Agents that reduce myocardial oxygen demand have yielded limited clinical results for salvaging ischemic myocardium, suggesting other pathophysiologic processes contribute to irreversible damage.
In the early 1970s Maroko, Braunwald, and others demonstrated the im portance of myocardial oxygen supply and demand as a major determinant of the extent of myocardial injury 0-3). A variety of agents that reduced myocar dial oxygen demand, B-adrenoceptor antagonists and calcium channel blockers for example, were shown to be beneficial in animal models of myocardial ischemia. The time for clinical testing of agents that improve myocardial oxygenation was said to have come (4). A decade later, however, the limited clinical results have been far from exciting. This approach to reducing isch emia-induced myocardial injury suffers from three major problems. Implicit in the concept of salvaging ischemic myocardium by altering myocardial oxygen supply and demand is the assumption that myocardial tissue injury results solely from an inability of the coronary vasculature to deliver necessary oxygen and nutrients to maintain myocyte viability. However, we believe that other pathophysiologic processes contribute to irreversible myocar dial damage. It is also assumed that the restoration of coronary blood flow to the ischemic myocardium would, of itself, prevent the development of irreversible damage. However, reperfusion of jeopardized myocardium may lead to cellular pro cesses that extend the area of cell necrosis beyond that which could be attributed
Lucchesi et al. (Tue,) conducted a review in Ischemia-induced myocardial injury. Agents that reduce myocardial oxygen demand was evaluated. Agents that reduce myocardial oxygen demand have yielded limited clinical results for salvaging ischemic myocardium, suggesting other pathophysiologic processes contribute to irreversible damage.