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Vascular and Endovascular Surgery
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Prostacyclin—Thromboxane Ratio as a Noninvasive Screening Test for Pulmonary Embolism

Enver Duran

Department of Cardiovascular Surgery, GATA Haydarpasa Hospital

Haldun Y. Karagoz

Department of Cardiovascular Surgery, GATA Haydarpasa Hospital

Askin Isimer

Department of Pharmacology, GATA Haydarpasa Hospital, Istanbul, Turkey

Nevzat Dogan

Department of Cardiovascular Surgery, GATA Haydarpasa Hospital

Ali Kocailik

Department of Cardiovascular Surgery, GATA Haydarpasa Hospital

Kunter Balkanli

Department of Cardiovascular Surgery, GATA Haydarpasa Hospital

Mutasim Sungun

Department of Cardiovascular Surgery, GATA Haydarpasa Hospital

The effect of pulmonary embolism (PE) on prostacyclin (PGI2) and thromboxane A2 (TxA2) levels and PGI2- TxA2 ratio (PTR) was investigated in a series of canine experiments. Group I dogs (n = 8) underwent experimental PE with autologous clot. Group II dogs (n=8) received imidazole (30 mg/kg), five minutes before PE to inhibit thromboxane synthesis and to simulate antiplatelet drug therapy. Group III dogs (n=8) received only imidazole without PE. In Groups I and II, PGI2 levels (measured as the 6-keto PGF1{alpha} metabolite) increased significantly after PE (p < 0.05), whereas they were not altered in Group III. PE caused a sharper increase in TxA2 levels (measured as the thromboxane B 2 metabolite) in Group I (p < 0.001). Imidazole decreased TxA 2 levels both in Groups II and III (p < 0.05). The reference values (ie, before PE and before imidazole) of PTR were not significantly different among the three groups: 3.8±0.4 in Group I, 3.6±0.2 in Group II, and 3.8 ±0.1 in Group III (mean 3.7±0.2). In Group I, PE resulted in a decrease in the PTR (p < 0.05), which reached its peak significance at ten minutes (from 3.8±0.4 to 1.8±0.2). Imidazole-treated groups showed a significant increase in the PTR irrespective of PE (p < 0.05) by virtue of the decreased thromboxane B2 values. It is concluded that, a PTR ratio of 2 or less is suggestive of PE in patients who do not receive antiplatelet therapy.

Vascular and Endovascular Surgery, Vol. 26, No. 4, 317-321 (1992)
DOI: 10.1177/153857449202600411
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