• Hyperlipidemia is a known risk factor for atherosclerosis and the problems and complications associated with atherosclerosis. The blood lipids include the total cholesterol, HDL cholesterol, LDL cholesterol, VLDL cholesterol, and triglycerides. • Use of statins decreases primary and secondary risks for cardiac disease and stroke. In addition to lowering lipid levels, statins appear to have protective and healing effects on the endothelium. Cardiovascular disease risk is decreased with statin use even if the LDL baseline is not considered elevated when therapy is started. • Many patients being treated for elevated cholesterol levels do not achieve the recommended treatment goals of total cholesterol under 200 mg/dL, LDL under 100 mg/dL, and HDL above 40 mg/dL. • Lovastatin, the prototype statin, lowers LDL, VLDL, triglyceride levels, and total cholesterol levels, and raises HDL levels. It has been shown to decrease mortality from cardiovascular complications associated with elevated cholesterol levels and LDL levels. • Lovastatin is metabolized through the hepatic enzyme CYP3A4. All other drugs or agents that are inhibitors of this pathway may have a drug interaction with lovastatin, decreasing lovastatin metabolism and sometimes dramatically raising blood levels of lovastatin. • All lipid-lowering drugs can elevate liver enzyme levels. This elevation is not normally serious, although the patient's liver enzyme levels should be monitored closely for up to the first year of therapy. Liver enzyme levels usually return to normal spontaneously while drug therapy continues; if this does not occur, then enzyme levels return to normal with either a dose reduction or discontinuation of the drug. • Lipid-lowering drugs can produce myalgias and potentially serious myopathies. These occur most frequently with high doses of statins, or the combination of another antilipid with a statin. Some patients may be genetically predisposed to these adverse effects due to inherited differences in P-450 isoenzymes, because the statins are metabolized via these pathways. • Dietary modifications to limit fat and cholesterol intake should be implemented before starting any drug to lower lipid levels. These modifications need to be continued once drug therapy has begun. • The fibric acid derivatives gemfibrozil and fenofibrate lower triglyceride levels and increase HDL cholesterol. Their effect on LDL cholesterol can be either to lower it slightly or to increase it slightly. They are usually coprescribed with a statin. Gemfibrozil reduces hepatic triglyceride production. The mechanisms of fenofibrate are not clear. • A cholesterol absorption inhibitor is ezetimibe, which decreases the absorption of cholesterol in the small intestine to lower serum LDL levels. It is also available in combination with the statin simvastatin. • Nicotinic acid (niacin or vitamin B3) reduces triglycerides, reduces LDL cholesterol, and increases HDL. Although the exact mode of action is unknown, nicotinic acid is known to inhibit lipolysis in adipose tissue, decrease esterification of triglyceride in the liver, and increase lipoprotein lipase activity. • The bile acid sequestrants cholestyramine, colestipol, and colesevelam decrease LDL. They work differently than other lipid-lowering drugs by binding with the bile acids in the intestine so that the bile acids are nonresorbable and are eliminated in the stool. The decrease in available bile acid causes the body to convert cholesterol to bile acids.
|Original language||English (US)|
|Title of host publication||Drug Therapy in Nursing|
|Publisher||Wolters Kluwer Health Adis (ESP)|
|Number of pages||17|
|State||Published - Nov 7 2012|
ASJC Scopus subject areas