Aortic dissection remains a highly lethal disease because of several persisting problems. First， the well-known difficulties in making a rapid diagnosis often result in delayed treatment or death. Secondly， current approaches to medical management do not reliably prevent descending thoracic aortic expansion and rupture. Furthermore， it is difficult to predict which patients will develop significant aortic expansion despite appropriate medical management. Finally， the timely detection of disease progression requires aggressive lifelong surveillance with imaging studies; lapses in follow-up are often fatal. Solving these problems and improving our ability to treat patients with this catastrophic disease are the principal goals of the research focusing on the pathobiology of aortic dissection. 

In contrast to the substantial advances in our understanding of the cellular and molecular processes involved in abdominal aortic aneurysm formation， the mechanisms underlying thoracic aortic disease remain poorly understood; this is particularly true for aortic dissection. Beyond the well-described， classic histological features of aortic dissection-elastic fiber fragmentation， medial degeneration， and fibrosis－our understanding of the changes in the aortic wall that follow acute dissection is limited. Current efforts toward improving this understanding focus heavily on the roles of inflammatory cells and proteolytic enzymes in the progressive degeneration of the aortic extracellular matrix. 

An enhanced understanding of the pathobiology of aortic dissection may be translated to patient care in two major ways. First， uncovering the cellular and molecular processes that cause the aortic wall to weaken may reveal novel opportunities to block disease progression and prevent aortic expansion and rupture. Secondly， understanding the pathobiology may lead to the identification of new biomarkers. Such biomarkers could be used to rapidly diagnose acute dissection， detect disease progression， predict prognosis， and guide therapy.