Acute Aortic Syndrome (AAS) represents a heterogeneous spectrum of highly fatal vascular emergencies characterized by acute compromise of the structural integrity of the aortic wall. This spectrum primarily includes aortic dissection (AD), intramural hematoma (IMH), and penetrating atherosclerotic ulcer (PAU). Clinically, it manifests as sudden, severe chest or abdominal pain, frequently accompanied by hemodynamic instability and an imminent risk of tissue malperfusion within the first 48 hours. The underlying pathophysiology involves complex degenerative processes of the tunica media, tissue elastic fiber fragility, marked immune dysregulation with neutrophil recruitment and neutrophil extracellular trap (NET) formation, and genetic predisposition, such as that associated with Marfan syndrome, acting synergistically with acquired risk factors, particularly systemic arterial hypertension, smoking, and atherosclerosis. Effective therapeutic management in emergency departments is based on rapid and accurate anatomical stratification using computed tomography angiography (CTA). The Stanford classification guides immediate management: cases involving the ascending aorta (Stanford type A) require urgent open surgical intervention to prevent life-threatening complications such as aortic rupture and cardiac tamponade, whereas lesions confined to the descending aorta (Stanford type B) require rigorous intensive medical management for hemodynamic control, with thoracic endovascular aortic repair (TEVAR) reserved for complicated presentations. Given the time-sensitive nature of the disease, coordinated multidisciplinary care and the implementation of rapid clinical pathways are essential to reduce diagnostic delays and optimize clinical outcomes.
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Abatt et al. (2026) studied this question.
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