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SummaryTissue thromboplastin injected into the femoral vein of anesthetized rabbits produced intravascular clotting in the vessels through which the thromboplastin flowed. In the systemic arteries macroscopically visible clots were never observed. No trace of tissue thromboplastin could be demonstrated in blood drawn from the carotid artery following infusion of tissue thromboplastin into the femoral vein. The slight, transient enhancement of coagulation of the arterial blood following tissue thromboplastin infusion was caused by a serum effect. After intravenous injection of serum, enhanced activation of coagulation could be observed for a period of up to 2 hrs. It is concluded that tissue thromboplastin, intravenously injected, is removed from the blood during its passage from the femoral vein to the systemic arteries, probably in the capillaries of the lung. True hypercoagulability appears to be due to a serum effect or caused by partial activation of the intrinsic coagulation system. The levels of coagulation precursors in blood are of minor significance.

SummaryThe effects of infusion of homologous tissue thromboplastin in the jugular vein of the rabbit was followed by determination of levels of coagulation factors in samples of blood obtained from the systemic arterial circulation by appropriate one-stage methods. The presence of active coagulation components was studied by appropriate two- or three-stage methods. There was marked consumption of coagulation factors, including fibrinogen. No macroscopically visible thrombi were seen in the major vessels of the systemic circulation indicating absence of tissue thromboplastin in the greater circulation. Two-and three-stage tests indicated presence of coagulation enhancing agents different from tissue thromboplastin and of a serum-like nature. Tissue thromboplastin, being bound to particulate matter, was most probably retained in the capillary bed of the lungs, thereby being prevented from appearing in the systemic circulation. The results confirm our previous findings obtained by infusion in the femoral vein. They are discussed and compared with the behavior of infused blood or tissue thromboplastin reported by other authors. Discrepancies in reported data could be traced to differences in sites of infusion or of collection of samples of blood. Changes in plasminogen concentration or in plasma euglobulin fibrinolytic activity on normal and heated fibrin plates were slight.

Predictability of prosthesis- and sudden heart-related complications was examined in 121 patients who were alive 30 days after valve replacement (1965-86) for aortic regurgitation. A variety of prosthetic valves, mainly mechanical, were used. The Cox regression model was used to identify independent risk factors and to estimate the predicted freedom of events relative to combinations of these risk factors. In the following, linearized event-rates (LER) are given as number of events per 100 patient years +/- standard error. No risk factors could be identified for endocarditis (LER: 0.3 +/- 0.2) or anticoagulant-related hemorrhage (LER: 1.7 +/- 0.6). Only factors underlying deranged preoperative patient and heart status and cardioplegic method, but not the type of prosthetic valve, had predictive influence on the other complications. Predicted 10-year event-freedoms for low- versus high-risk estimate were 98% versus 46% for thromboembolism (LER: 2.1 +/- 0.6), 87% versus 68% for all prosthesis-related complications (LER: 5.0 +/- 0.8), 100% versus 0% for sudden heart-related events (LER: 2.0 +/- 0.5; myocardial infarction and arrhythmia), and 72% versus 38% for combined prosthesis- and sudden heart-related morbidity and mortality (LER: 7.0 +/- 1.0). By deciding to operate early in the course of aortic regurgitation, the rate of these complications may be "actively" reduced, and longevity and life quality of the patients improved.

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