Author + information
- Received November 18, 1986
- Revision received March 25, 1987
- Accepted June 3, 1987
- Published online November 1, 1987.
- Christian W. Hamm, MD*,1,
- Reinhard L. Lorenz, MD1,
- Walter Bleifeld, MD, FACC1,
- Wolfram Kupper, MD1,
- Wolfgang Wober, MD, PhD1 and
- Peter C. Weber, MD1
- ↵*Address for reprints: Christian W. Hamm, MD, Medizinische Klinik, Abteilung für Kardiologie, Universitätskrankenhaus Eppendorf, Martinistr. 52, D-2000 Hamburg 20, West Germany.
Thromboxane released from activated platelets and prostacyclin of the vessel wall may act as potent antagonistic modulators of platelet aggregability and coronary vascular tone. Therefore, urinary excretion of their major metabolites, 2,3-dinor-thromboxane B2and 2,3-dinor-6-ketoprostaglandin F1α, was studied in 16 patients presenting with prolonged angina at rest. The 10 patients whose condition did not improve under vigorous antianginal treatment within 48 hours exhibited higher thromboxane metabolite excretion than did the 6 patients who responded to therapy (2,208 ± 1,542 versus 609 ± 312 ng/g creatinine; p < 0.01). Elevated values were also found in four of eight patients with sustained postinfarction angina. Enhanced thromboxane metabolite excretion was frequently associated with angiographic evidence of thrombus formation.
When nine patients were restudied in a stable phase after 11 ± 5 months, thromboxane metabolite excretion was consistently normal or high normal. Excretion of prostacyclin metabolites was not depressed in any patient but correlated weakly with thromboxane (r = 0.41). Thus, enhanced thromboxane production as an index of platelet activation may identify patients with active thrombus formation who could benefit most from platelet inhibitory treatment.
- Received November 18, 1986.
- Revision received March 25, 1987.
- Accepted June 3, 1987.
- American College of Cardiology Foundation