Plasma cholesterol levels are determined by the balance between dietary intake, de novo biosynthesis, and reabsorption processes in the gut as well as by biliary clearance and excretion. While the majority of plasma cholesterol concentrations are derived from cellular biosynthesis in the body, primarily in the liver, about one-third is accounted for from absorption after dietary intake. Prior to the late 1980s, few alternatives existed to lower plasma cholesterol levels. While changes in lifestyle and diet were recommended, polymeric resins that sequestered bile acids in the gut, such as cholesteryamine and colestipol, were used to lower LDLc. While these agents were extremely safe due to their lack of systemic absorption, the high doses required for clinical efficacy limited patient compliance. Even at maximal doses of grams per day, these resins only achieved LDLc reductions of no more than 25%. Over the last 25 years, tremendous progress has been made in providing alternatives for lipid-lowering therapies. Two complementary, pharmacological intervention approaches have been successfully utilized in clinical settings to reduce coronary events by lowering total plasma cholesterol and LDLc levels: cholesterol biosynthesis inhibitors (statins) and cholesterol absorption inhibitors.
As discussed below, the results generated from controlled trials with these new agents have been an important contributor to the changes in drug treatment guidelines proposed by the NCEP Adult Treatment Panel based on patient lipid levels and relative CHD risk (see 6.19 Diabetes/Syndrome X). For moderately high-risk patients (two or more risk factors), reducing LDLc level below 130mgdL_ 1 was recommended, with more aggressive treatment to lower plasma LDLc below 100mgdL_ 1 being considered. For very-high-risk patients, particularly those diagnosed with CHD, reducing LDLc levels below 100mgdL_ 1 was recommended, and more aggressive treatment to lower plasma LDLc below 70mgdL_ 1 was strongly advised.26
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