Chronic ischaemic ('hibernating') and postischaemic ('stunned') dysfunctional but viable myocardium.
Myocardial stunning might be defined as a transient postischaemic contractile abnormality seen after reperfusion has been achieved. The benefits of reperfusion therapy might be delayed, but will occur within hours to days after reperfusion. Consequently, the stunned myocardium is viable, but its full recovery might be delayed for a few weeks. While multiple pathophysiological mechanisms are reported to be responsible for the stunning phenomenon, a partial failure of calcium cycling seems to be the cause of the electromechanical uncoupling demonstrated in the stunned myocardium. No pharmacological or other means were used to detect myocardial viability in the stunned myocardium since it is, by definition, a viable myocardium. The 'hibernating' myocardium differs from the stunned myocardium in that it is a viable (partially or completely), chronically underperfused myocardium with an impaired metabolism and function which is slowly reversible when adequate blood flow is restored. This condition represents an 'extreme defence mechanism' in response to profound and chronic ischaemia; however, it does not occur in all patients with chronic myocardial ischaemia. In some circumstances the myocardium might undergo ischaemic necrosis instead of hibernation, with irreversible structural and functional damage. The mechanism leading to one or other response to chronic ischaemia is unclear and might depend on the degree and duration of myocardial ischaemia and histopathological response. Thus, the detection of hibernated myocardium is highly significant because it constitutes a potentially salvageable myocardium. The gold standard for the clinical detection of these conditions is positron emission tomography (PET), but it is uncertain what role echocardiography and pharmacological tests could play in this field.
Trevi
G P
GP
Istituto di Clinica Cardiovascolare, Università Chieti, Italy.
Sheiban
I
I
D003327:Coronary Disease / Q000503:physiopathology* / Q000628:therapy; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D015425:Myocardial Reperfusion