Endothelin-1 release from atherosclerotic plaque after percutaneous transluminal coronary angioplasty in stable angina pectoris and single-vessel coronary artery disease.

To assess the effects of percutaneous transluminal coronary angioplasty on endothelin-1 (ET-1) release, we assessed ET-1 concentrations at different sites of the coronary circulation in patients submitted to elective procedures. ET-1 levels immediately downstream from the plaque and ET-1 aortocoronary gradient increased significantly after the procedure, which was related to mechanical wall stress in patients only receiving balloons, but not in those undergoing stent percutaneous transluminal coronary angioplasty. No changes were found in the coronary sinus; these results suggest ET-1 release from the plaque rather than an ischemia/reperfusion-related production from the distal myocardium.

Platelet activation in outpatients undergoing esophagogastroduodenoscopy.

To evaluate the influence of emotional stress on platelet function, we have measured by radio-immunoassay in plasma two platelet-secreted proteins, beta-thromboglobulin and platelet factor 4, in a series of outpatients undergoing esophagogastroduodenoscopy for upper digestive complaints. The plasma levels of beta-thromboglobulin and platelet factor 4, determined just before the instrumental examination, were significantly more elevated as compared to basal values, checked a week later. These results provide evidence of enhanced in vivo platelet release reaction during emotional stress.

Molecular markers of hemostasis activation in nephrotic syndrome.

Fibrinopeptide A (FPA), a sensitive index of in vivo thrombin activity, beta-thromboglobulin (beta TG) and platelet factor 4 (PF4), specific markers of platelet intravascular activation, have been measured in plasma by radioimmunoassays in 23 patients with nephrotic syndrome and in 32 normal subjects. FPA concentration was 2.40 +/- 1.42 ng/ml (mean +/- SD) in nephrotic patients and 1.16 +/- 0.58 ng/ml in normal controls (p less than 0.001); beta TG concentration was 57.9 +/- 33.2 ng/ml in nephrotic patients and 25.7 +/- 7.4 ng/ml in controls (p less than 0.001); PF4 level was not different from controls. These data indicate in vivo blood hypercoagulability and platelet hyperfunction in nephrotic syndrome. Moreover, we have documented a slow in vitro FPA generation pattern (delta FPA): 0.97 +/- 0.51 ng/ml/10 min; this suggests that thrombin activity is predominantly local.

Comprehensive study of haemostasis in chronic uraemia.

A comprehensive study of haemostasis has been performed in a homogeneous group of 25 adult patients with conservatively treated chronic uraemia. We have found prolonged bleeding time, impaired platelet adhesiveness and aggregation, and decreased platelet factor 3 activity, increased values of fibrinogen, of factor VIII activity and related antigen, and of combined levels of factors II, VII and X. Non-significantly abnormal concentrations of factor XIII and of plasminogen and significantly lower values of plasminogen activators and higher values of urokinase inhibitors and anti-plasmin have also been found. Fibrinogen degradation products were detected in the urine of some patients.

Comprehensive study of haemostasis in nephrotic syndrome.

A comprehensive study of haemostasis has been performed in a homogeneous group of 20 patients with nephrotic syndrome without renal failure. We have found unchanged number of platelets and a significant increase of platelet adhesiveness and aggregation; increased levels of activity and related antigen of fibrinogen, of factor VIII, of activity of factors II, VII and X and of antigens of factors XIII. Antithrombin III was unchanged in plasma and was detected in the urine. Euglobulin lysis times were decreased, and levels of plasminogen and its activators were increased after a venous occlusion test. At the same time urokinase inhibitors and antiplasmins were increased not only after, but also before a venous occlusion test. Fibrinogen degradation products have been found in the urine of all our patients but not in their sera.

Characterization of heterogeneity of haemophilia B for the detection of carriers.

Factor IX activity (IX:C) and antigern (IX:Ag) as well as factor VII, prothrombin time, Normotest and Thrombotest were determined in 37 haemophiliacs B from 26 kindreds, in 30 carriers of haemophilia B and in 40 healthy subjects. In 15 obligatory carriers from 9 kindreds, in which haemophiliacs did not exhibit IX:Ag in excess of IX:C, IX:C was parallel with IX:Ag, but in 4 from 4 kindreds, in which haemophiliacs exhibit excess of IX:Ag, there was a discrepancy between IX:C and IX:Ag. Among the obligatory carriers 6 from 3 kindreds, in which haemophiliacs did not have IX:Ag in excess of IX:C, showed that the anomaly M is not a sign of genetic variability of haemophilia B.

Antithrombin III, heparin cofactor and antifactor Xa in relation to age, sex and pathological condition.

Antithrombin III (At-III) activity and protein, heparin cofactor activity, antifactor Xa activity were determined in 200 healthy adults, evenly distributed within age and sex groups, in 60 patients with cerebral thrombosis and in 20 oral contraceptive users. There was a positive correlation between At-III protein and its activities in normal subjects and in patients with cerebral thrombosis. The mean At-III protein and heparin cofactor activity values decreased with age in men and in women of fertile age. The mean values of At-III protein and its activities did not show any variation in the patients with cerebral thrombosis when compared with the normals. In oral contraceptive users a positive correlation was also found between At-III protein and its activities, antifactor Xa activity excepted. The mean antifactor Xa activity value in these women decreased during treatment, whereas the other At-III activities and At-III protein were unchanged.