Superoxygen Therapy

Abstract

In North America, every 25 seconds someone will have a coronary event and every minute someone will die of one.1 ST elevation myocardial infarction (STEMI) is the most dramatic manifestation of coronary artery disease and remains as one of the most important causes of mortality in the industrialized world. Prompt and successful reperfusion therapy (either pharmacologically with use of fibrinolytic therapy or mechanically with primary percutaneous coronary intervention [PCI]) is currently the cornerstone of acute management of STEMI to salvage ischemic myocardium and limit infarct size. Although undoubtedly beneficial, reperfusion of an occluded artery represents “a double-edge sword,”2 because restoration of epicardial coronary flow initiates a series of complex biochemical and molecular phenomena, which will ultimately mitigate myocardial healing. Thus, with reperfusion comes reperfusion injury.3 Article see p 366 Although the concept of cardioprotection (myocardial salvage) was first suggested by Braunwald,4 it was the seminal works of Reimer et al who crystallized the fact that there exists a window of opportunity to act to limit myocardial injury. They postulated that a “wavefront phenomenon” of cardiac necrosis, if left unchecked, would extend the infarct from the subendocardial region to the subepicardial region by using canine models of transiently or permanently occluded coronary arteries.5 Thereafter, over the course of 3 decades, mixed and disappointing results have plagued both experimental and clinical attempts to limit the deleterious effects of early reperfusion through either pharmacological (adenosine, calcium channel blockers, Na+/H+ exchange inhibitors, KATP channel openers, and glucose-insulin-potassium infusion) or nonpharmacological (therapeutic hypothermia) means.3,6 The reasons for such inconsistent findings in cardioprotection are multifold. First, reperfusion injury encompasses numerous, overlapping mediators of cardiomyocyte death from oxidative stress and Ca2+ overload to alterations in cellular pH, as well as an inflammatory process with a central …