Attenuation of reperfusion microvascular ischemia by aqueous oxygen: experimental and clinical observations

It is being increasingly recognized that, in patients with acute myocardial infarction, angiographically successful recanalization of the occluded artery cannot be used as a reliable indicator of successful myocardial perfusion. Postischemic myocardial reperfusion is commonly associated with focal regions of microvascular impairment, even when global coronary artery flow is normal. This problem ranges in severity from microvascular stunning to no reflow, depending principally on the duration and severity of ischemia. Reperfusion microvascular ischemia is not an instantaneous single event that occurs just at the moment of reperfusion. Rather, it is a progressive process that increases with time. Of importance, it is associated with poor recovery of left ventricular (LV) function and a worsened clinical outcome at follow-up. An increasing body of experimental and clinical data suggests a valuable role for high concentrations of oxygen (O2), delivered directly to the coronary artery, in reducing microvascular injury. Recently, a catheter-based method has been developed for infusion of O2 , dissolved in a crystalloid solution at extremely high concentrations (ie, 1-3 mL O2 /g [aqueous oxygen {AO}]), into blood without bubble formation to provide hyperoxemic treatment of tissue ischemia. In experimental studies, AO hyperoxemia has been found to improve LV function and electrocardiographic evidence of ischemia. This is thought to be the result of augmentation of oxygen delivery in plasma. Marked improvement in myocardial flow has been consistently found. These observations may explain the improvement of LV function after AO treatment noted in clinical studies.