The growing use of imaging examinations has led to increased detection of spontaneous coronary artery dissection (SCAD) as a non-atherosclerotic cause of acute coronary syndrome (ACS). Since a greater awareness of pathophysiologic mechanisms has relevant implications in clinical practice, we aim to provide an update to current knowledge of SCAD pathophysiology. We discuss the most common conditions associated with SCAD, including predisposing factors and triggers, and focus on potential mechanisms leading to SCAD development. Furthermore, we report the main genetic research findings that have shed further light on SCAD pathophysiology. Finally, we summarize practical considerations in SCAD management based on pathophysiologic insights.
