Carrasco OF, Vidrio H

Idioma: Español
Referencias bibliográficas: 19
Paginas: 207-210
Archivo PDF: 73.63 Kb.

FRAGMENTO

En las últimas décadas se ha hecho un progreso considerable en el esclarecimiento de la relación entre los desórdenes lipídicos y la prevención de enfermedades cardiacas isquémicas. La identificación de nuevos fármacos lipoactivos aumenta las opciones terapéuticas para los médicos. Los inhibidores de la 3-hidroxi-3-metilglutaril coenzima A (HMG-CoA) reductasa o estatinas, son considerados en la actualidad como una de las más poderosas clases de agentes farmacológicos para la reducción lipídica y en general para el tratamiento de la enfermedad cardiovascular.

REFERENCIAS (EN ESTE ARTÍCULO)

1. Goldstein JL, Brown MS. Regulation of the mevalonate pathway. Nature 1990; 343: 425-30.

2. Halcox J, Deanfield J. Beyond the laboratory: clinical implications for statin pleiotropy. Circulation 2004; 109 suppl II: II-42-8.

3. Malek AM, Alper SL, Izumo S. Hemodynamic shear stress and its role in atherosclerosis. JAMA 1999; 282: 2035-42.

4. Mason R, Walter M, Jacob R. Effects of HMG-CoA reductase inhibitors on endothelial function. Circulation 2004; 109 suppl II: II-34-41.

5. Vane JR, Anggard EE, Botting RM. Regulatory functions of the vascular endothelium. N Engl J Med 1990; 323: 27-36.

6. John S, Schneider MP, Delles C. Lipid-independent effects of statins on endothelial function and bioavailability of nitric oxide in hypercholesterolemic patients. Am Heart J En prensa 2005.

7. Laufs U, Wassmann S, Hilguers S et al. Rapid effects on vascular function after initiation and withdrawal of atorvastatin in healthy, noncholesterolemic men. Am J Cardiol 2001; 88: 1306-7.

8. Anderson TJ, Meredith IT, Yeung AC et al. The effect of cholesterol-lowering and antioxidant therapy on endothelium-dependent coronary vasomotion. N Engl J Med 1995; 332: 488-93.

9. Feron O, Dessy C, Desager JP et al. Hydroxy-methylglutaryl-coenzyme A reductase inhibition promotes endothelial nitric oxide synthase activation through a decrease in caveolin abundance. Circulation 2001; 103: 113-8.

10. Laufs U, La Fata V, Plutzky J et al. Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors. Circulation 1998; 97: 1129-35.

11. Wassman S, Laufs U, Baumer AT et al. HMG-CoA reductase inhibitors improve endothelial dysfunction in normocholesterolemic hypertension via reduced production of reactive oxygen species. Hypertension. 2001; 37: 1450-7.

12. Laufs U, Liao JK. Post-transcriptional regulation of endothelial nitric oxide synthase mRNA stability by Rho GTPase. J Biol Chem 1998; 273: 24266-71.

13. Wassmann S, Laufs U, Muller K et al. Cellular antioxidant effects of atorvastatin in vitro and in vivo. Arterioscler Thromb Vasc Biol 2002; 22: 300-5.

14. Vasa M, Fichtlscherer S, Adler K et al. Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease. Circulation 2001; 103: 2885-90.

15. Weber W. Drug firm withdraws statin from market. Lancet 2001; 358: 568.

16. Pasternak RC, Smith SC, Bairey-Merz CB et al. ACC/AHA/NHLBI Clinical advisory on the use of safety of statins. Circulation 2002; 106: 1024-8.

17. Davidson MH. Safety profiles for the HMG-CoA reductase inhibitors: treatment and trust. Drugs 2001; 61: 197-206.

18. Greur PJ, Vega JM, Mercuri MF et al. Concomitant use of cytochrome P450 3A4 inhibitors and simvastatin. Am J Cardiol 1999; 84: 811-5.

19. Williams D, Feely J. Pharmacokinetic-pharmacodynamic drug interactions with HMG-CoA reductase inhibitors. Clin Pharmacokinet 2002; 41: 343-70.