title: Statin therapy and myocardial no-reflow.
abstract: HMG-CoA reductase inhibitors (statins) have now become one of the most powerful pharmacological strategies in the treatment of cardiovascular diseases. Originally, the cardioprotective effects of statins were thought to be mediated through lipid lowering actions. However, it has now become increasingly clear that the beneficial effects of statins are not related to the lipid lowering effects, but rather to a number of pleiotropic actions. Of particular interest, statins have been shown to increase bioavailability of nitric oxide and protect against vascular inflammation and cardiac cell death in a number of cardiovascular disease states. In this present issue of the British Journal of Pharmacology, Zhao and colleagues provide a novel mechanism of action for statins with the observation that simvastatin reduces myocardial 'no-reflow' after ischemia and reperfusion by activating the mitochondrial K(ATP) channel. The findings of the present study have very profound implications for the treatment of cardiovascular disease. This commentary discusses the implications of these findings and how they relate to the established cardioprotective actions of statins.
authors.affiliation: Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
authors.forename: J W
authors.initials: JW
authors.lastname: Calvert
authors.forename: D J
authors.initials: DJ
authors.lastname: Lefer
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D019157:Ischemic Preconditioning, Myocardial; D009569:Nitric Oxide / Q000502:physiology; D015221:Potassium Channels / Q000187:drug effects; D019821:Simvastatin / Q000494:pharmacology
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015221:Potassium Channels; C117780:mitochondrial K(ATP) channel; D009569:Nitric Oxide; D019821:Simvastatin