LAUSR

O utcomes have improved after acute myocardial infarction (MI) with earlier patient presentation and widespread application of timely reperfusion therapy. However, patients with MI complicated by heart failure, cardiogenic shock, and/or cardiac arrest continue to have high mortality (1,2). In patients with large MI with left ventricular (LV) dysfunction, there is an unmet need for treatments to reduce infarct size, improve LV remodeling, and reduce cardiovascular adverse events. Inflammation is important in the pathophysiology of atherosclerosis and of acute coronary syndromes. CANTOS (Canakinumab Antiinflammatory Thrombosis Outcome Study) has re-energized the targeting of inflammatory pathways to improve clinical outcomes, by showing that an inhibitor of interleukin (IL)-1b can reduce both C-reactive protein (CRP) and cardiovascular events in a population with prior (by $30 days) MI (3). In acute MI, inflammatory activity in the vessel wall contributes to plaque instability. However, inflammation immediately after an MI is in large part a response to the myocardial injury, as well as a consequence of the stress and hypoperfusion that may occur. A comprehensive study of 6,809 patients with acute coronary syndromes showed that elevated CRP, in the acute phase of MI, is associated independently