If you look at the study of Fedak and collegues "Vascular remodeling of patints with congenital bicuspid aortic valve", you will see, that there is evidence of systemic deficiency of connective tissue elements, like fibrillin-1. There are also evidenced deficiencies of eNOS. There are elevated productions of MMP's, triggering aortic dilatations. However, these findings are not sufficient to do the conclusion for the BAV disease at all! The reason... there are too much BAV persons in those studies, whos structural and molecular and histological statuses compare the general. Plus - there is trend of hereditary bAV in only 15-30% of the patients. What about the others? That's why, the investigators are targeting their researches in some other, more complicated mechanisms, which may explain the BAV in non-familial, or non-genetical BAV.
Best regards,
Ivo
I think I get what you're saying now, but tell me if I'm wrong: There could be something as simple as vibrations from the BAV causing issues within the blood vessels, and stuff like that....? Or (going out on a limb) maybe something like hemolysis from the odd shape and turbulence of the BAV can cause problems...?