TABLE 9-10

Medications for Managing Hyperlipidemia

Type of MedicationMechanism of ActionMajor EffectsExamplesAdverse ReactionsFDA Approval in Youths (as of This Writing)
HMG-CoA reductase inhibitors (statins)Inhibits cholesterol synthesis in hepatic cells; decreases cholesterol pool, resulting in upregulation of LDL receptorsMainly lowers LDL cholesterol; some decrease in triglycerides and modest increase in HDL cholesterolAtorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatinRaised hepatic enzymes, raised creatine kinase, myopathy possibly progressing to rhabdomyolysisAll statins listed are approved as an adjunct to diet to lower LDL cholesterol in adolescent boys and postmenarcheal girls aged 10–18 y (≥8 y for pravastatin) with heFH and LDL cholesterol ≥190 mg/dL, or ≥160 mg/dL with family history of premature CVD and ≥2 CVD risk factors in the pediatric patient
Bile acid sequestrantsBinds intestinal bile acids, interrupting enterohepatic recirculation; more cholesterol converted into bile acids; decreases hepatic cholesterol pool; upregulates LDL receptorsLowers LDL cholesterol; small increase in HDL cholesterol; raises triglyceridesCholestyramine, colestipol, colesevelamLimited to gastrointestinal tract: gas, bloating, constipation, crampsNo pediatric indication listed for cholestyramine or colestipol; colesevelam indicated as monotherapy or with statin for LDL cholesterol reduction in boys and postmenarcheal girls aged 10–17 y with family history after diet trial if LDL cholesterol ≥ 190 mg/dL or if LDL cholesterol ≥ 160 mg/dL with family history of premature CVD or ≥2 CVD risk factors in the pediatric patient
Cholesterol absorption inhibitorsInhibits intestinal absorption of cholesterol and plant sterols; decreases hepatic cholesterol pool; upregulates LDL receptorsMainly lowers LDL cholesterol; some decrease in triglycerides and small increase in HDL cholesterolEzetimibeMyopathy, gastrointestinal upset, headacheNot approved
Fibric acid derivativesAgonist for PPAR-α nuclear receptors that upregulate LPL and downregulate apolipoprotein C-III, both increasing degradation of VLDL cholesterol and triglycerides; hepatic synthesis of VLDL cholesterol may also be decreasedMainly lowers triglycerides and raises HDL cholesterol; little effect on LDL cholesterolFenofibrate, gemfibrozilDyspepsia, constipation, myositis, anemiaNot approved
Nicotinic acid (extended release)Inhibits release of FFA from adipose tissue; decreases VLDL and LDL cholesterol production and HDL cholesterol degradationLowers triglycerides and LDL cholesterol and raises HDL cholesterol; can decrease lipoprotein(a)Niacin, extended releaseFlushing, hepatic toxicity, can increase fasting blood glucose, uric acid; can cause hyperacidityUse not recommended in children <2 y old
ω-3 fish oilDecreases hepatic FA and triglycerides synthesis while enhancing FA degradation/oxidation, with subsequent reduced VLDL cholesterol releaseLowers triglycerides; raises HDL cholesterol; increases LDL cholesterol and LDL cholesterol particle sizeω-3 acid ethyl estersOccasional adverse gastrointestinal effects but no adverse effect on glucose levels or muscle or liver enzymes or bleedingOnly 1 fish-oil preparation is FDA-approved for adults, but many generic fish-oil capsules are commercially available
  • HMG-CoA indicates hydroxymethylglutaryl coenzyme A; heFH, heterozygous hypercholesterolemia; PPAR-α, peroxisome proliferator-activated receptor; LPL, lipoprotein lipase; VLDL, very low density lipoprotein; FFA, free fatty acid; FA, fatty acid.

  • Adapted from McCrindle BW, Urbina EM, Dennison BA, et al; American Heart Association Atherosclerosis, Hypertension, and Obesity in Youth Committee; American Heart Association, Council of Cardiovascular Disease in the Young; American Heart Association, Council on Cardiovascular Nursing. Circulation. 2007;115(14):1948–1967.