SummaryBleeding complications occurred in 30 (11%) out of 280 patients who received continuous heparin infusion for deep venous thrombosis (DVT). 22 (8%) had minor while 8 patients (3%) had major bleeding complications (1 intrathoracic [fatal], 2 gastrointestinal and 5 retroperitoneal). Heparin activity, in daily drawn blood samples, was determined by four assays (chromogenic substrate [CS] assay, activated partial thromboplastin time [APTT], thrombin time with citrated plasma [CiTT] and thrombin time with recalcified plasma [CaTT]). The differences in median heparin activity between patients with minor bleeding and patients with no bleeding did not reach significance for any of the tests. In patients with major bleeding, the differences were significant with the CS (p = .011) and the CaTT (p = .030) assays. Patients with retroperitoneal bleeding had significantly increased median activity judged by all four assays: CS (p = .002), CaTT (p = .003), APTT (p = .010), CiTT (p = .029). The difference was most pronounced after four days of heparin treatment, but there was a considerable overlap with patients without bleeding.
In a prospective study, 280 patients with phlebographically proven deep venous thrombosis intravenous heparin infusion; 224 of the patients were subjected to control phlebography after 5–8 days of treatment. Females above 70 years showed least phlebographic improvement despite similar heparin dosage and heparin activity. Heparin activity in daily drawn blood samples was determined by four different assays. Chromogenic substrate (CS) assay (Coatest heparin), activated partial thromboplastin time (Cephotest), and thrombin time with recalcified plasma (CaTT) showed weak but significant correlations with thrombus resolution judged by phlebography (p=0.004, 0.003 and 0.018, respectively). A linear prediction equation showed that the phlebographic result was about equally influenced by the mean dose and by the result of any of the three heparin assays. Thrombin time with citrated plasma showed no correlation. CS assay and CaTT showed significantly lower mean heparin activity in patients with (n=13) than without clinically diagnosed pulmonary embolism (p=0.012 and 0.001, respectively).
Plasma antithrombin (AT) measured as heparin cofactor activity decreased 0.16 ± 0.13 U/ml (mean ± SD) in 198 patients who received heparin infusion during 1 wk for deep venous thrombosis (DVT). The decrease was weakly, but significantly correlated to heparin dose (r = 0.15, p = 0.02) and to heparin plasma concentration (r = 0.12, p = 0.05). In patients with subnormal AT at start of heparin treatment, AT decreased less and tended to normalize at the end of heparin infusion, suggesting increased synthetic rate. The decrease in AT was apparently unrelated to the extension or the fate of the thrombus, and also unrelated to other patient and disease characteristics apart from a significantly higher decrease in diabetics. 5 out of 9 patients with AT values below 0.60 U/ml had serious disease, and 1 died from pulmonary embolism (PE) shortly after cessation of heparin (AT 0.22 U/ml). We conclude that the main decrease in AT occurs during the initial 3 d of heparin treatment. If AT stays above 0.70 U/ml after 3 d of treatment, further AT monitoring is hardly indicated.
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