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Drug Treatment for Lipid Disorders

Agent Mechanism of Action Dosage Benefits Side Effects Notes
Colestipol (Colestid®) Interrupts bile-acid reabsorption requiring bile acid synthesis from cholesterol. 2 scoops bid or tid (use bulk form). Begin with 1 scoop in the morning. 30 minutes before meal, increase to bid, then to 2 scoops bid. Nonabsorbed with long-term safety established. LDL-C lowering 10%–15% (LRC-CPPT1). Taste/texture, bloating, heartburn, constipation, drug interaction (avoidable by administration of drugs 1 hour before or 4 hours after) and TG increase. Drug of choice for LDL-C lowering in children and in women with childbearing potential. Often used as second-line drug with statins because it acts synergistically to induce LDL receptors. Do not use in patients with TG >300 or in those with GI motility disorders.
Colesevelam hydrochloride (WelChol®) Interrupts bile-acid reabsorption requiring bile acid synthesis from cholesterol. Three 625-mg tablets bid (3.8 g total). 3 tablets with breakfast and 3 tablets with dinner. Nonabsorbed with long-term safety established. LDL-C lowering 10%–15%.1 Taste/texture, bloating, heartburn, constipation, drug interaction (avoidable by administration of drugs 1 hour before or 4 hours after) and TG increase. Drug of choice for LDL-C lowering in children and in women with childbearing potential. Often used as second line drug with statins because it acts synergistically to induce LDL receptors. Do not use in patients with TG >300 or those with GI motility disorders.
Ezetimibe (Zetia®) Selectively inhibits the intestinal absorption of cholesterol and related phytosterols. 10 mg qd. Decreases the delivery of intestinal cholesterol to the liver, thereby reducing hepatic cholesterol stores and increases the clearance of cholesterol from the blood rather than inhibiting cholesterol synthesis. Reduces LDL-C by 18%, TG by 8%, and apolipoprotein B by 16%(EASE2). Well tolerated with few adverse reactions similar to placebo. Can use in combination with statins; however, contraindicated in patients with active liver disease or elevated LFTs. When used in combination with statins, yields an additional LDL-C reduction of 12%, an increase in HDL-C of 3%, and a TG reduction of 8%. Statin plus ezetimibe yield a total LDL-C reduction of 25.8%2. Do not use in combination with resins, fibrates, or cyclosporine. May take at the same time as statin.
Ezetimibe and simvastatin (Vytorin®) Combination of intestinal absorption blocker and statin. Both selectively inhibit the intestinal absorption of cholesterol and partially inhibit HMG-CoA reductase. Ezetimibe: 10 mg Simvastatin: 10, 20, 40, or 80 mg qhs. Combination therapy fosters patient adherence with dosing. Synergistic benefits of both inhibition of intestinal cholesterol absorption by 54% and statin LDL-C lowering of 45%–60% depending on dose3. Abnormal LFTs, myositis/myalgias. Contraindicated in patients with active liver disease or elevated LFTs, pregnant patients, and nursing mothers. Do not use in combination with gemfibrozil, other fibrates, >1 g niacin amiodarone, or verapamil due to an increased risk of myopathy.
Gemfibrozil (Lopid®) Reduces VLDL-C synthesis and induces lipoprotein lipase. 600 mg bid. Best TG-reducing drugs, lowering 50% or more in many patients. Raises HDL-C 15%. Reduces CHD events by 24% in patients with low HDL-C, high TGs (Helsinki4, VA-HIT5). Nausea and skin rash. Does not lower LDL-C reliably or LDL-C may increase in one third of patients. Used in combination therapy with statins for combined hyperlipidemia; however use should be cautious, due to increased myositis/myalgias. Alters statin metabolism and causes an increase in statin plasma concentration. Use with caution in patients with renal insufficiency and gallbladder disease.
Fenofibrate (Tricor®, Antara™, Lofibra™) Reduces VLDL-C synthesis and induces lipoprotein lipase. Tricor: 48, 145 mg/d Antara: 43, 87, 130 mg/d Lofibra: 54, 67, 134, 160, 200 mg/d. Best TG-reducing drugs, lowering TG 50% or more in many patients. Raises HDL-C 15%. Reduces CHD in patients with low HDL-C, high TG.4-5 Nausea and skin rash. Does not lower LDL-C reliably or LDL-C may increase in one third of patients. Used in combination therapy with statins for combined hyperlipidemia; however use should be cautious, due to increased myositis/myalgias. Use with caution in patients with renal insufficiency and gallbladder disease. Use with repaglinide (Prandin®) may cause prolonged severe hypoglycemia.
Atorvastatin (Lipitor®) Partially inhibits HMG-CoA reductase, the rate-limiting step of cholesterol synthesis. This induces LDL receptor formation and removal of LDL-C from blood. 10–80 mg qd. Well-studied for safety and efficacy in many trials. Lowers LDL-C 39%–60% depending on dose and drugs. Raises HDL-C 5%–9%; however, at higher doses (>40 mg), can lower HDL-C. Lowers TG 19%–37%.6 Abnormal LFTs, myositis/myalgias. Drug of choice for elevated LDL-C based on safety and efficacy. Intensive lipid lowering with 80 mg of atorvastatin in patients with CHD provides significant benefit (percent reduction in CHD events) compared with 10 mg.6 Liver function abnormalities less common than previously thought. The 6 statins have different metabolism allowing substitution if side effects occur. Used in combination with bile-acid binding resins to synergistically lower
LDL-C. Used in combination with niacin and fibrates in patients with combined hyperlipidemia. Use cautiously in patients on fibrates due to increased risk of myalgia/myositis.
Amlodipine and atorvastatin (Caduet®)   Amlodipine: 10, 20, 40, or 80 mg Atorvastatin: 5 or 10 mg qd. Combination therapy fosters patient adherence with dosing. Treats both lipid disorder and hypertension concomitantly using a statin and calcium channel blocker. Edema, dizziness, headache, flushing, and palpitations. Do not use in patients with congestive heart failure or severe aortic stenosis.
Fluvastatin (Lescol®, Lescol® XL) Partially inhibits HMG-CoA reductase, the rate-limiting step of cholesterol synthesis. This induces LDL receptor formation and removal of LDL-C from blood.

Lescol: 20–40 mg qhs

Lescol XL: 80 mg qhs

Well-studied for safety and efficacy in many trials. Lowers LDL-C 22%–36% depending on dose and drugs. Raises HDL-C 3%–11%. Lowers TG 12%–25%.7 Abnormal LFTs, myositis/myalgias. Drug of choice for elevated LDL-C based on safety and efficacy. Liver function abnormalities less common than previously thought. The 6 statins have different metabolism allowing substitution if side effects occur. Used in combination with bile-acid binding resins to synergistically lower
LDL-C. Used in combination with niacin and fibrates in patients with combined hyperlipidemia. Use cautiously in patients on fibrates due to increased risk of myalgia/myositis.
Niacin and lovastatin Combination product of both extended-release niacin (niaspan) and statin (lovastatin). Niacin: 500 mg Lovastatin: 20 mg Niacin: 2000 mg lovastatin: 40 mg qhs. Combination therapy fosters patient adherence with dosing. Lowers LDL-C 30%–42%. Raises HDL-C 20%–30%. Reduces TG 32%–44%.8 Flushing, nausea, glucose intolerance, gout, LFT abnormalities, and elevated uric acid levels. Myositis/myalgias. Drug of choice for combined hyperlipidemia and for patients who require simplified dosing. May use a nonenteric coated aspirin taken 1 hour before evening dose along with a light snack to minimize flushing. Do not take with hot beverage.
Lovastatin (Mevacor®, Altoprev™) Partially inhibits HMG-CoA reductase, the rate-limiting step of cholesterol synthesis. This induces LDL receptor formation and removal of LDL-C from blood. 20–80 mg qhs. Well-studied for safety and efficacy in many trials. Lowers LDL-C 20%–60% depending on dose and drugs. Raises HDL-C 10%. Lowers TG 15%–25%. (4S9, WOSCOPS10, CARE11) Abnormal LFTs myositis/myalgias. Drug of choice for elevated LDL-C based on safety and efficacy. Liver function abnormalities less common than previously thought. The 6 statins have different metabolism allowing substitution if side effects occur. Used in combination with bile-acid binding resins to synergistically lower
LDL-C. Used in combination with niacin and fibrates in patients with combined hyperlipidemia. Use cautiously in patients on fibrates, due to increased risk of myalgia/myositis.
Pravastatin (Pravachol®) Partially inhibits HMG-CoA reductase, the rate-limiting step of cholesterol synthesis. This induces LDL receptor formation and removal of LDL-C from blood. 10–40 mg qhs. Well-studied for safety and efficacy in many trials. Lowers LDL-C 20%–40% depending on dose and drugs (28% decrease in LDL-C in the ALLHAT-LLT12 trial). Raised HDL-C 10%. Lowers TG 15%–25%.10-11 (WOSCOPS, CARE). Reduces the risk of major CHD events by 19%–24%.13 Abnormal LFTs, myositis/myalgias. Drug of choice for elevated LDL-C based on safety and efficacy. Liver function abnormalities less common than previously thought. The 6 statins have different metabolism allowing substitution if side effects occur. Used in combination with bile-acid binding resins to synergistically lower
LDL-C. Used in combination with niacin and fibrates in patients with combined hyperlipidemia. Use cautiously in patients on fibrates, due to increased risk of myalgia/myositis.
Aspirin and pravastatin (Pravigard™ PAC) Aspirin: 81 or 325 mg
Pravastatin: 20, 40, or 80 mg qhs.		      
Rosuvastatin (Crestor®) Partially inhibits HMG-CoA reductase, the rate-limiting step of cholesterol synthesis. This induces LDL receptor formation and removal of LDL-C from blood. 5–40 mg qhs. Effective in lowering LDL-C 45%–63% depending on dose and drugs. Raises HDL-C 8%–14%. Lowers TG 10%–35% (STELLAR trial14). Abnormal LFTs, myositis/myalgias. Newest of the 6 statins and therefore not as heavily studied in clinical trials to date; however, numerous industry trials having been conducted. Do not coadminister with warfarin or gemfibrozil. May be coadministered with fenofibrate and bile acid-binding resins to synergistically lower
LDL-C.
Simvastatin (Zocor®) Partially inhibits HMG-CoA reductase, the rate-limiting step of cholesterol synthesis. This induces LDL receptor formation and removal of LDL-C from blood. 5–80 mg qhs. Well-studied for safety and efficacy in many trials. Lowers LDL-C 20%–60% depending on dose and drugs. Raises HDL-C 10%. Lowers TG 15%–25% (4S). Abnormal LFTs, myositis/myalgias. Drug of choice for elevated LDL-C based on safety and efficacy. Liver function abnormalities less common than previously thought. The 6 statins have different metabolism allowing substitution if side effects occur. Used in combination with bile acid binding resins to synergistically lower
LDL-C. Used in combination with niacin and fibrates in patients with combined hyperlipidemia. Use cautiously in patients on fibrates, due to increased risk of myalgia/myositis.
Niacin Largely unknown. Reduces hepatic production of B-containing lipoproteins, increases HDL-C production. 500 mg to 1 g tid. Lowers LDL-C and TG 10%–30%. Most effective drug at raising HDL-C (25%–35%). Long-term efficacy studies (CDP15). Flushing, nausea, glucose intolerance, gout, LFT abnormalities, and elevated uric acid levels. May potentially increase homocysteine levels. Drug of choice for combined hyperlipidemia and in patients with low HDL-C. Extended-release preparations limit flushing and LFT abnormalities. OTC long-acting niacin preparations are not recommended as they increase the incidence of hepatotoxicity. Also lowers lipoprotein (a). Used in combination with statins or bile-acid binding resins in combined hyperlipidemia. To minimize flushing, nonenteric coated aspirin can be taken 1 hour before evening dose along with a light snack. Do not take with hot beverages such as tea or coffee.
Niacin (Niaspan extended release®) Largely unknown. Reduces hepatic production of B-containing lipoproteins, increases HDL-C production. 500 mg to 2 g qhs. Lowers LDL-C and TG 10%–30%. Most effective drug at raising HDL-C (25%–35%). Long term efficacy studies.15 Flushing, nausea, glucose intolerance, gout, LFT abnormalities, and elevated uric acid levels. May potentially increase homocysteine levels. Drug of choice for combined hyperlipidemia and in patients with low HDL-C. Extended-release preparations limit flushing and LFT abnormalities. Also lowers lipoprotein (a). Used in combination with statins or bile-acid binding resins in combined hyperlipidemia. To minimize flushing, nonenteric coated aspirin can be taken 1 hour before evening dose along with a light snack. Do not take with hot beverages such as tea or coffee.
Omega-3 polyunsaturated fatty acids (Lovaza™) Inhibits hepatic TG synthesis and augments chylomicron TG clearance secondary to increased activity of lipoprotein lipase. 4 g/d (4 tablets). Effective in controlling TG levels up to 45%. Raises HDL-C 9%.16 Dyspepsia, nausea. Can increase LDL-C in some patients with hypertriglyceridemia. May increase bleeding time; therefore, use with caution in patients receiving anticoagulant therapy.

ALLHAT-LLT = Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial; bid= twice daily; CARE= Cholesterol and Recurrent Events; CHD = coronary heart disease; GI = gastrointestinal; HDL-C = high-density lipoprotein-cholesterol; HMG-CoA = 3-hydroxy-3-methylglutaryl coenzyme A; LDL-C = low-density lipoprotein -cholesterol; LFT = liver function test; LIPID = Long-Term Intervention with Pravastatin in Ischaemic Disease; LRC-CPPT = Lipid Research Clinics Coronary Primary Prevention Trial; OTC = over the counter; qd = once daily; qhs = every night; STELLAR = Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin; TG = triglycerides; tid= three times daily; VA-HIT = Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial; VLDL = very–low-density lipoprotein-cholesterol; WOSCOPS = West of Scotland Coronary Prevention Study

1Schucker B, Wittes JT, Cutler JA, et al. Change in physician perspective on cholesterol and heart disease. Results from two national surveys. JAMA. 1987;258(24):3521-3526.
2Pearson TA. EASE Trial: Ezetimibe Add-on to Statin for effectiveness Trial. Presented at the American College of Cardiology 53rd Annual Scientific Session; March 7-10, 2004; New Orleans, LA.
3Vytorin [PI]. North Wales, PA: Merck/Schering-Plough Pharmaceuticals; 2004.
4Levine GN, Keaney JF, Vita JA. Cholesterol reduction in cardiovascular disease. Clinical benefits and possible mechanisms. N Engl J Med. 1995;332(8):512-521.
5Rubins HB, Robins SJ. Conclusions from the VA-HIT study. Am J Cardiol. 2000;86(5):543-544.
6Lipitor [PI]. New York, NY: Pfizer Inc.; 1997.
7Lescol and Lescol XL extended-release [PI]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; May 2003.
8Niaspan [PI]. Cranbury, NJ; Kos Pharmaceuticals, Inc.; 2006
94S Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344(8934):1383-1389.
10Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med. 1995;333(20):1301-1307.
11Sacks FM, Rouleau JL, Moye LA, et al. Baseline characteristics in the Cholesterol and Recurrent Events (CARE) trial of secondary prevention in patients with average serum cholesterol levels. Am J Cardiol. 1995;75(8):621-623.
12The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in moderately hypercholesterolemic, hypertensive patients randomized to pravastatin vs usual care: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT). JAMA. 2002;288(23):2998-3007.
13Pravachol [PI]. Princeton, NJ: Bristol-Myers Squibb Company; 1991.
14Jones PH, Davidson MH, Stein EA, et al, for the STELLAR Study Group. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR Trial). Am J Cardiol. 2003;92(2):152-160.
15Canner PL, Berge KG, Wenger NK, et al. Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J Am Coll Cardiol. 1986;8(6):1245-1255.
16Lovaza™ [package insert]. Liberty Corner, NJ: Reliant Pharmaceuticals, Inc.;2007.