Spontaneous Coronary Artery Dissection Unveiled: Pathophysiology, Imaging, and Evolving Management Strategies

Spontaneous coronary artery dissection (SCAD) is increasingly recognized as a significant cause of acute coronary syndrome (ACS), particularly among younger women who do not have traditional cardiovascular risk factors. Despite its prevalence in this demographic, SCAD is often underdiagnosed due to its non-atherosclerotic nature and the variability in its angiographic presentations. This review provides a comprehensive overview of SCAD, emphasizing its pathophysiology, clinical presentation, diagnostic methods, and evolving treatment strategies. SCAD results from either an intimal tear or an intramural hematoma, which leads to the compression of the coronary lumen and subsequent myocardial is-chemia. It is closely associated with conditions such as fibromuscular dysplasia, hormo-nal influences, and acute stressors. Angiographically, SCAD is categorized into different types based on the morphology of the lesions, with Type 2 being the most common. Diag-nosis primarily relies on coronary angiography; however, adjunctive imaging techniques, such as optical coherence tomography (OCT) or intravascular ultrasound (IVUS), can en-hance detection, particularly in atypical cases. For hemodynamically stable patients, con-servative management is typically preferred due to the high rates of spontaneous healing. While invasive interventions may sometimes be necessary, they are technically challeng-ing and carry a higher risk of complications. SCAD represents a unique, non-atherosclerotic mechanism of myocardial infarction, underscoring the importance of early recognition and targeted management. Advances in imaging and increased aware-ness have improved detection rates; however, significant gaps remain in risk stratification and long-term care. Future research should focus on genetic predispositions, hormonal mechanisms, and optimized pharmacological protocols to further enhance patient care.