Prostacyclin—Thromboxane Ratio as a Noninvasive Screening Test for Pulmonary Embolism

Abstract

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 PGF1α 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.