REPLY
Prinzmetal Angina and Cyproheptadine
Alison D. Schecter;
James H. Chesebro; and
Valentin Fuster
15 January 1995 | Volume 122 Issue 2 | Page 155
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.
1. DeCaterina R, Carpeggiani C, L'Abbate A. A double-blind, placebo-controlled study of ketanserin in patients with Prinzmetal's angina. Circulation. 1984; 69:889-94.
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