Matrix Metalloproteinase-9 for the Earliest Stage Acute Coronary Syndrome : Comparison With High-Sensitivity Troponin T
cute coronary syndrome (ACS) is evoked by rupture or erosion of vulnerable atherosclerotic plaques, which contain large lipid cores underneath thin and collagen-poor fibrous caps, followed by thrombus formation. The consequent luminal occlusion or critical narrowing of a coronary artery causes myocardial necrosis or ischemic damage.1 Thus, the identification of biomarkers that can detect plaque rupture or vulnerability might allow earlier diagnosis of ACS, although acute myocardial infarction (AMI) is currently diagnosed using biomarkers of myocardial necrosis or damage, such as creatine kinase-MB (CK-MB)2 and cardiac troponins.3–7 In recent years, highly sensitive assays for cardiac troponins have been developed.8,9 These high-sensitivity troponins, however, may be insufficient for diagnosing the earliest stages of ACS.10 Matrix metalloproteinases (MMPs), which are expressed in atherosclerotic plaques, induce degradation of extracellular matrix proteins, including collagens and elastins, in atherosclerotic fibrous caps.11,12 ACS is evoked by expression and activation of MMPs through disruption of the atherosclerotic fibrous caps and subsequent thrombus formation.12,13 Among MMPs, MMP-9, known as gelatinase B or 92-kDa type IV collagenase, is expressed in atherosclerotic plaques, especially