A guide to therapeutic decision-making in patients with non-ST-segment elevation acute coronary syndromes.

Recent clinical trial evidence supports an inflammatory etiology in acute ischemic heart disease. When a segment of coronary artery becomes inflamed, important cytokines, such as tissue factor, are released, facilitating thrombosis. Serum inflammatory markers are elevated in most acute coronary syndrome patients at presentation. Mortality risk has been shown to be associated with increased levels of high-sensitivity C-reactive protein (CRP), interleukin 6, and serum vascular cell adhesion molecule. Platelets, which are rich in inflammatory mediators (CD40 and its ligand thrombospondin, and phospholipase A2), also supply important triggers for the inflammatory cascade. In addition, more than 35 platelet-associated messenger ribonucleic acid mediators involved in arterial injury and inflammation have been found. The use of biomarkers of inflammation, such as CRP, and of the sequelae of embolization, such as troponin, provide a window into the underlying pathophysiology of acute ischemic heart disease. New agents from three distinct drug classes have recently flooded the therapeutic armamentarium. Decision-making is further complicated by the choice of an invasive (aggressive) or a medical (conservative) strategy of management with respect to coronary revascularization. For patients at highest risk, aspirin, beta-blockers, nitrates, and a statin should be given, and clopidogrel, enoxaparin, a glycoprotein (GP) IIb/IIIa inhibitor, plus an invasive strategy should be considered. For intermediate- and low-risk patients, a "sliding-scale" approach may be best. Decisions about the three classes of antithrombotics--low-molecular-weight heparins, GP IIb/IIIa inhibitors, and thienopyridines--along with whether to adopt an early invasive strategy, should be made on an individual basis.