As the most common congenital heart defect, bicuspid aortic valve (BAV) occurs in 1–2 % of the population and has been associated with serious complications such as aortic valve dysfunction, infective endocarditis, aortic dilatation, aortic aneurysm, and aortic dissection [1, 2]. While the pathogenesis of this valve malformation has been postulated to be genetic, the resulting vascular environment and abnormal hemodynamics are hypothesized to contribute to the progression of the disease and its subsequently high morbidity and mortality (greater than 33% of patients with BAV develop serious complications from the disease) [1]. However, clinical details supporting the causality between altered local blood flow dynamics and development of structural abnormality at the aortic root are still lacking.

This content is only available via PDF.
You do not currently have access to this content.