Abstract
<jats:p>The aortic wall layers separate in abdominal aortic dissection (AAD), a rare but potentially fatal vascular condition that impairs blood flow, increases the risk of rupture, and causes substantial morbidity and mortality. Combining clinical and molecular viewpoints is necessary to comprehend its pathogenesis. Clinically, AAD is linked to demographic factors like age, sex, and family history, as well as conventional cardiovascular risk factors like smoking, hypertension, atherosclerosis, and connective tissue disorders. Although diagnostic accuracy has increased due to advancements in imaging modalities, timely recognition is still difficult because of its heterogeneous presentation. The aortic wall is weakened, and susceptibility is increased at the molecular level by changes in extracellular matrix remodeling, inflammation, dysregulated signaling of the transforming growth factor-β (TGF-β) pathway, and genetic predispositions involving mutations in genes like FBN1, COL3A1, TGFBR1/2, and ACTA2. In addition to improving risk stratification, the integration of these clinical and molecular correlates directs surveillance procedures, preventative measures, and customized treatment plans. The clinical and molecular determinants of AAD are summarized in this chapter, along with their significance for diagnosis, treatment, and the creation of future focused interventions.</jats:p>