Bicuspid aortic valve (BAV) patients are identified by a lesion of the tricuspid aortic leaflets in which only two ‘functional’ leaflets are visibly present. This lesion occurs in 0.5–2% of the population and is accompanied by a significant incidence of morbidity and mortality related to aortic valve dysfunction, aortic dilatation, aortic aneurysm, and aortic dissection. [1] The pathogenesis of the malformation has been postulated to be the result of a congenital or inflammatorily-mediated fusion of two of the three aortic leaflets. In addition, BAV is accompanied by a variety of heterogeneous complications and is considered a complex disease with many cofactors, the importance of which continue to be debated. Among these cofactors, the most commonly identified vascular manifestation is aortic dilatation. [1] There are two hypotheses for this manifestation: the first postulates the coexistence of BAV and genetically-based aortic fragility; the second proposes that BAV morphology and incomplete valve opening induces hemodynamic forces that influence structure and function at the aorta.

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