Thromboxane A2in Vasotonic Angina Pectoris

Abstract

Thromboxane A₂ (TxA₂), an arachidonic acid metabolite causing vasoconstriction and platelet aggregation, is a putative mediator of coronary-artery vasospasm. To determine whether platelet-released TxA₂ causes coronary arterial vasospasm, we measured plasma thromboxane B₂ (TxB₂, the inactive hydration product of TxA₂) in the radial-artery and coronary-sinus blood of seven patients and performed therapeutic trials of antiplatelet agents in nine. Although coronary-sinus TxB₂ levels rose from the base line approximately fivefold with spontaneous ischemia, samples drawn early in ischemia showed no rise over base-line values. Although a 150-mg dose of aspirin reduced urinary dinor-TxB₂ levels by over 75 per cent, it had no effect on the course of the chronic recurrent form of angina pectoris due to vasospasm ("vasotonic angina"). Similarly, indomethacin had no effect on the frequency or duration of ischemia. TxA₂ is unlikely to cause vasotonic angina, but it may be released during coronary vasospasm. (N Engl J Med. 1981; 304:998–1003.)