Assessing Reperfusion and Prognostic Infarct Sizing with Biochemical Markers

Abstract

Pioneering work in the early 1970s initiated the “thrombolytic era” (1). During this era the therapeutic approach to acute myocardial infarction (AMI) focused on treatments aimed at limiting infarct size by improving myocardial oxygen supply, lowering myocardial oxygen demand, and minimizing autolytic damage to myocytes (2,3). The thrombus became the primary therapeutic target for reperfusion therapy and monitoring because it is a keystone pathophysiological feature of the “acute coronary syndromes” (ACS), a continuum of ischemic disease ranging from unstable angina, associated with reversible myocardial cell injury, to frank MI with large areas of necrosis. This approach was validated in large randomized clinical trials during the 1980s and 1990s that unequivocally demonstrated the benefit of thrombolytic therapy (4, 5). Thrombolytic therapy has become critically important for AMI patients having characteristic electrocardiographic (ECG) features for resolving the thrombotic occlusion, reestablishing patency to the infarct-related artery (IRA), and improving “downstream” tissue reperfusion (6). This chapter focuses on the utilization of cardiac markers for noninvasively assessing the success of reperfusion therapies and use of biochemical marker release to determine “infarct size” and, more important, prognosis. Prognostic infarct sizing is based on the notion that as myocytes die, cardiac function is compromised proportionately, resulting in a worse clinical outcome. The bridge uniting reperfusion assessment and prognostic infarct sizing is that both utilize serial monitoring of biochemical marker release. The contrast is that the focus of reperfusion assessment is the early 90-min time frame after thrombolytic therapy, whereas prognostic infarct sizing involves examining the entire cardiac marker release curve.