Inflammation is a major contributor in the development and progression of coronary artery disease (CAD). Preclinical studies have demonstrated that inflammatory processes, by means of specific cytokines and enzymes, promotes plaque formation, progression and instability [1,2]. Furthermore, patients with chronic inflammatory disease (e.g. rheumatoid arthritis, gout) have a high incidence of CAD [3,4]. Hence, by targeting inflammatory pathways, the risk for cardiovascular (CV) events may potentially be diminished [5,6].
