ABSTRACT
INTRODUCTION Inflammation is a critical participant in all aspects of the cardiovascular disease process, spanning from generation of the first foam cell and atherosclerotic lesion, to development of the vulnerable plaque and consequent fissuring, rupture, and thrombosis [1,2]. The assumption that high-grade coronary artery stenoses are the cause of most acute coronary events has now been challenged from pathologic, invasive, and noninvasive techniques showing that most coronary events occur in lesions that obstruct less than 50% of the coronary lumen [3-6]. It is now clear that patients presenting with unstable angina have diffuse coronary inflammation regardless of the site of culprit lesion, indicating that patients with acute coronary syndromes have a heightened degree of systemic inflammation [7]. With the recognition that adverse coronary events predominantly arise from inflamed vulnerable plaque, and not flow-limiting stenoses, research has shifted focus to the role of inflammatory processes and molecular markers that serve to monitor these pathways. Biomarkers such as the acute phase reactant C-reactive protein (CRP), and more recently soluble CD40 ligand (sCD40L) and myeloperoxidase (MPO), are gaining in recognition as potential prognostic and diagnostic tools to detect ‘‘vulnerable patients’’ with ‘‘vulnerable plaques.’’ The prognostic and diagnostic role of these and other novel inflammatory markers in acute coronary syndromes, and atherosclerotic risks, will be reviewed in this chapter.
