Spontaneous Coronary Artery Dissection: Pathophysiology, Outcomes, and Management

Purpose of Review Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndrome, particularly in younger women without traditional cardiovascular risk factors. This review summarizes recent advances in SCAD pathophysiology, diagnosis, and management, highlighting evolving clinical concepts and areas of uncertainty. Recent Findings SCAD is a non-atherosclerotic cause of myocardial infarction driven by intramural hematoma formation or intimal tear, both resulting in subsequent luminal compression. Advances in coronary imaging have improved recognition of diverse angiographic patterns. Selective use of intracoronary imaging and emerging noninvasive modalities is further refining diagnosis and surveillance. Observational data support a conservative management strategy in hemodynamically stable patients, given high rates of spontaneous healing. Emerging evidence supports beta-blockers for recurrence prevention while questioning the use of routine dual antiplatelet therapy. Long-term morbidity, including recurrent symptoms, coronary microvascular dysfunction, and psychosocial burden, is increasingly recognized. Summary SCAD is a distinct clinical entity with diagnostic and management considerations that differ from atherosclerotic disease. Despite improved recognition, key gaps remain in risk stratification, recurrence prediction, and optimal therapy. Ongoing international registries and emerging clinical trials are expected to address these gaps and inform a more individualized, mechanism-based approach to care.