Prodromal angina limits infarct size: A role for ischemic preconditioning: Filippo Ottani, Marcello Galvani, Donatella Ferrini, Francesco Sorbello, Patrizia Limonetti, Denis Pantoli, Franco Rusticali. Divisione di Cardiologia and Fondazione Cardiologica “M.Z. Sacco,” Ospedale G.B. Morgagni, Forli, Italy. Circulation. 1995;91: 291–7

Abstract

Myocardial ischemia, even if it persists for a prolonged period of time, does not inevitably induce irreversible damage. Recent studies have identified 2 phenomena that are characterized by endogenous cardioprotective features, i.e., myocardial hibernation and ischemic preconditioning. Myocardial hibernation is characterized by chronic contractile dysfunction during persistent ischemia. The myocardium remains viable, and function is restored upon reperfusion. Ischemic preconditioning is characterized by delayed development of infarct size when prolonged and severe myocardial ischemia is preceded ≥1 short-lasting episodes of ischemia and reperfusion. While ischemic preconditioning involves the activation of the adenosine A1 receptor, the bradykinin receptor, and activation of adenosine triphosphate (ATP)-dependent potassium channels, the mechanisms underlying myocardial hibernation are still unclear.