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How Statins Work: The Development of Cardiovascular Disease and Its Treatment With 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors

  • Authors: Authors: Michael H. Davidson, MD, FACC; Terry A. Jacobson, MD
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Target Audience and Goal Statement

This activity is intended for cardiologists, primary care physicians, and specialists in internal medicine and family medicine.

The goal of this activity is to describe the development of atherosclerosis and to discuss the use of the "statins," or 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, in the treatment of dyslipidemia.

On completion of this continuing medical education offering, participants will be able to:

  1. Describe the process by which fatty acids are transported through the vasculature.
  2. Explain how plaque is deposited in the blood vessel walls.
  3. Identify the main target points for combating dyslipidemia.
  4. Detail the mechanisms through which the statins prevent the synthesis of cholesterol.


  • Michael H. Davidson, MD, FACC

    President and Chief Executive Officer, Chicago Center for Clinical Research; Executive Medical Director, Protocare Trials; Director, Preventive Cardiology Center; Associate Professor of Medicine, Rush Presbyterian-St. Luke's Medical Center, Chicago, Illinois


    Disclosure: Michael H. Davidson, MD, FACC, has no significant financial interests to disclose.

  • Terry A. Jacobson, MD

    Professor, Department of Medicine, Emory University; Director, Office of Health Promotion and Disease Prevention, Department of Medicine, Grady Health Systems, Atlanta, Georgia


    Disclosure: Terry A. Jacobson, MD, has disclosed that he receives funding for clinical grants from Merck and Pfizer. He holds consulting agreements with Reliant, Merck, and Novartis.

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    For Physicians

  • Medical Education Collaborative, a nonprofit education organization, is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

    Medical Education Collaborative designates this educational activity for a maximum of 1 hour in Category 1 credit towards the AMA Physician's Recognition Award. Each physician should claim only those hours of credit that he/she actually spent in the educational activity.

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How Statins Work: The Development of Cardiovascular Disease and Its Treatment With 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors


Classification of Lipoproteins


Slide. Classification of Lipoproteins

There are 3 major types of lipids that circulate in the plasma: cholesterol and cholesterol esters, phospholipids, and triglycerides. Because lipids are not soluble in water, the principal constituent of blood, they must be packaged in some way in order to be suspended in the plasma. During the initial pass through the gastrointestinal system, they are packaged as chylomicrons, secreted into the circulation, transformed into chylomicron remnants, and then finally delivered to the liver. There they are repackaged as a series of smaller, denser lipoprotein "particles" and are resecreted back into the circulation.

Although there is an entire spectrum of these lipoprotein particles, they share most of the same components, the principal difference being their size and density. The figure depicts the major divisions in this spectrum and their principal components: cholesterol (red stars), apolipoprotein B (keys), apolipoprotein A (y shapes), and membrane proteins (blue dots).

Each of these lipoprotein particles serves an important step in the body's metabolic process. As they pass through the intestines and into the circulation with their contents of fatty acids, they act as little "food trucks," delivering the nutrients in their core to the adipose and muscle tissues. However, some of these particles, when they occur in the wrong amount in the wrong place, can begin to cause problems -- problems so severe that they ultimately lead to CVD, the primary cause of death in the industrialized world.

The difficulty for the physician and for the patient is that most dyslipoproteinemias have few, if any, symptoms and only rarely cause clinical signs evident on physical exam. It is thus important to have a working knowledge of the elements of lipid metabolism in order to ensure proper recognition and management of dyslipoproteinemia.

In the panels that follow, we will discuss how each of these lipoproteins is created and what role it plays. Note that these particle subtypes can be further subdivided. For example, the low-density lipoprotein (LDL) particles can be further subdivided into a range of sizes, from "light, fluffy" LDL particles down to "small, dense" LDL particles, with the smaller particles being more atherogenic (ie, causing atherosclerosis). However, measuring these subfractions of the LDL particles requires sophisticated analytical systems that are generally too expensive and complicated to be used in ordinary medical practice. Therefore, tests that distinguish only the general class of "LDL" particles are considered adequate for the purpose of diagnosis.

In addition, analysis of recent clinical trial data (eg, from the Scandinavian Simvastatin Survival Study, 4S) has shown that assessment of an aggregate of the lipoprotein subfractions other than HDL (ie, very low-density lipoprotein [VLDL] + intermediate-density lipoprotein [IDL] + LDL) is at least as effective, and perhaps more linear, than assessment of LDL alone as a predictor of future CVD events. Thus, in the new US National Cholesterol Education Program (NCEP) guidelines, the "non-HDL" subfraction of cholesterol has become the new target of measurement and treatment. To calculate this parameter, the clinician measures total cholesterol (TC) and then determines the non-HDL level according to the formula:


non-HDL = TC - HDL