Reperfusion injury quantification remains unreliable in patients; leaves open validation of cardioprotective strategies in vivo.
Key Points
To evaluate whether post-ischemic reperfusion injury represents a clinically meaningful barrier to myocardial salvage or an artifact predominantly observed in experimental models.
Reviewed laboratory data from in vitro preparations assessing isolated hearts subjected to periods of normothermic global ischemia.
Analyzed in vivo diagnostic approaches and confounding factors influencing the quantification of myocardial salvage and infarct size.
In vitro models consistently demonstrated reperfusion-associated injury through intracellular enzyme washout, ultrastructural damage, elevated resting tension, and calcium overload.
In vivo verification remains problematic due to variable collateral blood flow, systemic hemodynamic shifts, and difficulties in standardizing infarct localization.