ABSTRACT
In recent years the pathophysiology of coronary artery disease (CAD) has been unraveled, yielding a much deeper understanding of the mechanisms leading to acute coronary syndromes (ACS). Atherosclerosis is currently regarded as a dynamic process originating from endothelial dysfunction to plaque initiation, plaque progression, and finally to the development of either stable or unstable vulnerable plaques. Whereas stable plaques might cause mycocardial ischemia and angina pectoris at exertion because of relevant lumen narrowing, rupture or erosion of high-risk vulnerable plaques with subsequent thrombus formation is responsible for the development of acute ischemic events. In this atherothrombotic process the interaction of endothelial dysfunction, inflammation, and enhanced blood thrombogenicity plays the key role.
