The emergence of novel biomarkers of inflammation, platelet activation, plaque instability, and hemodynamic stress, along with more sensitive biomarkers of necrosis, has made possible the potential to (a) noninvasively characterize the participation of these different contributors in any individual patient, (b) detect patients at higher risk of complications despite normal concentrations oftraditional markers of necrosis, and (c) improve targeting of therapy to the underlying pathobiology (2). Contemporary investigation ofbio-markers has put a strong emphasis on elucidating the pathobiological correlates of newer and established biomarkers. This avenue, in particular, has supported the concept that novel biomarkers may be used to direct therapy. For example, elevated levels of cardiac troponin in the blood of patients with non-ST-elevation ACS (NSTEACS) are associated with the presence of intracoronary thrombus, distal embolization of platelet microaggregates, and impaired microvascular flow in the myocardium (5,6). These observations have moved forward hand in hand with the demonstration of greater benefits of potent antithrombotic agents in patients with increased levels of troponin and proven this biomarker extremely useful for therapeutic decision making (see Chapter 5) (7,8). This paradigm
exemplified by cardiac troponin has provided a blueprint for the clinical evaluation of newer biomarkers of cardiovascular risk.
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