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INTRODUCTION

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Atherosclerosis is the leading cause of death in the Western world. Drugs discussed in this chapter prevent the sequelae of atherosclerosis (heart attacks, angina, peripheral arterial disease, ischemic stroke) and decrease mortality in patients with a history of cardiovascular disease and hyperlipidemia. Although the drugs are generally safe and effective, they can cause problems, including drug-drug interactions and toxic reactions in skeletal muscle and the liver.

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HYPERLIPOPROTEINEMIA

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A. Pathogenesis
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Premature or accelerated development of atherosclerosis is strongly associated with elevated concentrations of certain plasma lipoproteins, especially the low-density lipoproteins (LDLs) that participate in cholesterol transport. A depressed level of high-density lipoproteins (HDLs) is also associated with increased risk of atherosclerosis. In some families, hypertriglyceridemia is similarly correlated with atherosclerosis. Chylomicronemia, the occurrence of chylomicrons in the serum while fasting, is a recessive trait that is correlated with a high incidence of acute pancreatitis and managed by restriction of total fat intake (Table 35–1).

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Table Graphic Jump Location
TABLE 35–1Primary hyperlipoproteinemias and their drug treatment.
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Regulation of plasma lipoprotein levels involves a complex interplay of dietary fat intake, hepatic processing, and utilization in peripheral tissues (Figure 35–1). Primary disturbances in regulation occur in a number of genetic conditions involving mutations in apolipoproteins, their receptors, transport mechanisms, and lipid-metabolizing enzymes. Secondary disturbances are associated with a Western diet, many endocrine conditions, and diseases of the liver or kidneys.

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FIGURE 35–1

Metabolism of lipoproteins of hepatic origin. The heavy arrows show the primary pathways. Nascent VLDL are secreted ...

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