Inflammatory Biomarkers in Acute Coronary Syndromes

Abstract

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–ST-elevation 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. Pathophysiological sequence of inflammatory biomarkers in ACS. In this schematic diagram showing the development of an atherosclerotic plaque and the local vascular events that surround an ACS, the inflammatory biomarkers are superimposed with a semiquantitative representation of their relative importance during the sequence of events shown. Cytokines and acute-phase reactants such as IL-6, MCP-1, TNF-α, IL-18, IL-10, CRP, and serum amyloid A (SAA) may establish or be surrogate markers for basal inflammation that leads to development of atherosclerotic plaque. Activation of endothelial adhesion molecules such as …