Treatments

Treatment options

Statins:
Epidemiological and clinical studies have clearly established the link between elevated LDL-C and cardiovascular morbidity and mortality.¹ This positive relationship is observed over a wide range of LDL-C levels, and it has been shown that the higher the LDL-C level, the greater the individual’s risk of developing cardiovascular disease.¹

Statins (HMG-CoA reductase inhibitors) are the most effective class of drugs in reducing LDL-C levels and have also been shown to be very effective in improving the overall lipid profiles in patients with dyslipidaemia. Key studies have shown that statins effectively:

reduce coronary events in subjects with and without coronary heart disease (CHD)^8-14
slow progression and even promote regression of atherosclerosis^2-7
reduce cardiovascular morbidity and mortality^8-16

The benefits of statin therapy on morbidity and mortality from cardiovascular disease have also been demonstrated in patients with a wide range of cardiovascular risk factors, including those with type 2 diabetes, metabolic syndrome, and multiple risk factors.^14,17,18

International guidelines formulated in recent years recommend that lowering elevated LDL-C in order to reduce cardiovascular risk is the primary goal in the management of dyslipidaemia.^1,19 These guidelines recommend assessment of an individual’s risk factors in order to determine the LDL-C levels to be achieved, depending on the patient’s overall level of cardiovascular risk. However, it is clear that despite these guidelines and the availability of statins, significant numbers of patients are under-treated and fail to reach recommended guideline LDL-C levels, and therefore, optimal outcomes.^20,21

Currently, there are six statins available: atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin and simvastatin.

In addition to statin therapy, several medical treatments as well as changes in diet and exercise can also contribute to LDL-C reduction.

References:
1. Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults. JAMA 2001;285:2486-2497.
2. Blankenhorn DH et al. Ann Intern Med 1993;119(10):969-976.
3. Waters D et al. Circulation 1994;89(3):959-968.
4. MAAS Investigators. Lancet 1994;344:633-638.
5. Pitt B et al. J Am Coll Cardiol 1995;26(5):1133-1139.
6. Brown BG et al. N Engl J Med 1990;323(19):1289-1298.
7. Nissen S. JAMA 2004;291:1071-1080.
8. The SPARCL Investigators N Engl J Med 2006; 355: 549-559.
9. Sacks FM et al, for the Cholesterol and Recurrent Event Trial Investigators. N Engl J Med 1996;335:1001-1009.
10. The Scandinavian Simvastatin Survival Study Group. Lancet 1994;344:1383–1389.
11. Shepherd J et al, for the West of Scotland Coronary Prevention Study (WOSCOPS) Group. N Engl J Med 1995;333:1301-1307.
12. The Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. N Engl J Med 1998;339:1349-1357.
13. Heart Protection Study Collaborative Group. Lancet 2002;360:7-22.
14. Sever PS et al. Lancet 2003;361:1149-1158.
15. LaRosa J et al. N Engl J Med 2005;352:1425-1435.
16. Cannon C et al. N Engl J Med 2004;350:1495-1504.
17. Shepherd J et al. Diabetes Care 2006; 29:1220-1226.
18. Ott C, Schmieder RE. Curr Hypertens Rep. 2009 Apr;11:143-149.
19. Grundy SM et al. Circulation 2004;110:227-239.
20. Pearson TA et al. Arch Intern Med 2000;160:459-467.
21. EUROASPIRE II Study Group. Eur Heart J 2001;22:554-572.