title: Are we ignoring the dilated thoracic aorta?
abstract: 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.
authors.affiliation: Zena and Michael A. Wiener Cardiovascular Institute.|Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York, New York.
authors.forename: Jose M
authors.initials: JM
authors.lastname: Castellano
authors.affiliation: Zena and Michael A. Wiener Cardiovascular Institute.|Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York, New York.
authors.forename: Jason C
authors.initials: JC
authors.lastname: Kovacic
authors.affiliation: Zena and Michael A. Wiener Cardiovascular Institute.|Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York, New York.
authors.forename: Javier
authors.initials: J
authors.lastname: Sanz
authors.affiliation: Zena and Michael A. Wiener Cardiovascular Institute.|Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Mount Sinai School of Medicine, New York, New York.|Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
authors.forename: Valentin
authors.initials: V
authors.lastname: Fuster
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000784:Aortic Dissection / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D017545:Aortic Aneurysm, Thoracic / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D001021:Aortic Valve / Q000002:abnormalities; D004535:Ehlers-Danlos Syndrome / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D020022:Genetic Predisposition to Disease; D006439:Hemodynamics; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D055947:Loeys-Dietz Syndrome / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D018810:Magnetic Resonance Angiography; D008382:Marfan Syndrome / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D012307:Risk Factors; D014057:Tomography, X-Ray Computed
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000900:Anti-Bacterial Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors