Update on the Inflammatory Hypothesis of Coronary Artery Disease.

Purpose of review The pathogenesis and progression of coronary artery disease (CAD) is now known to be largely driven by inflammation on top of the well-accepted role for the disequilibrium between cholesterol deposition and removal from the arterial wall. Recent clinical trials have supported the inflammatory hypothesis of CAD and will be discussed in this review. Recent findings The clinical trial Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) found that treatment with canakinumab, an anti-interleukin-1β agent, resulted in a reduction in non-fatal myocardial infarction, non-fatal stroke, or death. This provided evidence for the inflammatory hypothesis of CAD. However, canakinumab is not cost-effective for widespread therapy and more cost-effective treatments are warranted. The Cardiovascular Inflammation Reduction Trial (CIRT), Colchicine Cardiovascular Outcomes Trial (COLCOT), and Low-Dose Colchicine 2 (LoDoCo2) are recent clinical trials that increased the understanding of the inflammatory hypothesis of CAD. Cost-effective therapies targeting inflammation are the future of preventative CAD treatment. Additional clinical trials with anti-inflammatory and anti-cytokine agents would help delineate the most beneficial target for CAD prevention.