Perspective:

The presence of AAo dilation among patients with BAV variably has been attributed to a genetically based primary aortopathy or to mechanical forces caused by altered hemodynamics associated with the BAV. This study appears to add evidence to support a theory that hemodynamics at least plays a contributing role. Study limitations include its retrospective nature (potentially excluding patients with more advanced aortic valve or aortic disease who would have undergone intervention before the minimum 5-year follow-up interval), small sample size of both patients with BAV and healthy controls, and AAo measurement that apparently excluded the sinuses of Valsalva and used an average rather than a maximal AAo dimension. That more rapid AAo growth was not limited to patients with greater degrees of elevated WSS suggests that other factors (potentially including a primary bicuspid aortopathy) also were playing a role. The study had a counter-intuitive finding that therapy with a beta-blocker was associated with a higher risk for AAo growth, potentially attributable to bias that past AAo growth or other high-risk features led to a higher rate of beta-blocker use in some patients––reinforcing the pitfalls of drawing too firm of conclusions from this retrospective study.