A de Boer

Platelet release and thromboxane synthesis in symptomatic coronary artery disease.

The incidence and significance of platelet activation in myocardial ischemia was evaluated by serial measurement of plasma thromboxane B2 (TXB2) and β thromboglobulin (,βTG) in plasma and urine in 98 patients admitted to a coronary care unit with chest pain. All measurements were normal in the 26 patients with noncardiac chest pain. Mean plasma TXB2 and βTG concentration, but not urine βTG, were elevated in the 25 patients with myocardial infarction and the 47 patients with angina. The βTG levels remained normal in 61% of the patients with angina or infarction. The TXB2 levels were significantly higher in patients with recurrent episodes of angina at rest than in those without ischemic episodes after admission. There was a weak correlation between plasma TXB2 and plasma, βTG (r = 0.20, p < 0.01) and between plasma and urine βTG (r = 0.31, p < 0.01). Results indicate that platelets are frequently activated with myocardial ischemia or infarction. However, the measurement of βTG and TXB2 is of limited value in detecting or differentiating myocardial ischemia from infarction and therefore lacks clinical value in the management of patients with ischemic heart disease.

Highly variable anticoagulant response after subcutaneous administration of high-dose (12,500 IU) heparin in patients with myocardial infarction and healthy volunteers.

BackgroundIn this study, the anticoagulant response of 12,500 IU heparin s.c. was investigated in patients with myocardial infarction and healthy volunteers to determine variabilities in response and modifying factors. Methods and ResultsOn the fourth day after thrombolytic therapy, blood samples were taken before and at frequent intervals until 10 hours after the injection of 12,500 IU heparin s.c. Plasma anti-Xa activity, anti-Ha activity, and the activated partial thromboplastin time (APTT) were measured in addition to body weight and thickness of the abdominal subcutaneous fat layer. Contrary to expectations, the increase of anti-Xa activity, anti-lla activity, and APTT compared with baseline (predrug) levels was very small, with an average maximal APYIT of 42.6 seconds (SD, 12.4 seconds; range, 30.4–70.7 seconds). Subsequently, the influence of the length of the injection needle on the anticoagulant effect of 12,500 IU heparin s.c. was studied in 10 healthy volunteers to find a factor that could be responsible for the poor response in the patients. The length of the injection needle did not influence the anticoagulant effect of heparin. Large interindividual and intraindividual variabilities were seen in the volunteers. The majority of volunteers had minimal prolongation of the APWT, but very strong prolongation was also seen (maximal APIT, 163 seconds). There was no correlation between the abdominal skinfold thickness and anti-Xa activity, anti-Ha activity, or APTT (p>0.05), but in the patient study, there was a correlation between weight and anti-Xa activity and anti-Ila activity (p<0.05), and in the volunteer study, there was a correlation between weight and anti-Xa activity and APIT (p<0.05). ConclusionsSubcutaneous administration of heparin in a fixed dose for prophylactic and therapeutic purposes may be inadequate because of the large interindividual and intraindividual variations in anticoagulant effect.

Plasma betathromboglobulin and serum fragment E in acute partial stroke

Plasma betathromboglobulin (BTG) and serum fragment E (FgE) were measured serially by radioimmunoassay for 7 d in 67 patients admitted with acute partial stroke. Twelve patients progressed within 7 d of admission. Plasma BTG was not different from normal in patients with acute partial stroke and did not increase significantly with stroke progression. Serum FgE was elevated in patients with acute partial stroke compared with normal values, and was significantly higher in patients who progressed compared with those who remained stable. The results indicate that fibrin formation may be more important in the process of stroke progression than activation of platelets.

Measurement of antithrombin III, α2-macroglobulin and α1-antitrypsin in patients with deep venous thrombosis and pulmonary embolism

Abstract Antithrombin III (AT III) activity, α 2 -macroglobulin ( α 2 -M) and α 1 -antitrypsin ( α 1 -AT) concentration was determined in 101 non-surgical patients including 45 patients with deep venous thrombosis and 15 patients with pulmonary embolism. 9 (20%) patients with deep venous thrombosis (DVT) and 6 patients (40%) with pulmonary embolism had lowered AT III activity during the acute episode. In the group of patients with pulmonary embolism, mean AT III activity was lowered compared to control patients (86% and 97% respectively), although the difference was not significant. Some months after the thromboembolic event 7 patients with lowered AT III activity were investigated again. All had normal AT III activity by then, suggesting that decreased AT III activity in patients with thromboembolic disease is a temporary phenomenon. α 2 -M and α 1 -AT were significantly decreased in control patients compared to normal persons. In patients with thromboembolic disease no further lowering was seen. Both inhibitors may contribute to the hypercoagulable state, which is often seen in severely ill patients.

An evaluation of suloctidil in the prevention of deep vein thrombosis in neurosurgical patients

Suloctidil (200 mg t.i.d.) was compared with placebo in a randomized, double-blind trial to assess its value in preventing deep venous thrombosis (DVT) in high-risk neurosurgical patients, comprising 136 patients with brain or spinal tumour, head or spinal injury, or subarachnoid or intracranial hemorrhage. 125I fibrinogen leg scanning and impedance plethysmography were performed for up to 14 days to detect DVT. The two groups were also evenly balanced for DVT risk factors. Seventeen of 68 patients (25%) (95% confidence interval, 15-35%) treated with suloctidil and 12 of 68 patients (21%) (95% confidence interval, 11-32%) treated with placebo developed deep venous thrombosis. This observed difference in outcomes is not statistically significant (X2 = 1.096; p = 0.30). The estimated 95% confidence interval for the true difference in the incidence of DVT between suloctidil-treated and placebo-treated patients ranges from an 11% benefit in favour of suloctidil to an 18% benefit in favour of placebo. Major deep vein thrombosis occurred in two patients on suloctidil and three patients in the placebo group; there were no fatal pulmonary emboli during the 14-day study period, during which time four patients in each group died of non-thromboembolic complications. There was no observed difference in hemorrhagic complications. Long-term outcomes at three-months follow-up were similar between the two treatment groups. It is concluded that there is no real evidence that suloctidil (200 mg t.i.d.) is an effective regimen for the prevention of DVT in high-risk neurosurgical patients.

The value of adding thermographic leg scanning to impedance plethysmography in the detection of deep vein thrombosis

The clinical value of adding thermographic leg scanning to impedance plethysmography was evaluated and compared in 52 patients with clinically suspected deep venous thrombosis. Both tests were performed on the day of referral and phlebography within 72 hours. The sensitivity of thermography was 83%, the specificity 41% and the accuracy 61%. In comparison IPG had a sensitivity of 83%, a specificity of 96% and an accuracy of 90% The combination of thermography and IPG showed a sensitivity of 92%, a specificity of 41% and an accuracy of 65%. It is concluded that the addition of thermography to IPG is of no clinical value.