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Saturday, 17 May, 2008



Presenter Profile

Dr Philip Barter
  Philip J Barter, MD PhD FRACP The Heart Research Institute, Sydney, Australia

Philip Barter is Director of The Heart Research Institute in Sydney, Australia and Professor of Medicine at the University of Sydney. He is secretary of the International Atherosclerosis Society. He is also a member of the Board of Directors of the International Task Force for Prevention of Coronary Heart Disease. He was a member of the executives of the steering committees of two large international trials investigating the effects of lipid lowering in the prevention of coronary disease (the FIELD study and the TNT study) and is chairman of the steering committee of the recently terminated ILLUMINATE trial, which was investigating the effects of inhibiting cholesteryl ester transfer protein in humans. His basic research interests involve the study of plasma lipids and lipoproteins, specifically high-density lipoproteins, the factors that regulate them and the mechanism by which they protect against coronary heart disease.

Recent articles by Philip Barter

New Insights Into the Role of HDL as an Anti-inflammatory Agent in the Prevention of Cardiovascular Disease.
Effects of Torcetrapib in Patients at High Risk for Coronary Events.
Remodelling of apolipoprotein E-containing spherical reconstituted high density lipoproteins by phospholipid transfer protein.
Identification and characterization of two non-secreted PCSK9 mutants associated with familial hypercholesterolemia in cohorts from New Zealand and South Africa.

Presentation

An Evolutionary Journey Towards Comprehensive Patient Care


Conquering Atherosclerosis - From Science to Clinical Practice - Sponsored by AstraZeneca
76th Congress of the European Atherosclerosis Society in Helsinki, Finland
June 11th, 2007


Despite the proven efficacy of statins in clinical trials, dyslipidaemia remains poorly controlled in routine clinical practice.1 Possible reasons for this include use of less effective agents, lack of dose titration, and poor patient awareness leading to non-adherence to treatment. In addition, the broad range of patients at risk of cardiovascular disease (CVD) presents different challenges to physicians and this may impair optimal dyslipidaemia management.

Statins differ in their efficacy for LDL cholesterol (LDL-C) lowering2 and dose titration may be required to achieve an adequate level of reduction with some statins. Selecting a statin that gets the majority of patients to guideline goals at starting dose is important to reduce the need for dose titration and simplify dosing regimens.

The efficacy and tolerability of statins have been established in several patient groups including those at high CVD risk,3–5 and those with diabetes6–9 or metabolic syndrome.10,11 The effects of statins in other patients that may benefit from treatment but in whom efficacy has not yet been determined is the subject of current investigation. These include patients with acute coronary syndromes, an enhanced inflammatory response, chronic renal failure 12–14 or heart failure,15–17 as well as patients with or at risk of Alzheimer’s disease18 or osteoporosis.19,20 The use of a statin that offers a favourable benefit:risk profile and ease of administration across a wide range of patients will facilitate effective comprehensive management of dyslipidaemia, with benefits for improved CVD prevention.




References:

1. Assmann G, Benecke H, Neiss A, Cullen P, Schulte H, Bestehorn K. Gap between guidelines and practice: attainment of treatment targets in patients with primary hypercholesterolemia starting statin therapy. Results of the 4E-Registry (Efficacy Calculation and Measurement of Cardiovascular and Cerebrovascular Events Including Physicians' Experience and Evaluation). Eur J Cardiovasc Prev Rehabil 2006; 13: 776–783.
2. Jones PH, Davidson MH, Stein EA, et al. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial). Am J Cardiol 2003; 92: 152–160.
3. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002; 360: 7–22.
4. Clearfield MB, Amerena J, Bassand JP, et al. Comparison of the efficacy and safety of rosuvastatin 10 mg and atorvastatin 20 mg in high-risk patients with hypercholesterolemia – Prospective study to evaluate the Use of Low doses of the Statins Atorvastatin and Rosuvastatin (PULSAR). Trials 2006; 7: 35.
5. Leiter LA, Rosenson RS, Stein E, et al. Efficacy and safety of rosuvastatin 40mg versus atorvastatin 80 mg in high-risk patients with hypercholesterolemia: Results of the POLARIS study. Atherosclerosis 2007; Epub ahead of print.
6. Colhoun HM, Betteridge DJ, Durrington PN, et al. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet 2004; 364: 685–696.
7. Collins R, Armitage J, Parish S, Sleigh P, Peto R, Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial. Lancet 2003 361: 2005–2016.
8. Berne C, Siewert-Delle A, and the URANUS study investigators. Comparison of rosuvastatin and atorvastatin for lipid lowering in patients with type 2 diabetes mellitus: results from the URANUS study. Cardiovasc Diabetol 2005; 4: 7.
9. Wolffenbuttel BH, Franken AA, Vincent HH, Dutch CORALL Study Group. Cholesterol lowering effects of rosuvastatin compared with atorvastatin in patients with type 2 diabetes – CORALL study. J Intern Med 2005; 257: 531–539.
10. Deedwania P, Barter P, Carmena R, et al. Reduction of low-density lipoprotein cholesterol in patients with coronary heart disease and metabolic syndrome: analysis of the Treating to New Targets study. Lancet 2006; 368: 919–928.
11. Stalenhoef AF, Ballantyne CM, Sarti C, et al. A comparative study with rosuvastatin in subjects with metabolic syndrome: results of the COMETS study. Eur Heart J 2005; 26: 2664–2672.
12. Fellstrom B, Zannad F, Schmieder R, et al. Effect of rosuvastatin on outcomes in chronic haemodialysis patients – design and rationale of the AURORA study. Curr Control Trials Cardiovasc Med 2005; 6: 9.
13. Saltissi D, Westhuyzen J, Morgan C, Healy H. Efficacy, safety and tolerability of atorvastatin in dyslipidemic subjects with advanced (non-nephrotic) and endstage chronic renal failure. Clin Exp Nephrol 2006; 10: 201–209.
14. Wanner C, Krane V. Lessons learnt from the 4D trial. Nephrol Ther 2006; 2: 3–7.
15. Tavazzi L, Tognoni G, Franzosi MG, et al. Rationale and design of the GISSI heart failure trial: a large trial to assess the effects of n-3 polyunsaturated fatty acids and rosuvastatin in symptomatic congestive heart failure. Eur J Heart Fail 2004; 6: 635–641.
16. Khush KK, Waters DD, Bittner V, et al. Effect of high-dose atorvastatin on hospitalizations for heart failure: subgroup analysis of the Treating to New Targets (TNT) study. Circulation 2007; 115: 576–583.
17. Kjekshus J, Dunselman P, Blideskog M, et al. A statin in the treatment of heart failure? Controlled rosuvastatin multinational study in heart failure (CORONA): Study design and baseline characteristics. Eur J Heart Fail 2005; 7: 1059–1069.
18. Whitfield JF. Can statins put the brakes on Alzheimer's disease? Expert Opin Investig Drugs 2006; 15: 1479–1485.
19. Omiogui S. The Interleukin-6 inflammation pathway from cholesterol to aging – role of statins, bisphosphonates and plant polyphenols in aging and age-related diseases. Immun Ageing 2007; 4: 1.
20. Horiuchi N, Maeda T. Statins and bone metabolism. Oral Dis 2006; 12: 85–101.



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