title: Restoring the dysfunctional endothelium.
abstract: Nowadays the endothelium is considered a key determinant of vascular health. NO is the principal mediator of all endothelial protective effects, due to its antiinflammatory, antiproliferative, immunomodulatory and vasorelaxant properties. On the contrary, a growing body of evidence suggests that endothelial dysfunction is associated with cardiovascular events. Emerging data suggest that acute coronary syndromes (ACS) may involve a complex interplay between endothelial dysfunction, inflammation and thrombosis. Despite the success in reducing the mortality from acute cardiovascular events, the incidence of cardiovascular disease and its complication continues to increase. New insights into mechanisms of endothelial dysfunction, such as a better understanding of the regulation of vascular sources of oxygen radicals, may lead to novel therapeutic strategies with the potential to improve prognosis. The key pharmacological agents that improve clinical outcome in high-risk patients are statins, ACE-inhibitors or angiotensin receptor antagonists. Compelling scientific evidence suggests that these medications are effective in improving endothelial function. The present review focuses on the potential importance of benefits on endothelium of these medicaments in the management of acute coronary syndromes.
authors: Department of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padova, Italy.
authors: Elena
authors: E
authors: Osto
authors: Giuseppe
authors: G
authors: Coppolino
authors: Massimo
authors: M
authors: Volpe
authors: Francesco
authors: F
authors: Cosentino
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D002317:Cardiovascular Agents / Q000494:pharmacology* / Q000627:therapeutic use; D003327:Coronary Disease / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D065128:Endothelin Receptor Antagonists; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D017466:Receptors, Endothelin / Q000378:metabolism
chemical_list: D000319:Adrenergic beta-Antagonists; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D002317:Cardiovascular Agents; D065128:Endothelin Receptor Antagonists; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017466:Receptors, Endothelin; D009569:Nitric Oxide