ABSTRACT
The acute management of patients with acute coronary syndromes (ACS) proceeds from and has evolved with our understanding of the pathobiology of this complex syndrome and its complications. The spectrum of patients with ACS is heterogeneous, ranging from those with complete coronary occlusion resulting in ST segment elevation on the electrocardiogram and myocardial infarction that is typically transmural to patients presenting with severe, but not occlusive, coronary obstruction resulting in myocardial ischemia with or without myocyte necrosis. The varied risk of complications in this population demands a careful prognostic assessment as a guide to triage and individualized therapeutic decision making. Nevertheless, consistent pathobiological contributors across the entire spectrum of ACS support a common foundation of therapy, including anticoagulant and antiplatelet therapy, as well as agents to reduce myocardial oxygen demand. In addition, over the past decade substantial advances in vascular biology have shed new light on the complex processes that promote atherothrombosis. In particular, experimental, pathologic and clinical data have implicated inflammatory contributions at every stage of atherogenesis (1-3). Such observations have provided new directions for therapy designed to target specific steps in the inflammatory cascade believed to mediate atherothrombosis. A deeper understanding of the underlying mechanisms of atherogenesis and ACS is important to the clinician as this insight will continue to guide the contemporary and future management of patients with acute coronary ischemia.
