Pathophysiology of acute coronary syndromes

Plaque rupture has dominated our thinking about acute coronary syndromes (ACS) pathophysiology for decades. However, current evidence suggests that a sole focus on plaque rupture obscures other mechanisms that may mandate different management strategies. First, coronary artery thrombosis caused by plaque rupture can occur with or without signs of concomitant inflammation. This distinction may have substantial therapeutic implications as direct anti-inflammatory interventions for atherosclerosis are emerging. Coronary artery thrombosis caused by plaque erosion may be on the rise in an era of intense lipid lowering. Identification of patients with ACS resulting from erosion may permit a less invasive approach to management than the current standard of care; furthermore, new therapeutic targets are emerging as hyaluronic acid metabolism alterations seem to play a key role in this setting. Finally, ACS may occur without apparent epicardial coronary artery thrombus or stenosis. Such events may arise from spasm or coronary microvascular dysfunction. Emerging management strategies may likewise apply selectively to this category of ACS.