Inflammatory biomarkers in acute coronary syndromes: part I: introduction and cytokines.

Acute coronary syndromes (ACS) are multifactorial and occur in response to inflammation, plaque rupture and subsequent thrombosis, progressive mechanical obstruction, and dynamic obstruction.1 Patients with ACS span a large spectrum of risk that progresses from unstable angina (UA) to non–STelevation myocardial infarction (NSTEMI) to ST-elevation myocardial infarction (STEMI). ECG findings and markers of myocyte necrosis are used to define the type of ACS and guide reperfusion strategy in ST-elevation myocardial infarction. For patients with non–ST-elevation (NSTE) ACS, however, a large degree of uncertainty remains regarding long-term risk and optimal secondary prevention for the individual patient. Increasingly, biomarkers are being used as tools to identify subgroups of patients with ACS who are at increased risk for subsequent cardiovascular events. Among potential biomarkers, much interest has focused on biomarkers of inflammation. The process that leads to eventual plaque erosion or rupture involves a number of inflammatory mechanisms, including endothelial dysfunction, leukocyte migration, extracellular matrix degradation, and platelet activation (Figure).2 The optimal inflammatory biomarker would provide a method for quantitating cardiovascular-specific inflammation, thereby predicting the risk of recurrent atherothrombosis and its clinical sequelae. Because they address a separate aspect of ACS pathophysiology, biomarkers of inflammation may provide unique information to the clinician separate from that provided by biomarkers of myocyte necrosis and hemodynamic stress. The present review series summarizes our current understanding of inflammatory biomarkers and is based on their presumed pathophysiological role in ACS and the clinical evidence that supports their prognostic importance. The discussion is organized from early to late inflammatory mediators of plaque disruption; in reality, these processes are intertwined and simultaneous (Figure). Part I focuses on cytokines, part II on acute-phase reactants and biomarkers of endothelial cell activation, part III on biomarkers of oxidative stress and angiogenic factors, and part IV on matrix metalloproteinases and biomarkers of platelet activation.