ABSTRACT
It is well-known that cardiovascular disease is the leading cause of mortality, while coronary heart disease (CAD) accounts for more than 50 percent of all cases (Lloyd-Jones et al. 2010; Fonarow 2007; Steg et al. 2007). Anginal chest pain or other symptoms typical for an acute coronary syndrome (ACS) is the main cause of admission to an emergency department and remains the major clinical condition responsible for hospitalization (Braunwald et al. 2002; Bertrand et al. 2002; Antman et al. 2004). ACS covers the spectrum of clinical conditions ranging from unstable angina to non-Qwave myocardial infarction (MI) and Q-wave MI. In particular, an acute reduction in coronary blood fl ow and hence myocardial oxygen supply is usually the mechanism of ACS. In this case, recent events including rupture, erosion and hemorrhage often superimposed on thrombosis and/ or microembolism reduce coronary blood fl ow and lead to acute ischemic myocyte injury (Libby and Theroux 2005). The main pathophysiological mechanism contributing to the expression of the ACS is the progression of atherosclerosis, whereas the central process to the initiation of an ACS is disruption of an atheromatous plaque (Kampoli et al. 2012a).
