Myocardial release of lactate, hypoxanthine, and urate during and following percutaneous transluminal coronary angioplasty. Potential mechanism for the generation of free radicals

Until recently the assessment of alteration in myocardial metabolism in man early after an abrupt occlusion of a major coronary artery has not been feasible. PTCA however, now provides a unique opportunity to study the time course of these metabolic changes during the transient interruption of coronary flow by the balloon occlusion sequence in patients with single-vessel disease and without angiographically demonstrable collateral circulation (1, 2). The need to detect any persisting metabolic or mechanical dysfunction becomes of even greater concern as the number of dilated vessels and the duration of balloon inflation tend to increase, thereby enhancing both the extent and the severity of ischemia. The risk exists that the damage induced by the intervention may exceed its benefit.