestyle change is the first-line therapy for any lipoprotein disorder.

  • image 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.

  • image 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.

  • image If statin monotherapy is insufficient, patients may be treated with evidence-based combination therapy but should be monitored closely for drug-drug interactions.

  • image Reducing total cholesterol and LDL-C reduces CHD and total mortality.

  • image Lipid-lowering therapies that reduce ASCVD event rates are cost-effective.

  • image 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.

BEYOND THE BOOK

BEYOND THE BOOK

Watch these YouTube videos to learn about cholesterol basics as well as the physiology of lipoprotein cholesterol and metabolism:

INTRODUCTION

Cholesterol, triglycerides, and phospholipids are the major lipids that combine with proteins to be transported as complexes of lipid and proteins known as lipoproteins. Lipids, such as cholesterol and triglycerides, are insoluble in plasma, which is why the lipoproteins are required for transportation (Fig. 32-1).1,2

FIGURE 32-1

Intestinal cholesterol absorption and transportation. Cholesterol from food and bile enters the gut lumen and is emulsified by bile acids into micelles. Micelles bind to intestinal enterocytes and cholesterol, and other sterols are transported from the micelles to the enterocytes by sterol transporters. Triglycerides (TG) synthesized by absorbed fatty acids (FA) are incorporated into chylomicrons. Chylomicrons are released into lymphatic circulation and converted to chylomicron remnants (by losing triglyceride), and are then taken up by hepatic LDL-receptor–related protein. (Apo, apolipoprotein; ABC, ATP-binding cassette; CE, cholesterol ester; FA, fatty acid; NPC1L1, Niemann-Pick C1-Like1 protein; TG, triglyceride.) (Reproduced, with permission, from Chisholm-Burns MA, Schwinghammer TL, Malone PM, Kolesar JM, Bookstaver PB, Lee KC, eds. Pharmacotherapy Principles & Practice. 5th ed. New York: McGraw Hill; 2019.)

There are three major classes of lipoproteins in the serum. These include low-density lipoproteins (LDL), high-density lipoproteins (HDL), and very-low-density ...

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