An aneurysm occurs when a part or entire circumference of the vessel is pathologically dilated. A true aneurysm involves all three layers of the vessel, whereas pseudoaneurysm is characterized by disruption of the intima and media, and the dilated segment of the aorta is lined by adventitia alone. Thoracic aortic aneurysm (TAA) is a clinically silent and potentially fatal disease whose pathophysiology is poorly understood. Application of data derived from animal models and human tissue analysis of abdominal aortic aneurysms may prove misleading given current evidence of structural and biochemical aortic heterogeneity above and below the diaphragm. Genetic predisposition is more common in TAA and includes multi-faceted syndromes such as Marfan, Loeys-Dietz, and type IV Ehlers-Danlos as well as autosomal-dominant familial patterns of inheritance. Investigation into the consequences of these known mutations has provided insight into the cell signaling cascades leading to degenerative remodeling of the aortic medial extracellular matrix (ECM) with TGF-β playing a major role. Targeted research into modifying the upstream regulation or downstream effects of the TGF-β1 pathway may provide opportunities for intervention to attenuate TAA progression.
Thoracic aortic aneurysm pathophysiology
Aortic dissection pathophysiology
Aortic stenosis pathophysiology
Aortic sclerosis pathophysiology
Left ventricular aneurysm pathophysiology
Thoracic aortic aneurysm risk factors
Aortic regurgitation pathophysiology
Aortic sclerosis risk factors