Importance of early recanalization of the occluded coronary artery in acute myocardial infarction for preservation of left ventricular function

Stunning: Damaging or protective to the myocardium?

“…The first two forms of reperfusion injury refer to a fully reversible and transient abnormality with complete, although delayed, recovery in contractility. The others describe an almost irreversible condition that results in further depression of contractility [5].…”

“…The greatest benefit is observed in those patients who receive treatment within 1 hour of the onset of chest pain, but it is present, although to a reduced extent, up to approximately 4-6 hours [10]. Reperfusion after 6 hours neither iraproves myocardial function [5] nor prognosis [10]. Unfortunately, many patients will not reach medical attention within 6 hours and will not benefit from reperfusion.…”

Can We Improve Myocardial Protection during Ischaemic Injury?

“…This later event is particularly detrimental as the mitochondria, during reperfusion, may use the restored oxygen for calcium transport instead of ATP production, with the two processes competing for the same energy source, i.e. the ∆Ψ generated across the inner mitochondrial membrane [20]. As a consequence, it was logical to consider calcium antagonists to attenuate calcium overload.…”

“…The area not yet irreversibly damaged constitutes the so-called ‘area at risk'. The duration of ischaemia necessary to cause irreversible damage varies from seconds in isolated myocytes, a few minutes in small rodents, to about 30-40 min in large mammals and even longer in humans (perhaps as long as 6-8 h), although in humans it is difficult to establish with precision the onset of ischaemia [16,19,20]. It follows that the area at risk does not necessarily correspond to the actual infarct size, which normally begins in the inner myocardial layers and spreads transmurally and laterally.…”

“…Reperfusion seems to suddenly and massively potentiate myocardial damage, characterized by intense oedema and cytosolic and mitochondrial calcium overload, causing an increase of myofilament contracture and a further reduction of ATP production. Figure 7 shows that this type of reperfusion injury is evident in an isolated and perfused heart preparation when readmission of flow occurs rather late, after several (90) min of ischaemia, which roughly correspond to 6-12 h in humans [20]. …”