SummaryThe fibrinolytic system was investigated in 120 patients with spontaneous or recurrent deep vein thrombosis (DVT) without any known organic disease able to explain by itself the occurrence of a thrombosis and without any known defect of antithrombin III, Heparin Cofactor II, Protein C, or Protein S. The assays included: Euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator related antigen (t-PA-Ag) and plasminogen activator inhibitor activity (PA inhibitor), which were measured before and after 10 min of venous occlusion (V. O.). On the basis of the results, the patients could be classified in 3 groups:good responders with an at least two-fold increase of EFA after venous occlusion (n = 76), poor responders with a lesser increase of EFA due to deficient release of t-PA (n = 12), and poor responders with a normal t-PA release but an increased level of PA-Inhibitor (n = 32).The poor responders due to deficient t-PA release (10% of total) had a higher incidence of recurrence of deep vein thrombosis, than the other groups (p <0.01). An overall correlation was found between the level of PA-Inhibitor activity and the triglyceride level (r = 0.40, p <0.01), suggesting that these elevations may be due to a common cause, at least in some of the patients.It is concluded that a poor fibrinolytic response to venous occlusion occurs in 35 percent of DVT patients. Poor responders however fall into two categories, one fourth with deficient t-PA release who have a high risk for recurrent venous thrombosis, and three fourth with increased PA-Inhibitor levels which may be associated with underlying diseases also causing hypertriglyceridemia. Further elucidation of the correlation between recurrent venous thrombosis and deficient fibrinolysis is expected to result in more specific and adequate treatment and prevention of DVT.

The fibrinolytic activity of blood depends on the balance between the circulating level of tissue-type plasminogen activator (t-PA), which is secreted by endothelial cells, and plasminogen activator inhibitor-1 (PAI-1), 3 which is secreted by endothelial cells and hepatocytes and is also released by platelets. 4 Patients with coronary artery disease, either before or after myocardial infarction, have an increased plasma level of PAI activity, 5 -8 which may predispose to infarction. Received September 13, 1988; revision accepted December 13, 1988. stand the mechanisms that regulate PAI-1 production in patients at risk for myocardial infarction. Methods PatientsSixty-seven consecutive patients undergoing coronary angiography (51 men, mean age [SD] 61 [6], range 43 to 77) were studied; 22 had angina on exertion, 17 had angina at rest, four had mixed angina, and 24, unstable angina. Electrocardiographs (ECG) changes at rest were noted in 40 patients (ST segment depression of at least 1 mm or T wave inversion). Seven patients had ECG changes during painful episodes only. The other 20 had a normal ECG at rest. Of 44 patients, 31 had an abnormal exercise ECG. Previous myocardial infarction (more than 3 months before blood sampling) had occurred in 13 men and two women, and three patients had previous deep venous thrombosis. Patients received Ca ++ -antagonists (40 patients), ^-blocking agents (22 patients), nitrates (18 patients), heparin (18 patients), oral anticoagulants (three patients), or platelet aggregation inhibitors (13 patients).Body mass index (BMI) defined as body weight (kg) divided by the square of height (m), was (mean±SD): for men, 25±2.7, range 22 to 28 (normal value, 23); and for women, 24±3.6, range 21 to 28 (normal value, 21). The prevalence of risk factors is reported in Table 1.Coronary angiograms were performed with the femoral or brachial approach. The severity of coronary disease 362 Downloaded from http://ahajournals.org by on April 1, 2019

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Methods : in this prospective study, real time B Mode ultrasound imaging (USI) was compared to bilateral ascending contrast venography, double blindly, in 430 patients suspected of deep vein thrombosis (DVT) or pulmonary embolism.A complete scan of the venous system from the inferior vena cava to the calf veins, was performed with a high resolution duplex system (DIASONICS DRF 400) and coupled systematically with a C.W. Doppler examination. The results obtained by USI were thus compared to the venograms performed on a total of 854 legs.Results : there are corresponding results in 95% of the legs (808/854). If we consider venography as the standard of reference, the sensitivity of USI is 98% (325/333) and the specificity 94% (483/514). Isolated calf vein thrombosis are detected in 91% (84/92) of the legs and proximal DVT in 100% (241/241) in this series whatever the topography and the extension of the thrombosis and whatever the degree of the obstruction of the vein.Discrepancies found in 46 legs are related to :- 8 DVT located in the calf (6 in the presumed healthy leg) diagnosed only by venography.- 27 DVT (18 distal, 9 femoral or iliac) detected only by USI- 9 doubtful examinations with USI not confirmed by venography- 2 doubtful venograms with negative USI test.Comments : Calf vein thrombosis especially located in the soleal sinuses and the gastrocnemius with in most cases the direct image of the thrombus are more often detected by USI provided that the technique and the equipment are appropriate.The absence of visualisation of venous segments with venography is not specific of venous thrombosis. These veins non affected by the thrombosis are not filled by the contrast medium when located above in occluded ilio-femoral or ilio-caval junction or when they are the site of extrinsic compression. The direct image of the vein and the surrounding structures obtained with USI enhances the diagnostic sensitivity and specificity and provides precision of the exact extension of the thrombosis.Due to these differences, can venography still be considered as the standard of reference in the diagnosis of DVT and their precise localisation ?

Prostacyclin (PGI 2 ) and prostaglandin E 2 (PGE 2 ) production was Investigated in human aortas (five controls and 27 with atherosclerotic lesions). The specific activities of PGI 2 and PGE 2 synthetase were studied using radioimmunoassays of PGE 2 and 6-keto-PGE 1( , of aortic microsomes incubated in the presence of additional substrate and cofactors. The atherosclerotic lesions were examined under the light microscope and were classified as Stage 1 when the disease was restricted to the intima and as Stages 2 and 3 when there were moderate or advanced lesions. Prostaglandin production for the control group (n = 5), Stage 1 (n = 7), Stage 2 (n = 10), and Stage 3 (n = 10) were as follows: 454 ± 15, 162 ± 81, 92 ± 90, and 65 ± 61 pmol 6-K-PGF 1u /50 mg proteln/10 minutes; and 15 ± 12, 399 ± 406, 227 ± 174, and 366 ± 362 pmol PGEj/50 mg protein/10 minutes (mean ± SD) respectively. We conclude that: 1) In normal aortas, PGE 2 production was low, while PGI 2 synthesis activity was elevated. The reverse situation was observed In aortas with atherosclerosis lesions (p < 0.05). 2) There was an inverse relationship between PGE 2 and PGI, production (p < 0.05).3) There was a direct hlstologlc relationship between lower PGI 2 production and atherosclerosis progression. A decided decline In 6-K-PGF,,, production was detected in aortas In the early stages (65% of control values). 4) By contrast, a progressive increase In PGE 2 production was found In Stage 2 and Stage 3 groups (p < 0.05). These results demonstrate that there are correlations between the changes In prostaglandin production and the morphological features of atherosclerosis development. Because of the pharmacologlc properties of prostaglandins, these changes in prostaglandin production may promote the development of atherosclerosis. (Arteriosclerosis 4:70-78, January/February 1984)