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Prinzmetal Angina and Cyproheptadine
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IN RESPONSE:
Dr. Ambrus emphasizes that inhibition of platelet aggregation is a potential important pathophysiologic mechanism for serotonergic-receptor blockade in vasospasm. Serotonin is initially released when platelets aggregate and initiate a positive feedback loop by releasing adenosine diphosphate, thromboxane A2, and more serotonin.
An early study [1] failed to show a decrease in the number of ischemic episodes in patients with vasospastic angina who were treated with ketanserin, a selective serotonin-receptor (S2) antagonist. Ketanserin was given at concentrations that inhibited in vitro platelet aggregation. The presence of serotonin-receptor families, individual patient characteristics for platelet aggregation, and differing in vivo responses may make the use of other serotonin-receptor antagonists, such as cyproheptadine, clinically efficacious in selected patients.
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 Unpublished letters cannot be returned.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
