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Frank W. Sellke
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J Thorac Cardiovasc Surg 2007;133:1686-1687
© 2007 The American Association for Thoracic Surgery


Letter to the Editor

Reply to the Editor

Munir Boodhwani, MD, MMSc, Frank W. Sellke, MD

Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass

The first 20% of the full text of this article appears below.

Statins are increasingly being used in patients with coronary disease. Recently, there has been increasing evidence from studies conducted in both in vitro and murine models that low-dose statins promote angiogenesis and high-dose statins inhibit it.1Go The application of these findings to patients is limited because of the lack of translation of the experimental models to the human setting. It is in this context that we examined the in vivo effects of high-dose atorvastatin in a clinically relevant large animal model of chronic myocardial ischemia and hypercholesterolemia. We found that atorvastatin treatment did not improve endogenous myocardial angiogenesis2Go or response to growth factor therapy,3Go despite improvement in endothelial function.

Czepluch and Waltenberger make the important point that the dose of statins used may be too high for clinical relevance and indeed may be toxic. The first thing to note is that, for initial toxicity studies, as much as 80 . . . [Full Text of this Article]


Related Article

High-dose atorvastatin is associated with impaired myocardial angiogenesis in response to vascular endothelial growth factor in hypercholesterolemic swine: Relevance to the human situation?
Frauke S. Czepluch and Johannes Waltenberger
J. Thorac. Cardiovasc. Surg. 2007 133: 1685-1686. [Extract] [Full Text] [PDF]






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Copyright © 2007 by The American Association for Thoracic Surgery.