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Atorvastatin

An Updated Review of its Pharmacological Properties and Use in Dyslipidaemia

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Summary

Abstract

Atorvastatin is a synthetic hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. In dosages of 10 to 80 mg/day, atorvastatin reduces levels of total cholesterol, low-density lipoprotein (LDL)-cholesterol, triglyceride and very low-density lipoprotein (VLDL)-cholesterol and increases high-density lipoprotein (HDL)-cholesterol in patients with a wide variety of dyslipidaemias.

In large long-term trials in patients with primary hypercholesterolaemia, atorvastatin produced greater reductions in total cholesterol, LDL-cholesterol and triglyceride levels than other HMG-CoA reductase inhibitors. In patients with coronary heart disease (CHD), atorvastatin was more efficacious than lovastatin, pravastatin, fluvastatin and simvastatin in achieving target LDL-cholesterol levels and, in high doses, produced very low LDL-cholesterol levels. Aggressive reduction of serum LDL-cholesterol to 1.9 mmol/L with atorvastatin 80 mg/day for 16 weeks in patients with acute coronary syndromes significantly reduced the incidence of the combined primary end-point events and the secondary end-point of recurrent ischaemic events requiring rehospitalisation in the large, well-designed MIRACL trial.

In the AVERT trial, aggressive lipid-lowering therapy with atorvastatin 80 mg/day for 18 months was at least as effective as coronary angioplasty and usual care in reducing the incidence of ischaemic events in low-risk patients with stable CHD. Long-term studies are currently investigating the effects of atorvastatin on serious cardiac events and mortality in patients with CHD.

Pharmacoeconomic studies have shown lipid-lowering with atorvastatin to be cost effective in patients with CHD, men with at least one risk factor for CHD and women with multiple risk factors for CHD. In available studies atorvastatin was more cost effective than most other HMG-CoA reductase inhibitors in achieving target LDL-cholesterol levels.

Atorvastatin is well tolerated and adverse events are usually mild and transient. The tolerability profile of atorvastatin is similar to that of other available HMG-CoA reductase inhibitors and to placebo. Elevations of liver transaminases and creatine phosphokinase are infrequent. There have been rare case reports of rhabdomyolysis occurring with concomitant use of atorvastatin and other drugs.

Conclusion: Atorvastatin is an appropriate first-line lipid-lowering therapy in numerous groups of patients at low to high risk of CHD. Additionally it has a definite role in treating patients requiring greater decreases in LDL-cholesterol levels. Long-term studies are under way to determine whether achieving very low LDL-cholesterol levels with atorvastatin is likely to show additional benefits on morbidity and mortality in patients with CHD.

Pharmacodynamic Properties

Like other members of its class, atorvastatin inhibits hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase in vivo and in vitro, and impedes the formation of mevalonic acid, which is the rate-limiting step in the biosynthesis of cholesterol. The reduction in intracellular cholesterol increases the number of low-density lipoprotein (LDL) receptors, thus increasing the clearance of LDL-cholesterol from plasma.

Atorvastatin reduces plasma levels of total cholesterol, LDL-cholesterol, very low-density lipoprotein (VLDL)-cholesterol, triglycerides and apolipoprotein B, as demonstrated in a number of studies in human volunteers and patients (see Therapeutic Efficacy section). The greater efficacy of atorvastatin than other currently available HMG-CoA reductase inhibitors in reducing total cholesterol and LDL-cholesterol levels is believed to result from a prolonged duration of HMG-CoA reductase inhibition rather than the degree of inhibition.

The marked reductions in triglyceride levels with atorvastatin result mainly from decreases in VLDL production, caused in part by inhibition of cholesterol synthesis. In addition, the increase in number of LDL receptors, combined with the decrease in LDL particles available to bind to these receptors, may enhance the binding of VLDL particles, thus reducing triglyceride levels.

Atorvastatin reduces LDL-cholesterol levels in patients with homozygous familial hypercholesterolaemia despite the absence of any functional LDL receptors in these patients. This effect appears to result from marked inhibition of cholesterol synthesis, which in turn decreases the rate of LDL production. The reductions in overall levels of triglycerides and cholesterol by atorvastatin are accompanied by an improvement in the LDL subfraction profile, with a shift towards the larger subfractions.

There is some evidence that atorvastatin, like other drugs of its class, may have beneficial pharmacodynamic effects in addition to lipid-lowering in patients with atherosclerosis and CHD. Atorvastatin improved endothelial function in patients with hypercholesterolaemia or diabetes mellitus. The improvement did not correlate with the reduction in cholesterol levels and is likely to be due to enhanced endothelial production of nitric oxide (NO) and/or decreased formation of oxygen-derived free radicals.

As well, atorvastatin possibly plays a role in the stabilisation of atherosclerotic plaques by reducing the accumulation of inflammatory cells within them. The drug reduced the activation in vitro of nuclear factor Kappa-B, an inducer of chemokines involved in the inflammation in the atheromatous plaque. In studies of other effects, atorvastatin abolished macrophage infiltration in the arterial neointimal lesions in addition to reducing atheromatous lesion size in a rabbit model of atherosclerosis, and inhibited smooth muscle cell migration and proliferation in both in vitro and in vivo studies.

Treatment with atorvastatin has been shown to reduce spontaneous and ADP-and epinephrine-induced platelet aggregation, probably because of its effect on intraplatelet NO metabolism through an increase in intraplatelet NO synthase activity. Atorvastatin also reduced the enhanced susceptibility of LDL to oxidation, decreased cholesterol accumulation in macrophages and improved red cell deformability.

Most data indicate the drug has positive or negligible effects on non-lipid risk factors for CHD. The drug generally had no appreciable effect on fibrinogen levels, and most data from randomised trials demonstrated a possibly dose-dependent reduction in C-reactive protein levels. The drug generally had no effect on lipoprotein (a) levels in dosages up to 40 mg/day, but the largest such clinical trial (the ASAP study) showed a significant reduction in this parameter after 2 years’ therapy with atorvastatin 80 mg/day.

Pharmacokinetic Properties

About 30% of an oral dose of atorvastatin is absorbed and undergoes extensive first-pass metabolism. The drug has a bioavailability of about 14% and is >98% protein bound in the plasma. No significant changes in area under the plasma concentration-time curve or elimination half-life were observed with the administration of atorvastatin 30 minutes after food intake, although the rate of absorption was reduced.

The single-dose pharmacokinetic parameters of atorvastatin are linear. After single doses of atorvastatin 10, 20 or 40mg in healthy male volunteers, time to reach peak plasma concentration was 0.6 to 0.9 hours. The pharmacological response (lipid-lowering action) is more accurately predicted by the dose administered than the plasma drug concentrations.

Metabolism of atorvastatin by cytochrome P450 (CYP) 3A4 produces ortho-and para-hydroxylated derivatives and various β-oxidation products. 70% of the HMG-CoA reductase inhibitory activity associated with atorvastatin has been attributed to its active ortho- and para-hydroxylated metabolites, which are equipotent to the parent drug.

The peak plasma concentration of atorvastatin is significantly increased in patients with hepatic failure and dosage needs to be reduced in such patients. However, renal impairment has no significant effect on the pharmacokinetic parameters of atorvastatin.

Clinically significant interactions of atorvastatin are likely to occur with its concomitant use with other drugs metabolised by CYP 3A4 including erythromycin, itraconazole, ethinyl estradiol, fusidic acid and cyclosporin.

Therapeutic Efficacy

The lipid-lowering effects of atorvastatin have been investigated in patients with various types of dyslipidaemia. At present the only clinical outcomes data are from studies of aggressive atorvastatin therapy in patients with CHD, but many large trials of atorvastatin are under way to examine the effect of the drug on morbidity and mortality.

Primary hypercholesterolaemia. The lipid-lowering efficacy of atorvastatin in patients with primary hypercholesterolaemia is well established. The drug consistently reduces total and LDL-cholesterol levels in a nonlinear dose-dependent manner, with atorvastatin 10 to 80 mg/day producing reductions in serum LDL-cholesterol levels of about 35 to 60% in various placebo-controlled and non-comparative trials. Atorvastatin 10 to 80 mg/day reduced triglyceride levels by 17 to 45% and apolipoprotein B levels by 17 to 50%.

Target US National Cholesterol Education Program (NCEP) LDL-cholesterol levels (<4.1 mmol/L) were achieved in 91 and 100% of patients with low CHD risk receiving 10 and 20 mg/day of atorvastatin, respectively, in a placebo-controlled study. In the high CHD risk group, 27, 40, 64 and 82% of patients receiving atorvastatin 10, 20, 40 and 80mg, respectively, reached their target serum LDL-cholesterol levels (≤2.6 mmol/L).

Atorvastatin was more efficacious in lowering serum levels of LDL-cholesterol, total cholesterol and triglycerides than milligram equivalent doses of other currently available HMG-CoA reductase inhibitors in patients with hypercholesterolaemia. In large double-blind 1-year trials, reductions in total cholesterol, LDL-cholesterol, apolipoprotein B and triglyceride levels were significantly greater with atorvastatin 10 to 20 mg/day than with lovastatin 20 to 40 mg/day, pravastatin 20 to 40 mg/day or simvastatin 10 to 20 mg/day.

As well, a greater number of patients tended to reach US NCEP LDL-cholesterol goals or European Atherosclerosis Society goals with atorvastatin than with lovastatin, pravastatin, fluvastatin and simvastatin. Fewer patients receiving atorvastatin than these other agents require upward dose titration. Atorvastatin increased high-density lipoprotein (HDL)-cholesterol levels by about 5 to 9% in most studies comparing the drug with others of its class.

Mixed hyperlipidaemia. In patients with mixed hyperlipidaemia, atorvastatin 10 to 20 mg/day produced greater reductions in serum LDL-cholesterol and total cholesterol but lesser reductions in serum triglyceride levels than fenofibrate 200 or 300 mg/day, bezafibrate 400 mg/day and nicotinic acid 3 g/day. The increase in HDL-cholesterol was less than that with fenofibrate and nicotinic acid and similar to that with bezafibrate.

Atorvastatin 10 mg/day was more efficacious in reducing serum LDL-cholesterol and triglyceride levels than simvastatin 10 mg/day in a well-designed, 6-week study involving 1378 evaluable patients with mixed dyslipidaemia (the ASSET trial), and than other comparator HMG-CoA reductase inhibitors in a smaller trial.

Type 2 diabetes mellitus. The efficacy of atorvastatin in lowering serum LDL-cholesterol levels is similar in patients with type 2 diabetes mellitus and those without the condition. Atorvastatin 10 mg/day produced a greater reduction in serum LDL-cholesterol levels than simvastatin 10 mg/day, pravastatin 20 mg/day or lovastatin 20 mg/day in patients with type 2 diabetes mellitus after 6 months, and the drug was superior to simvastatin after 54 weeks in the ASSET trial. More patients given atorvastatin 80 mg/day than 10 mg/day achieved target NCEP LDL-cholesterol goals in the DALI study.

Familial hypercholesterolaemia. Atorvastatin reduced serum LDL-cholesterol levels further in patients with familial hypercholesterolaemia who had previously received simvastatin alone, or in combination with cholestyramine. Reductions were similar to those in patients previously treated with combinations of simvastatin and fenofibrate or nicotinic acid. In the ASAP trial, atorvastatin 80 mg/day significantly reduced, and simvastatin 40 mg/day increased, carotid intimai media thickness in patients with familial hypercholesterolaemia after 2 years.

Atorvastatin 80 mg/day significantly reduced total cholesterol and LDL-cholesterol levels in small numbers of patients with homozygous familial hypercholesterolaemia treated for 2 months.

Aggressive therapy in patients with coronary heart disease.

Atorvastatin is generally more efficacious than the other HMG-CoA reductase inhibitors in achieving the stricter serum LDL-cholesterol target levels in patients with established CHD, in terms of the percentage of patients achieving the targets on monotherapy with these drugs as well as the proportion of patients requiring upward dose titration or a combination with other lipid-lowering agents. This has led to investigation of whether more aggressive therapy can provide clinical benefits.

Aggressive reduction of serum LDL-cholesterol to 1.9 mmol/L, well below the recommended target, with atorvastatin 80 mg/day for 16 weeks in patients with unstable angina or non-Q-wave myocardial infarction significantly reduced the incidence of the combined primary end-point (p = 0.048 vs placebo) and the secondary end-point of recurrent ischaemic events requiring rehospitalisation (p = 0.02) in the large (n = 3086) randomised, double-blind, placebo-controlled MIRACL trial. There were no significant differences in other secondary end-points (death, myocardial infarction and cardiac arrest).

As well, the results of the AVERT trial showed that aggressive lipid-lowering therapy with atorvastatin 80 mg/day for 18 months was at least as effective as coronary angioplasty and usual care in reducing the incidence of ischaemic events in low-risk patients with stable CHD.

Other special patient groups. Use of atorvastatin in place of the previous unsuccessful lipid-lowering therapy in patients with severe resistant hypercholesterolaemia resulted in a significant further reduction in serum LDL-cholesterol and triglyceride levels and achievement of target serum LDL-cholesterol in a significant proportion of these patients.

Although there are no large controlled studies comparing atorvastatin with other HMG-CoA reductase inhibitors in patients with organ transplants, small studies, some of them retrospective, have found atorvastatin to further reduce serum LDL-cholesterol and triglyceride levels in patients with renal or cardiac transplants switched to this drug after previous unsuccessful therapy with simvastatin, pravastatin and fluvastatin. Atorvastatin was superior to pravastatin in a small 4-month trial in patients with cardiac transplants.

Similarly, preliminary results from generally small studies suggest that atorvastatin is effective in patients with end-stage renal disease undergoing dialysis.

Tolerability

Atorvastatin has been well tolerated in long-term clinical trials. In placebo-controlled studies, the incidence of adverse events (18%) in 1122 patients receiving atorvastatin up to 80 mg/day was similar to that in patients receiving placebo (18%; n = 270). No dose-related increase in adverse events was observed in these studies. Overall, the most frequently reported adverse events were constipation, flatulence, dyspepsia, abdominal pain, headache and myalgia. Adverse events reported with atorvastatin have been mild and transient.

Fewer than 2% of the 2502 patients who received atorvastatin withdrew from the trials because of adverse effects related to treatment. The incidence of withdrawal was not dose dependent. In general, the adverse event profile for ator- vastatin was similar to that observed with other HMG-CoA reductase inhibitors.

Mild hepatic involvement in the form of asymptomatic elevations in serum transaminase levels has been reported during treatment with atorvastatin in 0.7% of patients and was responsible for discontinuation of atorvastatin in 0.3%. The incidence of persistent elevation of transaminase levels was higher in patients receiving atorvastatin in doses of 80 mg/day (2.3%) than those receiving lower doses (up to 0.6%).

The incidence of myalgia with the use of atorvastatin (1%) has been found similar to that with placebo (1%) and other HMG-Coa reductase inhibitors (2%). Although isolated asymptomatic elevation of creatine phosphokinase (CPK) has been observed in patients receiving atorvastatin, persistent elevation of CPK (>10 times elevation on 2 consecutive occasions) along with muscle pain, tenderness or weakness has not so far been reported. Case reports of rhabdomyolysis are rare with atorvastatin use, most occurring with concomitant use with other drugs such as cyclosporin, fusidic acid and gemfibrozil.

Pharmacoeconomic Studies

Pharmacoeconomic studies have shown lipid-lowering with atorvastatin to be cost effective in patients with CHD, men with at least one risk factor for CHD and women with multiple risk factors for CHD. Atorvastatin has been found to be more cost effective than most other HMG-CoA reductase inhibitors, in terms of cost per year of life saved and cost of achieving target LDL-cholesterol levels. Atorvastatin 10 mg/day had the lowest acquisition cost per percent reduction in LDL-cholesterol levels among various dosages of the HMG-CoA reductase inhibitors investigated.

Dosage and Administration

Atorvastatin 10 to 80 mg/day may be used to reduce the raised lipid levels in patients with primary hypercholesterolaemia (heterozygous familial, homozygous familial or nonfamilial) or combined dyslipidaemia and diabetic dyslipidaemia.

The dosage of atorvastatin should be adjusted according to response. Atorvastatin may be taken at any time of day with or without food. Dosage reduction may be required in patients with hepatic insufficiency. The drug is contraindicated in patients with active hepatic disease or unexplained persistent elevations in serum transaminase levels.

Concomitant use of atorvastatin with cyclosporin, nicotinic acid, fibrates, erythromycin or azole antifungals is likely to increase the risk of adverse events such as myopathy and rhabdomyolysis.

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References

  1. Lea AP, McTavish D. Atorvastatin: a review of its pharmacology and therapeutic potential in the management of hyperlipidaemias. Drugs 1997 May; 53: 828–47

    Article  PubMed  CAS  Google Scholar 

  2. Moghadasian MH. Clinical pharmacology of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Life Sci 1999; 65(13): 1329–37

    Article  PubMed  CAS  Google Scholar 

  3. Illingworth DR. Management of hypercholesterolemia. Med Clin North Am 2000; 84(1): 23–42

    Article  PubMed  CAS  Google Scholar 

  4. Blum CBB. Comparison of properties of four inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Am J Cardiol 1994; 73 Suppl. D: 3D–11D

    Article  PubMed  CAS  Google Scholar 

  5. Rackley CE. Monotherapy with HMG-CoA reductase inhibitors and secondary prevention in coronary artery disease. Clin Cardiol 1996 Sep; 19:683–9

    Article  PubMed  CAS  Google Scholar 

  6. Bocan TMA, Ferguson E, McNally W, et al. Hepatic and non-hepatic sterol synthesis and tissue distribution following administration of a liver selective HMG-CoA reductase inhibitor, CI-981: comparison with selected HMG-CoA reductase inhibitors. Biochim Biophys Acta 1992 Jan 24; 1123: 133–44

    Article  PubMed  CAS  Google Scholar 

  7. Newton RS. Are all HMG-CoA reductase inhibitors (vastatins) alike? [abstract]. In: 66th Congress of the European Atherosclerosis Society Abstract Book: 1996 July 13–17, Florence Italy, 31

  8. Shaw MK, Newton RS, Sliskovic DR, et al. Hep-G2 cells and primary rat hepatocytes differ in their response to inhibitors of HMG-CoA reductase. Biochem Biophys Res Commun 1990; 170(2): 726–34

    Article  PubMed  CAS  Google Scholar 

  9. Auerbach BJ, Bousley RF, Stanfield RL, et al. Mechanism of cholesterol lowering in casein-fed rabbits treated with atorvastatin [abstract]. Atherosclerosis 1994 Sep 15; 109: 164–5

    Article  Google Scholar 

  10. Sliskovic DR, Roth BD, Bocan TMA. Tissue selectivity of HMG-CoA reductase inhibitors. Drug News Perspect 1992; 5(9): 517–33

    Google Scholar 

  11. Bocan TMA, Mazur MJ, Mueller SB, et al. Antiatherosclerotic activity of inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase in cholesterol-fed rabbits: a biochemical and morphological evaluation. Atherosclerosis 1994 Nov; 111: 127–42

    Article  PubMed  CAS  Google Scholar 

  12. Krause BR, Newton RS. Lipid-lowering activity of atorvastatin and lovastatin in rodent species: triglyceride-lowering in rat correlates with efficacy in LDL animal models. Atherosclerosis 1995 Oct; 117: 237–44

    Article  PubMed  CAS  Google Scholar 

  13. Auerbach BJ, Krause BR, Bisgaier CL. Comparative effects of HMG-CoA reductase inhibitors on apo B production in the casein-fed rabbit: atorvastatin versus lovastatin. Atherosclerosis 1995 Jun; 115: 173–80

    Article  PubMed  CAS  Google Scholar 

  14. Naoumova RP, Marais AD, Mountney J, et al. Plasma mevalonic acid, an index of cholesterol synthesis in vivo, and responsiveness to HMG-CoA reductase inhibitors in familial hypercholesterolaemia. Atherosclerosis 1996 Jan 26; 119: 203–13

    Article  PubMed  CAS  Google Scholar 

  15. Marais AD, Naoumova RP, Firth JC, et al. Decreased production of low density lipoprotein by atorvastatin after apheresis in homozygous familial hypercholesterolemia. J Lipid Res 1997; 38(10): 2071–8

    PubMed  CAS  Google Scholar 

  16. Cilia Jr DD, Gibson DM, Whitfield LR, et al. Pharmacodynamic effects and pharmacokinetics of atorvastatin after administration to normocholesterolemic subjects in the morning and evening. J Clin Pharmacol 1996 Jul; 36: 604–9

    Google Scholar 

  17. Le N-A, Innis-Whitehouse W, Li X, et al. Lipid and apolipoprotein levels and distribution in patients with hypertriglyceridemia: effect of triglyceride reductions with atorvastatin. Metabolism 2000; 49(2): 167–77

    Article  PubMed  CAS  Google Scholar 

  18. Mohammadi A, Macri J, Newton R, et al. Effects of atorvastatin on the intracellular stability and secretion of apolipoprotein B in HepG2 cells. Arterioscler Thromb Vase Biol 1998 May; 18: 783–93

    Article  CAS  Google Scholar 

  19. Naoumova RP, Dunn S, Rallidis L, et al. Prolonged inhibition of cholesterol synthesis explains the efficacy of atorvastatin. J Lipid Res 1997 Jul; 38: 1496–500

    PubMed  CAS  Google Scholar 

  20. Ness GC, Chambers CM, Lopez D. Atorvastatin action involves diminished recovery of hepatic HMG-CoA reductase activity. J Lipid Res 1998 Jan; 39: 75–84

    PubMed  CAS  Google Scholar 

  21. Bakker-Arkema RG, Davidson MH, Goldstein RJ, et al. Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia. JAMA 1996 Jan 10; 275: 128–33

    Article  PubMed  CAS  Google Scholar 

  22. Conde K, Vergara-Jinenez M, Krause BR, et al. Hypercholes-terolemic actions of atorvastatin are associated with alterations on hepatic cholesterol metabolism and lipoprotein composition in the guinea pig. J Lipid Res 1996; 37: 2372–82

    PubMed  CAS  Google Scholar 

  23. Ma PTS, Gil G, Südhof TC, et al. Mevinolin, an inhibitor of cholesterol synthesis, induces mRNA for low density lipoprotein receptor in livers of hamsters and rabbits. Proc Natl Acad Sci U S A 1986; 88: 8370–4

    Article  Google Scholar 

  24. Parhofer KG, Barrett PH, Schwandt P. Effect of atorvastatin on postprandial lipoprotein metabolism in normolipidemic subjects [abstract]. Circulation 2000 Oct 31; 102 Suppl.: 11–601

    Article  Google Scholar 

  25. Burnett JR, Barrett PHR, Vicini P, et al. The HMG-CoA reductase inhibitor, atorvastatin, increases the fractional clearance rate of postprandial triglyceride rich lipoproteins [abstract]. 13th International Symposium on Drugs Affecting Lipid Metabolism; 1998 May 30-Jun 3, Florence, 78

  26. Raal FJ, Pappu AS, Illingworth DR, et al. Inhibition of cholesterol synthesis by atorvastatin in homozygous familial hypercholesterolaemia. Atherosclerosis 2000; 150(2): 421–8

    Article  PubMed  CAS  Google Scholar 

  27. Postiglione A, Montefusco S, Pauciullo P, et al. Effects of atorvastatin in patients with homozygous familial hypercholesterolemia. Atherosclerosis 1999; 147(2): 423–4

    Article  PubMed  CAS  Google Scholar 

  28. Landray MJ, Hartland A, Hubscher D, et al. Effect of atorvastatin on low-density lipoprotein subfraction profile. Ann Clin Biochem 1999 Mar; 36 (Pt 2): 240–1

    PubMed  Google Scholar 

  29. Superko HR, Raul E, Davis V, et al. Atorvastatin and LDL subclass distribution. J Am Coll Cardiol 2001 Feb; 37(2) Suppl. A: 248A

    Article  Google Scholar 

  30. Aviram M, Rosenblat M, Bisgaier CL, et al. Atorvastatin and gemfibrozil metabolites, but not the parent drugs, are potent antioxidants against lipoprotein oxidation. Atherosclerosis 1998 Jun; 138: 271–80

    Article  PubMed  CAS  Google Scholar 

  31. Simons LA, Sullivan D, Simons J, et al. Effects of atorvastatin monotherapy and simvastatin plus cholestyramine on arterial endothelial function in patients with severe primary hyper-cholesterolaemia. Atherosclerosis 1998 Mar; 137: 197–203

    Article  PubMed  CAS  Google Scholar 

  32. Perticone F, Ceravolo R, Maio R, et al. Effects of atorvastatin and vitamin C on endothelial function of hypercholesterolemic patients. Atherosclerosis 2000; 152(2): 511–8

    Article  PubMed  CAS  Google Scholar 

  33. Marchesi S, Lupattelli G, Siepi D, et al. Short-term atorvastatin treatment improves endothelial function in hypercholesterolemic women. J Cardiovasc Pharmacol 2000 Nov; 36: 617–21

    Article  PubMed  CAS  Google Scholar 

  34. Wagner AH, Köhler T, Rückschloss U, et al. Improvement of nitric oxide-dependent vasodilatation by HMG-CoA reductase inhibitors through attenuation of endothelial Superoxide anion formation. Art Thrombosis Vasc Biol 2000; 20(1): 61–9

    Article  CAS  Google Scholar 

  35. Feron O, Dessy C, Desager J-P, et al. Hydroxy-methylglutarylcoenzyme A reductase inhibition promotes endothelial nitric oxide synthase activation through a decrease in caveolin abundance. Circulation 2001 Jan 2; 103: 113–8

    Article  PubMed  CAS  Google Scholar 

  36. Ortego M, Bustos C, Hernández-Presa MA, et al. Atorvastatin reduces NF-kappa B activation and chemokine expression in vascular smooth muscle cells and mononuclear cells. Atherosclerosis 1999; 147(2): 253–61

    Article  PubMed  CAS  Google Scholar 

  37. Bustos C, Hernández-Presa MA, Ortego M, et al. HMG-CoA reductase inhibition by atorvastatin reduces neointimal inflammation in a rabbit model of atherosclerosis. J Am Coll Cardiol 1998 Dec; 32: 2057–64

    Article  PubMed  CAS  Google Scholar 

  38. Bellosta S, Ferri N, Arnaboldi L, et al. Pleiotropic effects of statins in atherosclerosis and diabetes. Diabetes Care 2000 Apr; 23 Suppl. 2: B72–8

    PubMed  Google Scholar 

  39. Axel DI, Riessen R, Runge H, et al. Effect of the new HMG-CoA reductase inhibitor atorvastatin on human vascular cell growth in mono- and cocultures in comparison to lovastatin [abstract]. Eur Heart J 1997 Aug; 18 Abstr Suppl.: 370

    Google Scholar 

  40. Tannous M, Cheung R, Vignini A, et al. Atorvastatin increases ecNOS levels in human platelets of hyperlipidemic subjects. Thromb Haemost 1999; 82(5): 1390–4

    PubMed  CAS  Google Scholar 

  41. Viigimaa M, Valkman R. Lipid-lowering and anti-aggregatory efficacy of atorvastatin in coronary heart disease patients with combined hyperlipidemia [abstract]. Atherosclerosis 1999 May 24; 144 Suppl. 1: 24

    Article  Google Scholar 

  42. Fan B, Tomlinson B, Critchely JAJH. Effects of atorvastatin on platelet aggregation in whole blood [abstract]. Atherosclerosis 1999 May; 35(144) Suppl. 1: 35

    Article  Google Scholar 

  43. Porreca E, Di Febbo C, Amore C, et al. Effect of lipid-lowering treatment on factor VII profile in hyperlipidemic patients. Thromb Haemost 2000 Nov; 84: 789–93

    PubMed  CAS  Google Scholar 

  44. Atalar E, Acil T, Aytemir K, et al. Effects of atorvastatin treatment on global fibrinolytic capacity, apoptosis, and leukocyte activation in patients with coronary artery disease [abstract]. J Am Coll Cardiol 2001 Feb; 37 Suppl. A: 267A

    Google Scholar 

  45. Bocan TM, Mueller SB, Brown EQ, et al. HMG-CoA reductase and ACAT inhibitors act synergistically to lower plasma cholesterol and limit atherosclerotic lesion development in the cholesterol-fed rabbit. Atherosclerosis 1998 Jul; 139: 21–30

    Article  PubMed  CAS  Google Scholar 

  46. Jialal I, Stein D, Balis D, et al. Effect of HMG-CoA reductase inhibitors therapy on C-reactive protein levels [abstract]. Circulation 2000 Oct 31; 102 Suppl.: 11–833

    Article  Google Scholar 

  47. Aristegui R, Gomez-Gerique JA, Gil R, et al. Atorvastatin decreases elevated levels of C-reactive protein in patients with cardiovascular disease and mixed dyslipidaemia: the ATOMIX Study [abstract]. Eur Heart J 2000 Aug–Sep; 21 Suppl.: 497

    Google Scholar 

  48. Joukhadar C, Klein N, Prinz M, et al. Similar effects of atorvastatin, simvastatin and pravastatin on thrombogenic and inflammatory parameters in patients with hypercholesterolemia. Thromb Haemost 2001 Jan; 85: 47–51

    PubMed  CAS  Google Scholar 

  49. Van de Ree MA, Huisman MV, Princen HMG, et al. Dose dependent effects of atorvastatin on C-reactive protein in type 2 diabetes mellitus [abstract no. 684-P]. Diabetes 2001 Jun; 50 Suppl. 2

  50. Marais AD, Firth JC, Bateman ME, et al. Atorvastatin: an effective lipid-modifying agent in familial hypercholesterolemia. Art Thrombosis Vasc Biol 1997; 17: 1527–31

    Article  CAS  Google Scholar 

  51. Wierzbicki AS, Lumb PJ, Semra YK, et al. Effect of atorvastatin on plasma fibrinogen [letter] [see comments]. Lancet 1998 Feb 21; 351: 569–70

    Article  PubMed  CAS  Google Scholar 

  52. Nair DR, Papadakis JA, Jagroop IA, et al. Statins and fibrinogen [letter; comment]. Lancet 1998 May 9; 351: 1430. discussion 1431–2

    Article  PubMed  CAS  Google Scholar 

  53. Bertolotto A, Pucci L, Bandinelli S, et al. Effects of atorvastatin on plasma homocysteine levels in subjects with familial hypercholesterolemia [abstract]. Diabetologia 1999 Aug; 42 Suppl. 1: 288

    Google Scholar 

  54. Wierzbicki AS, Lumb PJ, Chik G, et al. Fibrinogen response with simvastatin versus atorvastatin in familial hypercholesterolemia. Am J Cardiol 2001 Feb 1; 87: 338–40

    Article  PubMed  CAS  Google Scholar 

  55. Jones P, Kafonek S, Laurora I, et al. Comparative dose efficacy study of atorvastatin versus simvastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia (the CURVES study) [published erratum appears in Am J Cardiol 1998 Jul 1;82(1):128] [see comments]. Am J Cardiol 1998 Marl; 81: 582–7

    Article  PubMed  CAS  Google Scholar 

  56. Otto C, Schwandt P. More on atorvastatin and fibrinogen. Atherosclerosis 2000; 151(2): 591–2

    Article  PubMed  CAS  Google Scholar 

  57. Davidson M, McKenney J, Stein E, et al. Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia. Atorvastatin Study Group I. Am J Cardiol 1997 Jun 1; 79: 1475–81

    CAS  Google Scholar 

  58. Goudevenos JA, Bairaktari ET, Chatzidimou KG, et al. The effect of atorvastatin on serum lipids, lipoprotein(a) and plasma fibrinogen levels in primary dyslipidaemia — a pilot study involving serial sampling. Curr Med Res Opin 2001; 16(4): 269–75

    Article  PubMed  CAS  Google Scholar 

  59. Rosenson RS, Tangney C, Schaefer EJ. Comparative study of HMG-CoA reductase inhibitors on fibrinogen. Atherosclerosis 2001; 155:463–6

    Article  PubMed  CAS  Google Scholar 

  60. Dart A, Jerums G, Nicholson G, et al. A multicenter, double-blind, one-year study comparing safety and efficacy of atorvastatin versus simvastatin in patients with hypercholesterolemia. Am J Cardiol 1997 Jul 1; 80(1): 39–44

    Article  PubMed  CAS  Google Scholar 

  61. Smilde TJ, van Wissen S, Wollersheim H, et al. Effect of aggressive versus conventional lipid lowering on atherosclerosis progression in familial hypercholesterolaemia (ASAP): a prospective, randomised, double-blind trial. Lancet 2001 Feb 24; 357: 577–81

    Article  PubMed  CAS  Google Scholar 

  62. Henderson AH. Endothelium in control. Br Heart J 1991; 65: 116–25

    Article  PubMed  CAS  Google Scholar 

  63. Boger RH, Bode-Boger SM, Froloch JC. The L-arginine-nitric oxide pathway: role in atherosclerosis and therapeutic implications. Atherosclerosis 1996; 127: 1–11

    Article  PubMed  CAS  Google Scholar 

  64. Schachinger V, Britten MB, Zeiher AM. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation 2000 Apr 25; 101(16): 1899–906

    Article  PubMed  CAS  Google Scholar 

  65. Åsberg A, Hartmann A, Fjeldsa E, et al. Atorvastatin improves endothelial function in renal transplant recipients [abstract]. Nephrol Dial Transplant 2001 Jun; 16(6): A214

    Article  Google Scholar 

  66. Mullen MJ, Wright D, Donald AE, et al. Atorvastatin but not L-arginine improves endothelial function in type I diabetes mellitus: a double-blind study. J Am Coll Cardiol 2000; 36(2): 410–6

    Article  PubMed  CAS  Google Scholar 

  67. Ohara Y, Peterson TE, Harrison DG. Hypercholesterolemia increases endothelial Superoxide anion production. J Clin Invest 1993; 91: 2546–51

    Article  PubMed  CAS  Google Scholar 

  68. Alber HFW, Dulak JJ, Hugal H, et al. Atorvastatin reduces the blood levels of vascular endothelial growth factor in patients with coronary artery disease [abstract]. J Am Coll Cardiol 2001 Feb; 37(2) Suppl. A: 237A

    Article  Google Scholar 

  69. Kumar S, Brown CD, Zhao Z, et al. Reduction in LDL cholesterol improves RBC deformability in patients with primary hypercholesterolemia [abstract]. J Invest Med 2001 Mar; 49(2): 195A

    Article  Google Scholar 

  70. Bertolotto A, Pucci L, Bandinelli S, et al. Effects of atorvastatin on the fibrinolytic system in patients with primary hypercholesterolemia [abstract]. Diabetologia 2000 Aug; 43 Suppl. 1:288

    Google Scholar 

  71. Tracy RP. Inflammation markers and coronary heart disease. Cur Opin Lipidol 1999; 10: 435–551

    Article  CAS  Google Scholar 

  72. Morrow DA, Ridker PM. C-reactive protein, inflammation, and coronary risk. Med Clin North Am 2000; 84: 149–61

    Article  PubMed  CAS  Google Scholar 

  73. Kent SM, Markwood TT, Coyle LC, et al. Do different statins possess different antiinflammatory and antithrombogenic properties? [abstract no. 1007-203]. J Am Coll Cardiol 2001 Feb; 37 Suppl. A: 267

    Google Scholar 

  74. Danesh J, Collins R, Appleby P, et al. Association of fibrinogen, C-reactive protein, albumin or leukocyte count with coronary artery disease: meta-analyses of prospective studies. JAMA 1998; 279: 1477–82

    Article  PubMed  CAS  Google Scholar 

  75. Salomaa V, Rasi V, Pekkanen J, et al. Hemostatic risk factors and prevalent coronary heart disease: the FINRISK study. Eur Heart J 1994; 15: 1293–9

    PubMed  CAS  Google Scholar 

  76. Athyros VG, Papageorgiou AA, Hatzikonstandinou HA, et al. Effect of atorvastatin versus simvastatin on lipid profile and plasma fibrinogen in patients with hypercholesterolaemia. A pilot, randomised, double-blind, dose-titrating study. Clin Drug Invest 1998; 16(3): 219–27

    CAS  Google Scholar 

  77. Black DM. Statins and fibrinogen [letter; comment]. Lancet 1998 May 9; 351: 1430; discussion 1431–2

    Article  PubMed  CAS  Google Scholar 

  78. Corsini A, Bellosta S, Baetta R, et al. New insights into the pharmacodynamic and pharmacokinetic properties of statins. Pharmacol Ther 1999; 84(3): 413–28

    Article  PubMed  CAS  Google Scholar 

  79. Gibson DM, Stern RH, Abel RB, et al. Absolute bioavailability of atorvastatin in man [abstract]. Pharm Res 1997 Nov; 14 Suppl.: 253

    Google Scholar 

  80. Nemoto H, Oyama T, Karasawa Y, et al. Pharmacokinetic studies on CI-981 (3): in vitro and in vivo plasma protein binding [in Japanese]. Yakuri to Chiryo 1998 Aug; 26: 1229–40

    CAS  Google Scholar 

  81. Whitfield LR, Stern RH, Sedman AJ, et al. Effect of food on the pharmacodynamics and pharmacokinetics of atorvastatin, an inhibitor of HMG-CoA reductase. Eur J Drug Metab Pharmacokinet 2000 Apr; 25(2): 97–101

    Article  PubMed  CAS  Google Scholar 

  82. Oishi S, Watanabe T, Higuchi S, et al. Atorvastatin (CI-981) clinical pharmacokinetic study (III) — effect of food on bioavailability of atorvastatin [in Japanese]. J Pharmacol Ther 1998; 26(8): 93–103

    Google Scholar 

  83. Oishi S, Watanabe T, Higuchi S, et al. Atorvastatin (CI-981) clinical pharmacokinetic study (II) — pharmacokinetics of single dose atorvastatin in healthy male volunteers [in Japanese]. J Pharmacol Ther 1998; 26(8): 79–92

    Google Scholar 

  84. Stern RH, Yang B-B, Hounslow NJ, et al. Pharmacodynamics and pharmacokinetic-pharmacodynamic relationships of atorvastatin, an HMG-CoA reductase inhibitor. J Clin Pharmacol 2000 Jun; 40: 616–23

    Article  PubMed  CAS  Google Scholar 

  85. Black AE, Hayes RN, Roth BD, et al. Metabolism and excretion of atorvastatin in rats and dogs. Drug Metab Dispos 1999 Aug; 27: 916–23

    PubMed  CAS  Google Scholar 

  86. Lipitor™ (atorvastatin calcium) tablets. Data sheet. Parke-Davis, Division of Warner-Lambert Company, Morris Plains, NJ 07950, USA. 1996. (Data on file)

  87. Oishi S, Watanabe T, Higuchi S, et al. Atorvastatin (CI-981) clinical pharmacokinetic study (IV) — pharmacokinetics of multiple dose atorvastatin in healthy male volunteers [in Japanese]. J Pharmacol Ther 1998; 26(8): 105–19

    Google Scholar 

  88. Heinonen T, Stein E, Issacsohn J, et al. Atorvastatin in the treatment of severe hypercholesterolemia [abstract]. In: 66th Congress of the European Atherosclerosis Society Abstract Book; 1996 Jul 13–17; Florence, Italy: 214

  89. Gibson DM, Bron NJ, Richens A, et al. Effect of age and gender on pharmacokinetics of atorvastatin in humans [437340]. J Clin Pharmacol 1996; 36: 242–6

    PubMed  CAS  Google Scholar 

  90. Gibson DM, Yang B-B, Abel RB, et al. Effects of hepatic and renal impairment on pharmacokinetics (PK) and pharmacodynamics (PD) of atorvastatin [abstract]. Pharm Res 1996; 13(9) Suppl.: S428

    Google Scholar 

  91. Yang B-B, Smithers JA, Abel RB, et al. Effects of Maalox TC on pharmacokinetics and pharmacodynamics of atorvastatin [abstract]. Pharm Res 1996; 13(9) Suppl.: S437

    Google Scholar 

  92. Stern RH, Gibson DM, Whitfield LR. Cimetidine does not alter atorvastatin pharmacokinetics or LDL-cholesterol reduction. Eur J Clin Pharmacol 1998 Feb; 53: 475–8

    Article  PubMed  CAS  Google Scholar 

  93. Vaughan CJ, Murphy MB, Buckley BM. Statins do more than just lower cholesterol. Lancet 1996 Oct 19; 348: 1079–82

    Article  PubMed  CAS  Google Scholar 

  94. Yang B-B, Smithers JA, Siedlik PH, et al. Atorvastatin pharmacokinetic interactions with other CYP3A4 substrates: erythromycin and ethinyl estradiol [abstract]. Pharm Res 1996; 13(9) Suppl.: S437

    Google Scholar 

  95. Kantola T, Kivisto KT, Neuvonen PJ. Effect of itraconazole on the pharmacokinetics of atorvastatin. Clin Pharmacol Ther 1998 Jul; 64: 58–65

    Article  PubMed  CAS  Google Scholar 

  96. Siedlik PH, Olson SC, Yang BB, et al. Erythromycin coadministration increases plasma atorvastatin concentrations. J Clin Pharmacol 1999 May; 39: 501–4

    PubMed  CAS  Google Scholar 

  97. Lilja JJ, Kivistö KT, Neuvonen PJ. Grapefruit juice increases serum concentrations of atorvastatin and has no effect on pravastatin. Clin Pharmacol Ther 1999 Aug; 66: 118–27

    PubMed  CAS  Google Scholar 

  98. Boyd RA, Stern RH, Stewart BH, et al. Atorvastatin coadministration may increase digoxin concentrations by inhibition of intestinal P-glycoprotein-mediated secretion. J Clin Pharmacol 2000 Jan; 40: 91–8

    Article  PubMed  CAS  Google Scholar 

  99. Carr RA, Andre AK, Bertz RJ, et al. Concomitant administration of ABT-378/ritonavir (ABT-378r) results in a clinically important pharmacokinetic (PK) interaction with atorvastatin (ATO) but not pravastatin (PRA) [abstract]. 40th Interscience Conference on Antimicrobial Agents and Chemotherapy; 2000 Sep 17–20; Toronto (ON), 334

  100. Chin C, Gamberg P, Miller J, et al. Efficacy and safety of atorvastatin after pediatric cardiac transplantation [abstract]. J Heart Lung Transplant 2001 Feb; 20: 230

    Article  PubMed  Google Scholar 

  101. Maltz HC, Balog DL, Cheigh JS. Rhabdomyolysis associated with concomitant use of atorvastatin and cyclosporine. Ann Pharmacother 1999; 33(11): 1176–779

    Article  PubMed  CAS  Google Scholar 

  102. Renders L, Mayer-Kadner I, Koch C, et al. Efficacy and drug interactions of the new HMG-CoA reductase inhibitors cerivastatin and atorvastatin in CsA-treated renal transplant recipients. Nephrol Dial Transplant 2001 Jan; 16: 141–6

    Article  PubMed  CAS  Google Scholar 

  103. Magnani G, Carinci V, Magelli C, et al. Role of statins in the management of dyslipidemia after cardiac transplant: randomized controlled trial comparing the efficacy and the safety of atorvastatin with pravastatin. J Heart Lung Transplant 2000 Jul; 19:710–5

    Article  PubMed  CAS  Google Scholar 

  104. Alvarez ML, Errasti P, Gomez G, et al. Effect of atorvastatin of the treatment of hypercholesterolemia after renal transplantation. Transplant Proc 1999 Sep; 31: 2328–9

    Article  PubMed  CAS  Google Scholar 

  105. Executive summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in adults (Adult Treatment Panel III). JAMA 2001 May 16;285(19): 2486–97

    Article  Google Scholar 

  106. Pyörälä K, De Backer G, Graham I, et al. Prevention of coronary heart disease in clinical practice: recommendations of the Task Force of the European Society of Cardiology, European Atherosclerosis Society and European Society of Hypertension. Eur Heart J 1994 Oct; 15: 1300–31

    PubMed  Google Scholar 

  107. Schrott H, Fereshetian AG, Knopp RH, et al. A multicenter, placebo-controlled, dose-ranging study of atorvastatin. Journal of Cardiovascular Pharmacology and Therapeutics 1998; 3(2): 119–24

    Article  PubMed  CAS  Google Scholar 

  108. Nakamura H, Ohashi Y, Maruhama Y, et al. Efficacy of atorvastatin in primary hypercholesterolemia. Am J Cardiol 1997; 79(9): 1248–52

    Article  Google Scholar 

  109. Davidson MH, Nawrocki JW, Weiss SR, et al. Effectiveness of atorvastatin for reducing low-density lipoprotein cholesterol to National Cholesterol Education Program treatment goals. Am J Cardiol 1997 Aug 1; 80: 347–8

    Article  PubMed  CAS  Google Scholar 

  110. Nawrocki JW, Weiss SR, Davidson MH, et al. Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG-CoA reductase inhibitor. Art Thrombosis Vasc Biol 1995 May; 15: 678–82

    Article  CAS  Google Scholar 

  111. Heinonen TM, Stein E, Weiss SR, et al. The lipid-lowering effects of atorvastatin, a new HMG-CoA reductase inhibitor: results of a double-masked study. Clin Ther 1996; 18(5): 853–63

    Article  PubMed  CAS  Google Scholar 

  112. Schrott HG, Knapp H, Davila M, et al. Effect of atorvastatin on blood lipid levels in the first 2 weeks of treatment: a randomized, placebo-controlled study. Am Heart J 2000 Aug; 140: 249–52

    Article  PubMed  CAS  Google Scholar 

  113. Kastelein JJP, Isaacsohn JL, Ose L, et al. Comparison of effects of simvastatin versus atorvastatin on high-density lipoprotein cholesterol and apolipoprotein A-I levels. Am J Cardiol 2000; 86(2): 221–3

    Article  PubMed  CAS  Google Scholar 

  114. Crouse III JR, Frohlich J, Ose L, et al. Effects of high doses of simvastatin and atorvastatin on high-density lipoprotein cholesterol and apolipoprotein A-I. Am J Cardiol 1999 May 15; 83: 1476–7

    Article  PubMed  CAS  Google Scholar 

  115. Nawrocki JW, Peters TK, Newell P, et al. Effect of statin therapy on HDL-C levels in patients with type Ha and type IIb hyperlipidemia [abstract]. Atherosclerosis 1999; 28 (144 Suppl. 1): 25–6

    Google Scholar 

  116. Farmer M, Portal J-J, Maigret P. Efficacy of atorvastatin compared with simvastatin in patients with hypercholesterolemia. J Cardiovasc Pharmacol Ther 2000; 5(1): 27–32

    Article  Google Scholar 

  117. Recto II CS, Acosta S, Dobs A. Comparison of the efficacy and tolerability of simvastatin and atorvastatin in the treatment of hypercholesterolemia. Clin Cardiol 2000 Sep; 23: 682–8

    Article  PubMed  Google Scholar 

  118. Davidson MH, Ma PTS, Stein E, et al. ZD4522 is superior to atorvastatin in decreasing low density lipoprotein cholesterol and increasing high density lipoprotein cholesterol in patients with type IIa or IIb hypercholesterolemia [abstract]. J Am Coll Cardiol 2001 Feb; 37(2) Suppl. A: 292A

    Article  Google Scholar 

  119. Assmann G, Hiiwel D, Schussman K-M, et al. Efficacy and safety of atorvastatin and pravastatin in patients with hypercholesterolemia. Eur J Intern Med 1999; 10(1): 33–9

    Article  CAS  Google Scholar 

  120. Barter PJ, O’Brien RC. Achievement of target plasma cholesterol levels in hypercholesterolaemic patients being treated in general practice. Atherosclerosis 2000; 149(1): 199–205

    Article  PubMed  CAS  Google Scholar 

  121. Bertolini S, Bon GB, Campbell LM, et al. Efficacy and safety of atorvastatin compared to pravastatin in patients with hypercholesterolemia. Atherosclerosis 1997 Apr; 130: 191–7

    Article  PubMed  CAS  Google Scholar 

  122. Hunninghake D, Bakker-Arkema RG, Wigand JP, et al. Treating to meet NCEP-recommended LDL cholesterol concentrations with atorvastatin, fluvastatin, lovastatin, or simvastatin in patients with risk factors for coronary heart disease. J Fam Pract 1998 Nov; 47: 349–56

    PubMed  CAS  Google Scholar 

  123. Illingworth DR, Crouse III JR, Hunninghake DB, et al. A comparison of simvastatin and atorvastatin up to maximal recommended doses in a large multicenter randomized clinical trial. Curr Med Res Opin 2001; 17(1): 43–50

    PubMed  CAS  Google Scholar 

  124. van Dam M, Basart DCG, Janus C, et al. Additional efficacy of milligram-equivalent doses of atorvastatin over simvastatin. Clin Drug Invest 2000; 19(5): 327–34

    Article  Google Scholar 

  125. White HD, Kush D, Bertolami M, et al. Simvastatin and atorvastatin have different effects at high doses on high density lipoprotein cholesterol and apolipoprotein A-I [abstract]. Atherosclerosis 1999; 144 Suppl. 1

  126. Schuster H, Berger J, Luft FC. Randomised, double-blind, parallel-group trial of atorvastatin and fluvastatin on plasma lipid levels in patients with untreated hyperlipidaemia. Br J Cardiol 1998; 5(11): 597–602

    Google Scholar 

  127. Edmundowicz D, Andrews TC, Shear CL, et al. Comparing treatment success with statins: results from the Atorvastatin Comparative Cholesterol Efficacy and Safety Study (ACCESS) [abstract]. J Am Coll Cardiol 2000; 35 Suppl. A: 314

    Google Scholar 

  128. Williams RR, Hopkins PN, Hunt SC, et al. Population-based frequency of dyslipidemia syndromes in coronary-prone families in Utah. Arch Intern Med 1990; 150: 582–8

    Article  PubMed  CAS  Google Scholar 

  129. Gaw A. Evidence based approach for management of mixed hyperlipidemia. Atherosclerosis 1998; 137: S97–100

    Article  PubMed  CAS  Google Scholar 

  130. Bairaktari ET, Tzallas CS, Tsimihodimos VK, et al. Comparison of the efficacy of atorvastatin and micronized fenofibrate in the treatment of mixed hyperlipidemia. J Cardiovasc Risk 1999 Apr; 6: 113–6

    PubMed  CAS  Google Scholar 

  131. Bottazzo S, Severi G, Fazzin G. Comparison of atorvastatin and bezafibrate treatment in dyslipidemic patients with metabolic syndrome (MS) [abstract]. 13th International Symposium on Drugs Affecting Lipid Metabolism; 1998 May 30–Jun 3; Florence, 59

  132. Ooi TC, Heinonen T, Alaupovic P, et al. Efficacy and safety of a new hydroxymethylglutaryl-coenzyme A reductase inhibitor, atorvastatin, in patients with combined hyperlipidemia: comparison with fenofibrate. Arterioscler Thromb Vasc Biol 1997 Sep; 17: 1793–9

    Article  PubMed  CAS  Google Scholar 

  133. McKenney JM, McCormick LS, Weiss S, et al. A randomized trial of the effects of atorvastatin and niacin in patients with combined hyperlipidemia or isolated hypertriglyceridemia. Collaborative Atorvastatin Study Group. Am J Med 1998 Feb; 104: 137–43

    CAS  Google Scholar 

  134. Branchi A, Fiorenza AM, Rovellini A, et al. Lowering effects of four different statins on serum triglyceride level. Eur J Clin Pharmacol 1999 Sep; 55: 499–502

    Article  PubMed  CAS  Google Scholar 

  135. Insull W, Kafonek S, Goldner D, et al. Comparison of efficacy and safety of atorvastatin (10 mg) with simvastatin (10 mg) at six weeks. Am J Cardiol 2001 Mar 1; 87: 554–9

    Article  PubMed  CAS  Google Scholar 

  136. Stein EA, Lane M, Laskarzewski P. Comparison of statins in hypertriglyceridemia. Am J Cardiol 1998 Feb 26; 81: 66B–9B

    Article  PubMed  CAS  Google Scholar 

  137. Best JD, O’Neal DN. Diabetic dyslipidaemia: current treatment recommendations. Drugs 2000; 59(5): 1101–11

    Article  PubMed  CAS  Google Scholar 

  138. Taskinen MR. Triglyceride is the major atherogenic lipid in NIDDM. Diabetes Metab Rev 1997; 13: 93–8

    Article  PubMed  CAS  Google Scholar 

  139. Stamler J, Vaccaro O, Neaton JD, et al. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care 1993; 16: 434–4

    Article  PubMed  CAS  Google Scholar 

  140. Taskinen M-R. Strategies for the management of diabetic dyslipidaemia. Drugs 1999; 58 Suppl. 1: 47–51

    Article  PubMed  Google Scholar 

  141. Aguilar-Salinas CA, Gomez-Perez FJ, Posadas-Romero C, et al. Efficacy and safety of atorvastatin in hyperlipidemic, type 2 diabetic patients. A 34-week, multicenter, open-label study. Atherosclerosis 2000; 152(2): 489–96

    CAS  Google Scholar 

  142. Posadas C, Aguilar C, Gomez Perez F, et al. Atorvastatin is effective and safe in patients with NIDDM: a multicenter, open-label study [abstract no. 1047]. Diabetes 2001 May; 47 Suppl. 1:23

    Google Scholar 

  143. Black DM, Bakker-Arkema R, Heinonen T, et al. Does the presence of either concurrent hypertension or non-insulin-dependent diabetes mellitus affect the efficacy and safety of atorvastatin in patients with hyperlipidaemia? [abstract]. Am J Hypertens 1998 Apr; 11 (Pt 2): 75

    Article  Google Scholar 

  144. Bogaty P, Leiter L, Murray P, et al. The Can-ADA Study: do lipid parameters respond differently to atorvastatin therapy in ischemic heart disease subjects with and without type 2 diabetes? [abstract]. Can J Cardiol 2000 Sep; 16 Suppl. F: 234F

    Google Scholar 

  145. Djordjevic PB, Lalic K, Lalic NM, et al. Effectiveness of statin treatment in reducing vascular risk in type 2 diabetes: comparison between fluvastatin, simvastatin and atorvastatin [abstract]. Diabetes Res Clin Pract 2000 Sep; 50 Suppl. 1: S347

    Google Scholar 

  146. Gentile S, Turco S, Guarino G, et al. Comparative efficacy study of atorvastatin vs. simvastatin, pravastatin, lovastatin and placebo in type 2 diabetic patients with hypercholesterolaemia. Diabetes Obes Metab 2000 Nov; 2: 355–62

    Article  PubMed  CAS  Google Scholar 

  147. Insull Jr W, The ASSET Investigators. The efficacy and safety of atorvastatin versus simvastatin in mixed dyslipidemic patients with type 2 diabetes mellitus during 54 weeks [abstract no. 576-P]. Diabetes 2001 Jun; 50 Suppl. 2: A143

    Article  Google Scholar 

  148. The Diabetes Atorvastatin Lipid Intervention (DALI) Study Group. The effect of aggressive versus standard lipid lowering by atorvastatin on diabetic dyslipidemia. The DALI Study: a double-blind, randomised placebo-controlled trial in patients with type 2 diabetes and diabetic dyslipidemia. Diabetes Care 2001 Aug; 24(8): 1335–41

    Google Scholar 

  149. Velussi M, Cernigoi AM, Tortul C, et al. Atorvastatin for the management of Type 2 diabetic patients with dyslipidaemia. A mid-term (9 months) treatment experience. Diabetes Nutr Metab 1999; 12(6): 407–12

    CAS  Google Scholar 

  150. Hoogerbrugge N, Jansen H. Atorvastatin increases low-density lipoprotein size and enhances high-density lipoprotein cholesterol concentration in male, but not in female patients with familial hypercholesterolemia. Atherosclerosis 1999 Sep; 146: 167–74

    Article  PubMed  CAS  Google Scholar 

  151. Wierzbicki AS, Lumb PJ, Chik G, et al. Comparison of therapy with simvastatin 80 mg and atorvastatin 80 mg in patients with familial hypercholesterolaemia. Int J Clin Pract 1999; 53(8): 609–11

    PubMed  CAS  Google Scholar 

  152. Wierzbicki AS, Lumb PJ, Semra YK, et al. High-dose atorvastatin therapy in severe heterozygous familial hypercholesterolaemia. Q J Med 1998 Apr; 91: 291–4

    Article  CAS  Google Scholar 

  153. Wierzbicki AS, Lumb PJ, Semra Y, et al. Atorvastatin compared with simvastatin-based therapies in the management of severe familial hyperlipidaemias. Q J Med 1999 Jul; 92(7): 387–94

    Article  CAS  Google Scholar 

  154. Hoogerbrugge N. Effects of atorvastatin on serum lipids of patients with familial hypercholesterolaemia. J Intern Med 1998 Aug; 244: 143–7

    Article  PubMed  CAS  Google Scholar 

  155. Stein E, Strutt KL, Miller E, et al. ZD4522 is superior to atorvastatin in the treatment of patients with heterozygous familial hypercholesterolemia [abstract]. J Am Coll Cardiol 2001 Feb; 37(2) Suppl. A: 292A

    Article  Google Scholar 

  156. Habib G, Paillard F, Charpentier G, et al. A multicenter, open-label, randomized study comparing the efficacy of atorvastatin versus usual care in reducing refractory hypercholesterolemia in high-risk patients to target levels. Curr Ther Res Clin Exp 2000; 61(4): 175–90

    Article  CAS  Google Scholar 

  157. Simons LA. Comparison of atorvastatin alone versus simvastatin ± cholestyramine in the management of severe primary hypercholesterolaemia (the Six Cities Study). Aust N Z J Med 1998 Jun; 28: 327–33

    Article  PubMed  CAS  Google Scholar 

  158. Brown AS, Bakker-Arkema RG, Yellen L, et al. Treating patients with documented atherosclerosis to National Cholesterol Education Program — recommended low-density-lipoprotein cholesterol goals with atorvastatin, fluvastatin, lovastatin and simvastatin. J Am Coll Cardiol 1998 Sep; 32: 665–72

    Article  PubMed  CAS  Google Scholar 

  159. März W, Wollschläger H, Klein G, et al. Safety of low-density lipoprotein cholesterol reduction with atorvastatin versus simvastatin in a coronary heart disease population (the TARGET TANGIBLE trial). Am J Cardiol 1999 Jul 1; 84: 7–13

    Article  PubMed  Google Scholar 

  160. McVey D, Patel H, Eminton Z, et al. An assessment of the efficacy of atorvastatin in treating patients with dyslipidaemia to target LDL-cholesterol goals: the Atorvastatin Matrix Study. Int J Clin Pract 1999; 53(7): 509–13

    PubMed  CAS  Google Scholar 

  161. Geiss HC, Parhofer KG, Schwandt P. Atorvastatin compared with simvastatin in patients with severe LDL hypercholesterolaemia treated by regular LDL apheresis. J Intern Med 1999 Jan; 245: 47–55

    Article  PubMed  CAS  Google Scholar 

  162. McPherson R, Angus C, Murray P, et al. Efficacy of atorvastatin in achieving National Cholesterol Education Program low-density lipoprotein targets in women with severe dyslipidaemia and cardiovascular disease or risk factors for cardiovascular disease: the Women’s Atorvastatin Trial on Cholesterol (WATCH). Am Heart J 2001; 141: 949–56

    Article  PubMed  CAS  Google Scholar 

  163. Schartl M, Bocksch W, Koschyk D, et al. Use of intravascular ultrasound to compare effects of different strategies of lipid-lowering therapy on plaque volume and composition in patients with coronary artery disease. Circulation 2001; 104: 387–92

    Article  PubMed  CAS  Google Scholar 

  164. Schwartz GG, Olsson AG, Ezekowitz MD, et al. Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes. The MIRACL study: a randomized controlled trial. JAMA 2001 Apr 4; 285(13): 1711–8

    CAS  Google Scholar 

  165. Pitt B, Waters D, Brown WV, et al. Aggressive lipid-lowering therapy compared with angioplasty in stable coronary artery disease. Atorvastatin versus Revascularization Treatment Investigators. N Engl J Med 1999 Jul 8; 341: 70–6

    CAS  Google Scholar 

  166. Brown WV, Avert I. Can aggressive lipid-lowering therapy provide additional clinical benefit? Subgroup analysis of the Atorvastatin VErsus Revascularization Treatments (AVERT) trial [abstract]. Eur Heart J 2000 Aug–Sep; 21 Suppl.: 157

    Google Scholar 

  167. Kobashigawa JA, Moriguchi JD, Ro TK, et al. Atorvastatin for refractory hypercholesterolemia in heart transplant patients [abstract]. J Am Coll Cardiol 1998 Feb; 31 Suppl. 2A: 157

    Article  Google Scholar 

  168. Patel DN, Pagani FD, Koelling TM, et al. Safety and efficacy of atorvastatin in heart transplant recipients [abstract]. J Heart Lung Transplant 2000 Jan; 19: 43

    Article  Google Scholar 

  169. Romero R, Calvifio J, Rodriguez J, et al. Short-term effect of atorvastatin in hypercholesterolaemic renal-transplant patients unresponsive to other statins. Nephrol Dial Transplant 2000; 15(9): 1446–9

    Article  PubMed  CAS  Google Scholar 

  170. Penzak SR, Chuck SK. Hyperlipidemia associated with HIV protease inhibitor use: pathophysiology, prevalence, risk factors and treatment. Scand J Infect Dis 2000; 32: 111–23

    Article  PubMed  CAS  Google Scholar 

  171. Henry K, Melroe H, Huebesch J, et al. Atorvastatin and gemfibrozil for protease-inhibitor-related lipid abnormalities [letter] [see comments]. Lancet 1998 Sep 26; 352: 1031–2

    Article  PubMed  CAS  Google Scholar 

  172. Murillas J, Martin T, Ramos A, et al. Atorvastatin for protease inhibitor-related hyperlipidaemia [letter]. AIDS 1999 Jul 30; 13: 1424–5

    Article  PubMed  CAS  Google Scholar 

  173. Kasiske BL. Hyperlipidemia in patients with chronic renal disease. Am J Kidney Dis 1998 Nov; 32(5) Suppl. 3: S142–56

    Article  PubMed  CAS  Google Scholar 

  174. Wheeler DC. Should hyperlipidaemia in dialysis patients be treated? [editorial comments]. Nephrol Dial Transplant 1997; 12: 19–21

    Article  PubMed  CAS  Google Scholar 

  175. Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 1998 Nov; 32(5) Suppl. 3: S112–9

    Article  PubMed  CAS  Google Scholar 

  176. Wheeler CD, Harris KPG, on behalf of the UK CAPD Investigators. A placebo-controlled trial examining the efficacy and safety of atorvastatin in dyslipidaemic patients undergoing CAPD [abstract]. Nephrol Dial Transplant 2001 Jun; 16(6): A196

    Google Scholar 

  177. Hufnagel G, Michel C, Vrtovsnik F, et al. Effects of atorvastatin on dyslipidaemia in uraemic patients on peritoneal dialysis. Nephrol Dial Transplant 2000; 15(5): 684–8

    Article  PubMed  CAS  Google Scholar 

  178. Le Roux CW, McCarthy HJ, Almond MK. Correction of hypercholesterolaemia in haemodialysis patients with atorvastatin [abstract no. 30]. Clin Sci 2000; 98(2): 11P

    Google Scholar 

  179. Stegmayr BG, Näsström BG, Brännström M, et al. Safety and efficacy of atorvastatin in patients with severe renal dysfunction [abstract no. P 35]. Int J Artif Organs 1998; 21(10): 631

    Google Scholar 

  180. Diepeveen SHA, Verhoeven GHWE, van der Palen J, et al. Vitaestat 1: a prospective randomised placebo controlled trial with a-tocopherol and atorvastatin in patients in hemo- and peritoneal dialysis [abstract]. Nephrol Dial Transplant 2001 Jun; 16(6): A87

    Google Scholar 

  181. Black DM, Bakker-Arkema RG, Nawrocki JW. An overview of the clinical safety profile of atorvastatin (Lipitor), a new HMG-CoA reductase inhibitor. Arch Intern Med 1998 Mar 23; 158: 577–84

    Article  PubMed  CAS  Google Scholar 

  182. Pfeiffer CM, Kazenoff S, Rothberg HD. Toxic epidermal necrolysis from atorvastatin [letter]. JAMA 1998 May 27; 279: 1613–4

    Article  PubMed  CAS  Google Scholar 

  183. Gonzalez-Ponte ML, Gonzalez-Ruiz M, Duvos E, et al. Atorvastatin-induced severe thrombocytopenia [letter]. Lancet 1998 Oct 17; 352: 1284

    Article  PubMed  CAS  Google Scholar 

  184. Bakker A-RG, Nawrocki JW, Black DM. Safety profile of atorvastatin-treated patients with low LDL-cholesterol levels. Atherosclerosis 2000; 149(1): 123–9

    Article  Google Scholar 

  185. Bakker-Arkema RG, Davidson M, Black DM. Two year safety of atorvastatin compared to lovastatin in patients with hypercholesterolemia [abstract]. 13th International Symposium on Drugs Affecting Lipid Metabolism; 1998 May 30–Jun 3; Florence, 58

  186. Wierzbicki AS, Crook MA. Cholestatic liver dysfunction [letter]. Lancet 1999 Sep 11; 354: 954

    Article  PubMed  CAS  Google Scholar 

  187. Jimenez-Alonso J, Osorio JM, Gutierrez-Cabello F, et al. Atorvastatin-induced cholestatic hepatitis in a young woman with systemic lupus erythematosus. Grupo Lupus Virgen de las Nieves. Arch Intern Med 1999 Aug 9; 159(15): 1811–2

    CAS  Google Scholar 

  188. Nakad A, Bataille L, Hamoir V, et al. Atorvastatin-induced acute hepatitis with absence of cross-toxicity with simvastatin [letter]. Lancet 1999 May 22; 353: 1763–4

    Article  PubMed  CAS  Google Scholar 

  189. Noel B, Cerottini J-P, Panizzon RG. Atorvastatin-induced dermatomyositis [letter]. Am J Med 2001; 110(8): 670–1

    Article  PubMed  CAS  Google Scholar 

  190. Duell PB, Connor WE, Illingworth DR. Rhabdomyolysis after taking atorvastatin with gemfibrozil. Am J Cardiol 1998 Feb 1; 81: 368–9

    Article  PubMed  CAS  Google Scholar 

  191. Wenisch C, Krause R, Fladerer P, et al. Acute rhabdomyolysis after atorvastatin and fusidic acid therapy [letter]. Am J Med 2000 Jul; 109:78

    Article  PubMed  CAS  Google Scholar 

  192. Montvale NJ. Physicians’ Desk Reference. 54th ed: Medical Economics Company, Inc., 2000

  193. Huse DM, Russell MW, Miller JD, et al. Cost-effectiveness of statins. Am J Cardiol 1998 Dec 1; 82: 1357–63

    Article  PubMed  CAS  Google Scholar 

  194. Elliott WJ, Weir DR. Comparative cost-effectiveness of HMG-CoA reductase inhibitors in secondary prevention of acute myocardial infarction. Am J Health Syst Pharm 1999 Sep 1; 56: 1726–32

    PubMed  CAS  Google Scholar 

  195. Hilleman DE, Phillips JO, Mohiuddin SM, et al. A population-based treat-to-target pharmacoeconomic analysis of HMG-CoA reductase inhibitors in hypercholesterolemia. Clin Ther 1999 Mar; 21: 536–62

    Article  PubMed  CAS  Google Scholar 

  196. Hilleman DE, Heineman SM, Foral PA. Pharmacoeconomic assessment of HMG-CoA reductase inhibitor therapy: an analysis based on the CURVES Study. Pharmacotherapy 2000; 20(7): 819–22

    Article  PubMed  CAS  Google Scholar 

  197. Smith DG, Leslie SJ, Szucs TD, et al. Cost of treating to a modified European Atherosclerosis Society LDL-C target. Comparison of atorvastatin with fluvastatin, pravastatin and simvastatin. Clin Drug Invest 1999 Mar; 17(3): 185–93

    Google Scholar 

  198. Koren MJ, Smith DG, Hunninghake DB, et al. The cost of reaching National Cholesterol Education Program (NCEP) goals in hypercholesterolaemic patients: a comparison of atorvastatin, simvastatin, lovastatin and fluvastatin. Pharmacoeconomics 1998; 14(1): 59–70

    Article  PubMed  CAS  Google Scholar 

  199. MacLaine GDH, Patel H. A cost-effectiveness model of alternative statins to achieve target LDL-cholesterol levels. Int J Clin Pract 2001; 55(4): 243–9

    PubMed  CAS  Google Scholar 

  200. Wlodarczyk J, Barter PJ, O’Brien R, et al. Cost of treatment of hypercholesterolaemia to NHF goals in Australia [abstract no. PCV39]. Value Health 2001 Mar–Apr; 4(2): 110

    Article  Google Scholar 

  201. Smith DG. The cost-effectiveness of statins: evidence from the ACCESS trial [abstract no. PCV37]. Value Health 2001 Mar–Apr; 4(2): 109

    Article  Google Scholar 

  202. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study Group (4S). Lancet 1994; 344: 1383–9

    Google Scholar 

  203. Attanasio E, Russo P, Allen SE. Cost-minimization analysis of simvastatin versus atorvastatin for maintenance therapy in patients with coronary or peripheral vascular disease. Clin Ther 2001; 23(2): 276–83

    Article  PubMed  CAS  Google Scholar 

  204. Lipitor prescribing information. Compendium of data sheets and summaries of product characteristics, pp. 1122–4

  205. Newman TJ, Kassler-Taub KB, Gelarden RT, et al. Safety of pravastatin in long-term trials conducted in the United States. J Drug Dev 1990; 3 Suppl. 1: 275–81

    Google Scholar 

  206. Thompson GR. Adverse reactions profile: 10. simvastatin and pravastatin. Prescr J 1990; 33: 217–20

    Google Scholar 

  207. Garnett WR. Interactions with hydroxymethylglutaryl-coenzyme A reductase inhibitors. Am J Health System Pharm 1995; 52: 1639–45

    CAS  Google Scholar 

  208. Safeer RS, Lacivita CL. Choosing drug therapy for patients with hyperlipidemia. Am Fam Physician 2000; 61(11): 3371–82

    PubMed  CAS  Google Scholar 

  209. Holme I. Lipid lowering in the patient at risk — the next decade of discovery. Br J Cardiol 2000; 7(4): 223–30

    Google Scholar 

  210. Stamler M, Wentworth D, Neaton JD, et al. Is the relationship between serum cholesterol and the risk of premature death from coronary heart disease continuous or graded? Findings in 356,222 screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA 1986; 256: 2823–8

    Article  PubMed  CAS  Google Scholar 

  211. Jacobson TA, Schein JR, Williamson A, et al. Maximizing the cost-effectiveness of lipid-lowering therapy. Arch Intern Med 1998 Oct 12; 158: 1977–89

    Article  PubMed  CAS  Google Scholar 

  212. Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med 1996; 335: 1001–9

    Article  PubMed  CAS  Google Scholar 

  213. Long term Intervention with Pravastatin in Ischemic disease (LIPID) study group: Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med 1998; 339: 1349–57

    Article  Google Scholar 

  214. Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med 1995; 333(20): 1301–7

    Article  PubMed  CAS  Google Scholar 

  215. Downs JR, Clearfield M, Weis S, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TEXCAPS. JAMA 1998; 279: 1615–22

    Article  PubMed  CAS  Google Scholar 

  216. Pedersen TR. Pro and con: low-density lipoprotein cholesterol lowering is and will be the key to the future of lipid management. Am J Cardiol 2001 Mar; 8(87) Suppl. 5A: 8B–12B

    Article  Google Scholar 

  217. Wilhelmsen L, Pyorala K, Wedel H, et al. Risk factors for a major coronary event after myocardial infarction in the Scandianavian Simvastatin Survival Study (4S): impact of predicted risk on the benefit of cholesterol-lowering treatment. Eur Heart J 2001 Jul; 22(13) 1119–27

    Article  PubMed  CAS  Google Scholar 

  218. Isaacsohn JL, Davidson MH, Hunninghake D, et al. Aggressive lipid-lowering initiation abates new cardiac events (ALLIANCE)-rationale and design of atorvastatin versus usual care in hypercholesterolemic patients with coronary artery disease. Am J Cardiol 2000; 86(2): 250–2

    Article  PubMed  CAS  Google Scholar 

  219. Dahlof B, Sever PS, Poulter NR, et al. The Anglo-Scandinavian Cardiac Outcomes Trial. Am J Hypertens 1998; 11: 9A–10A

    Article  Google Scholar 

  220. Gmerek A, McLain R, Nawrocki J. A 4-year, placebo-controlled study of atorvastatin as prevention of CHD endpoints in patients with non-insulin dependent diabetes mellitus [abstract]. Diabetes 1997 May; 46 Suppl. 1: 363

    Google Scholar 

  221. Atorvastatin International Trials Compendium. Pfizer Inc, 2001. (Data on file)

  222. Wanner C, Krane V, Ruf G, et al. Rationale and design of a trial improving outcome of type 2 diabetics on hemodialysis. Kidney Int 1999; 56 Suppl. 71: S222–6

    Article  Google Scholar 

  223. Pedersen TR, Faergeman O, Holme I, et al. Effect of greater LDL-C reductions on prognosis — the Incremental Decrease in Endpoints through Aggressive Lipid Lowering (IDEAL) trial [abstract]. Atherosclerosis 1999; 144 Suppl. 1: 38

    Article  Google Scholar 

  224. Goldstein LB, Welch KMA, Amarenco P, et al. Stroke prevention by aggressive reduction in cholesterol levels — the SPARCL study [poster]. Presented at the 25th International Stroke Conference; 2000 Feb 10–12; New Orleans

  225. LaRosa JC, for the TNT steering committee. Effect of lowering LDL-C beyond currently recommended targets — the treating to new targets study. Poster presented at the 13th International Symposium on Drugs Affecting Lipid Metabolism; 1998 May 30–Jun 3; Florence

  226. Raggi P, Callister TQ, Davidson M, et al. Aggressive versus moderate lipid-lowering therapy in postmenopausal women with hypercholesterolaemia: rationale and design of the Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES) trial. Am Heart J 2001; 141: 722–6

    Article  PubMed  CAS  Google Scholar 

  227. Nissen S, for the REVERSAL investigators. Assessing the effects of statins on atherosclerosis progression using intravascular ultrasound: rationale and design of the REVERSAL study [abstract]. Atherosclerosis 2001; 2(2) Suppl.: 51–2

    Google Scholar 

  228. Creager MA, Hiatt W, Mohler ER, et al. Effects of atorvasatin on exercise time in patients with intermittent claudication (IC) due to peripheral arterial disease (PAD) [poster]. Presented at the XIVth International Symposium on Drugs Affecting Lipid Metabolism, 2001 Sep 9–12; New York

  229. Ekonomidou D, Kokolina E, Manou E, et al. Effects of serivastatin and atorvastatin on dyslipidaemia of peritoneal dialysis patients [abstract]. Nephrol Dial Transplant 2001 Jun; 16(6): A191

    Google Scholar 

  230. Ma P, Hegele R, Yale JF, et al. CAVEAT: a randomised, double-blind, parallel group evaluation of cerivastatin 0.4mg and 0.8mg compared to atorvastatin 10mg and 20mg once daily in patients with combined (type IIB) dyslipidaemia. Br J Cardiol 2000; 7(12): 780–6

    Google Scholar 

  231. Hunninghake D, Insull W, Knopp R, et al. Comparison of the efficacy and safety of atorvastatin versus cerivastatin in patients with hypercholesterolemia [abstract]. Atherosclerosis 1999; 144 Suppl. 1:28–9

    Article  Google Scholar 

  232. Bayer drug linked to more deaths [online]. Available from: URL: http://news.bbc.co.uk/hi/english/business/newsidl488000/1488486.stm [Accessed 2001 Aug 14]

  233. Baycol news prompts EU review of cholesterol drugs [online]. Available from: URL: http://dailynews.yahoo.eom/h/nm/20010809/hl/baycol1.html [Accessed 2001 Aug 14]

  234. Goldstein MR. Should reductase inhibitor therapy to lower cholesterol be instituted in the setting of an acute coronary event? [1]. Atherosclerosis 2000; 149(1): 215–6

    Article  PubMed  CAS  Google Scholar 

  235. Cohen DJ, Carrozza JP, Baim DS. Aggressive lipid-lowering therapy compared with angioplasty in stable coronary artery disease [2] [in letter]. N Engl J Med 1999; 341(24): 1853–4

    Article  PubMed  CAS  Google Scholar 

  236. Waters D. Is a mechanical or a metabolic approach superior in the treatment of coronary disease? Results of the Atorvastatin Versus Revascularization (AVERT) Trial. Eur Heart J 2000; 21(13): 1029–31

    Article  PubMed  CAS  Google Scholar 

  237. West of Scotland Coronary Prevention Study Group. Influence of pravastatin and plasma lipids on clinical events in the West of Scotland Coronary Prevention Study (WOSCOPS). Circulation 1998; 97: 1440–5

    Article  Google Scholar 

  238. Sacks FM, Maye LA, Davis BR, et al. Relationship between plasma LDL concentrations during treatment with pravastatin and recurrent coronary events in the Cholesterol and Recurrent Events Trial. Circulation 1998; 97: 1446–52

    Article  PubMed  CAS  Google Scholar 

  239. Pendersen TR, Olsson AG, Faergeman O, et al. Lipoprotein changes and reduction in incidence of major coronary heart disease events in the Scandinavian Simvastatin Survival Study. Circulation 1998; 97: 1453–60

    Article  Google Scholar 

  240. Garg A. Treatment of diabetic dyslipidemia. Am J Cardiol 1998 Feb 26; 81: 47–51

    Article  Google Scholar 

  241. Kato T, Tokoro T, Namii Y, et al. Early introduction of HMG-CoA reductase inhibitors could prevent the incidence of transplant coronary artery disease. Transplant Proc 2000; 32(2): 331–3

    Article  PubMed  CAS  Google Scholar 

  242. Christians U, Jacobsen W, Floren LC. Metabolism and drug interactions of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in transplant patients: are the statins mechanistically similar? Pharmacol Ther 1998 Oct; 80: 1–34

    Article  PubMed  CAS  Google Scholar 

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    Harinder S. Malhotra & Karen L. Goa

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Malhotra, H.S., Goa, K.L. Atorvastatin. Drugs 61, 1835–1881 (2001). https://doi.org/10.2165/00003495-200161120-00012

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