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Ann Thorac Surg 2006;81:2225-2226
© 2006 The Society of Thoracic Surgeons

Original article: Cardiovascular

Invited commentary

Jun Feng, MD, PhD, Frank W. Sellke, MD

Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, DA 880, Boston, MA 02215

(Email: jfeng@caregroup.harvard.edu; fsellke@caregroup.harvard.edu).

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

Li and colleagues [1] in the present study provide provocative in vivo experimental data to support the notion that pravastatin (5 or 50 mg/kg/d) improves remodeling and cardiac function after acute myocardial infarction through anti-inflammatory mechanisms, rather than pro-angiogenic pathways. Furthermore, combination of pravastatin (50 mg/kg/d) with bone marrow mononuclear cells (BM-MNCs) implantation failed to induce synergistic effects of angiogenesis. These interesting and provocative findings heated current controversies on the issues of potential statins-related myocardial and angiogenic effects.

"From bench to bedside," statins have been found to reduce the risk of coronary event by cholesterol-lowering dependent and independent mechanisms [. . . [Full Text of this Article]






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