Much less is known about the pathogenesis of myocardial hibernation than about that of stunning and ischemic preconditioning. Mechanistic data are only available from animal models of short-term hibernation. Such studies have taken perfusion-contraction matching, recovery of metabolic markers, persistent inotropic reserve, and lack of infarction as criteria of hibernation. On these premises, a downregulation of ß-adrenoceptor density and an involvement of adenosine and activation of KATP channels have been excluded. The role of acidosis and triggering events is still unclear. Hibernating myocardium has, however, a reduced calcium responsiveness...