Inflammation and Atherothrombosis: The Beginning of the End of a Hypothesis

<p>Abstract: The inflammatory hypothesis for atherothrombosis posits that inflammation drives the development of atherosclerotic plaque and its progression to thrombosis. Empirical data have suggested the relation of inflammation to the Virchow’s triad: endothelial injury, blood stasis, and hypercoagulable state. Evidence from clinical studies also pointed to a potential benefit in thrombotic risk reduction from inhibiting inflammation. Until recently, interleukin-1β blockade with canakinumab has been investigated for preventing recurrent cardiovascular events among patients with prior myocardial infarction and demonstrated compelling outcomes. Furthermore, the results ascertain that a downstream inflammatory biomarker, high-sensitivity C-reactive protein, could be utilized to identify at-risk patient subsets associated with significant benefits from anti-inflammatory therapy. As research efforts are closing the knowledge gap between inflammation and thrombosis, the potential role of inflammation in other cardiovascular diseases also presents new challenges for future studies.</p