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(Hypertension. 2004;43:1171.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Statin Therapy: Having the Good Without the Bad

James K. Liao

From the Vascular Medicine Unit, Cardiovascular Division, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass.

Correspondence to James K. Liao, MD, Vascular Medicine Research, 65 Landsdowne Street, Room 275, Cambridge, MA 02139. E-mail jliao@rics.bwh.harvard.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Because serum cholesterol level is strongly associated with coronary heart disease, it has been generally assumed that cholesterol reduction by 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors or statins is the predominant mechanism underlying their beneficial effects. However, large prospective trials with statins suggest that these agents may have beneficial effects in cardiovascular disease in addition to their cholesterol-lowering effects. These so-called cholesterol-independent or "pleiotropic" effects include improving or restoring endothelial function, decreasing oxidative stress and inflammation, enhancing the stability of atherosclerotic plaques, and inhibiting the thrombogenic response in the vascular wall (Table). Many of these effects may explain some of the rapid actions of statin therapy on tissue perfusion in acute coronary syndrome and ischemic stroke, irrespective of baseline cholesterol levels.

View this table: [in this window] [in a new window]   ffects of Statins on the Vascular Wall

Recently, statins have also been found to increase the number of circulating endothelial progenitor cells (EPCs).¹ EPCs augment ischemia-induced neovascularization,² accelerate re-endothelialization after carotid balloon injury,³ and improve post-ischemic cardiac function.⁴ Indeed, statins induce angiogenesis by promoting the proliferation, migration, and survival of circulating EPCs.⁵ In patients with stable coronary artery disease, administration of statins for 4 weeks augmented the number of circulating EPCs and enhanced functional capacity in patients with stable coronary artery disease.⁶ These findings agree with earlier data showing that statins rapidly mobilize EPCs from the bone marrow and accelerates vascular structure formation via activation of phosphatidylinositol 3-kinase/protein kinase Akt and endothelial nitric oxide synthase.^5,7,8 These angiogenic effects were observed at lower concentrations of statins and were cholesterol-independent. At . . . [Full Text of this Article]

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