Are we ignoring the dilated thoracic aorta?

The pathophysiology of thoracic aortic aneurysm (TAA) formation involves a complex interplay of genetic predisposition, cardiovascular risk factors, and hemodynamic forces. The medical community has resorted to the use of pharmacologic agents based on weak data transplanted from either abdominal aortic aneurysms (AAAs) or Marfan syndrome. However, aneurysms differ significantly based on their anatomic location and etiology. Epidemiologic and experimental data demonstrate that different genetic and nongenetic risk factors as well as diverse physiologic processes are responsible for the development and progression of sporadic TAA, familial TAA, and AAA. Therefore, these disease processes need to be considered as distinct entities and not hastily grouped together. The extrapolation of data from one aneurysmal disease process to another is still ill-founded and potentially harmful. Clinical trials in TAA are required before medical therapies, such as β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, or macrolide antibiotics, can be recommended.