title: [Mechanisms of myocardial cell protection from ischemia/reperfusion injury and potential clinical implications].
abstract: Myocardial cell damage caused by myocardial ischemia results from several factors that include the duration of ischemia, oxygen demand by cardiomyocytes at the time of ischemia, and the presence and entity of collateral blood flow to the ischemic area. Importantly, myocardial cell injury may derive not only from ischemia itself but also from detrimental phenomena occurring during the restoration of myocardial blood flow after the ischemic episode (reperfusion damage). In the last decades a lot of studies have demonstrated that cardiomyocytes have several mechanisms that provide them protection against the damage deriving from ischemia-reperfusion, also allowing a prolongation of survival in the most severe cases. In this article we review some of these mechanisms, also discussing their present and/or potential therapeutic applications in the clinical setting. The topics include the interventions aimed at reducing cardiac work through a reduction of oxygen demand by myocardial cells or at optimizing the utilization of energetic resources by myocardial cells in situations of ischemia, the importance of phenomena such as ischemic preconditioning (early and delayed) and postconditioning of myocardial cells, and, finally, the theoretic possibility of interventions aimed at preventing cell death consequent to apoptosis.
authors.affiliation: Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Roma
authors.forename: Priscilla
authors.initials: P
authors.lastname: Lamendola
authors.forename: Antonio
authors.initials: A
authors.lastname: Di Monaco
authors.forename: Lucy
authors.initials: L
authors.lastname: Barone
authors.forename: Chiara
authors.initials: C
authors.lastname: Pisanello
authors.forename: Gaetano A
authors.initials: GA
authors.lastname: Lanza
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
mesh_terms: D000083:Acetanilides / Q000627:therapeutic use*; D054058:Acute Coronary Syndrome / Q000188:drug therapy; D000787:Angina Pectoris / Q000188:drug therapy / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D016923:Cell Death; D003097:Collateral Circulation; D004195:Disease Models, Animal; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D015201:Meta-Analysis as Topic; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism*; D010101:Oxygen Consumption; D010879:Piperazines / Q000627:therapeutic use*; D016032:Randomized Controlled Trials as Topic; D000069458:Ranolazine; D014292:Trimetazidine / Q000627:therapeutic use*; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: D000083:Acetanilides; D010879:Piperazines; D014665:Vasodilator Agents; D000069458:Ranolazine; D014292:Trimetazidine