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.

Links

Publisher Full Text

Authors

Castellano JM, Kovacic JC, Sanz J, Fuster V

Institution

Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.

Source

Annals of the New York Academy of Sciences 1254: 2012 Apr pg 164-74

MeSH

Adrenergic beta-Antagonists
Aneurysm, Dissecting
Angiotensin Receptor Antagonists
Angiotensin-Converting Enzyme Inhibitors
Animals
Anti-Bacterial Agents
Aortic Aneurysm, Thoracic
Aortic Valve
Ehlers-Danlos Syndrome
Genetic Predisposition to Disease
Hemodynamics
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Loeys-Dietz Syndrome
Magnetic Resonance Angiography
Marfan Syndrome
Risk Factors
Tomography, X-Ray Computed

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

22548582