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	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

I read the article by Batur et al,¹ which was accepted about a year ago by the ARCHIVES, the same journal where I published my original article in 1961.²

Fortunately, recent observations by a group in France³ have finally actually set the problem straight. As Vincentelli and coworkers³ have demonstrated, it now appears that in patients with tight aortic stenosis the huge von Willebrand factor molecule physically breaks up or functionally denatures as the blood is forced through a stenosed aortic valve, resulting in acquired von Willebrand factor deficiency syndrome. When the aortic stenosis was corrected by surgery, the functional von Willebrand defect was no longer present.

To my perhaps biased way of thinking, the explanation of aortic stenosis and unexplained gastrointestinal bleeding is now much more clearly defined, rather than attributing it to venous ectasias observed by gastroenterologists in many older patients. Perhaps vascular abnormalities such as these could . . . [Full Text of this Article]

Ralph C. Williams, Jr, MD
Albuquerque, NM

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