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HLA-B27-Associated Cardiac Disease
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
IN RESPONSE:
I appreciate Dr. Arnason's letter and his suggestion that transesophageal echocardiography may be more sensitive than transthoracic echocardiography for evaluating cardiac manifestations related to the HLA-B27-associated disease process. The increased sensitivity is analogous to what has been proven for bacterial endocarditis. In the hands of Dr. Arnason and his colleagues, the transesophageal echocardiography-derived observations regarding the subaortic structures also seemed to be specific for patients with ankylosing spondylitis [1]. If these results can be confirmed and extended, they may also expand the proportion of HLA-B27-positive patients with disease manifestations related to this genetic trait beyond the present figure of 20% to 25%.
I would, however, like to stress the fact that transesophageal echocardiography is still a “research tool” for this indication. Much work, such as longitudinal studies, needs to be done to prove the clinical value of repeated evaluations with this test, which was performed in only a minority of Arnason and colleagues' cohort of patients with ankylosing spondylitis.
For pathophysiologic reasons discussed in my review, I doubt that Arnason and colleagues' observations will have any predictive value with regard to the development of aortic valve insufficiency or atrioventricular conduction block.
Lennart Bergfeldt, MD, PhD
Karolinska Hospital; S-171 76 Stockholm, Sweden
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
