Aortic dissection (AD) is a fatal disease characterized by a ruptured intima that leads to the complete rupture of the aorta. The aim of this study is to examine the immunohistochemical expression of inflammation/fibrosis-associated chemical mediators in AD patients. Surgical specimens of aortic tissues were obtained from 37 patients who underwent an open thoracic aortic repair. AD was detected with histological staining. Local congestion and hemorrhage as well as chronic inflammatory cells infiltrations were observed at the dissection. Moreover, extensive disarrangement and disruption of elastic fibers were observed in the medial layer of the aorta with dissection. In summary, our study revealed that the apoptotic rate of vascular SMCs (VSMCs) in the vascular middle layer is higher in the dissected aortas than in the control aortas, suggesting that abnormally elevated apoptosis is correlated with AD pathogenesis. Functional studies of key genes identified in the apoptotic pathways as well as in extracellular matrix would be critical in thoroughly understanding the underlying mechanisms of AD development. Targeting the mediators related to TGF-β1, the Smad family proteins, and caspase 3 or anti-apoptotic agents may provide diagnostic markers and therapeutic targets that could be used to prevent AD.