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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An attempt was made to evaluate a thrombotic tendency in cases of infective endocarditis (IE) from the viewpoint of the changes of platelets and coagulo-fibrinolysis. Qualitative changes of platelets by thrombi formation were detected by showing activated responses of platelets to adenosine diphosphate or collagen and by showing a high level of plasma beta-thromboglobulin which is released by platelets during aggregation. A mild hypercoagulable state without acceleration of fibrinolysis was also detected by showing low levels of plasma antithrombin III which is the most potent antithrombin in the blood and normal levels of plasma alpha 2-plasmin inhibitor in the blood. From above findings, it was concluded that a thrombotic tendency in cases of IE was clearly detected by qualitative changes of platelets by thrombi formation and by mild hypercoagulability without acceleration of fibrinolysis.
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PMID:A thrombotic tendency in patients with infective endocarditis. 621 Jul 85

Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in IE patients with and without embolic events by measuring the plasma levels of prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasminogen activator inhibitor-1, beta-thromboglobulin, and platelet factor 4. The study included 76 consecutive patients with definite IE according to the Duke criteria. Among them, 13 (17.1%) had major embolic events. Plasma concentrations of prothrombin fragment 1 + 2 (3.2 +/- 1.3 vs 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/L, p <0.001, respectively) and thrombin-antithrombin (7.3 +/- 1.5 vs 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p <0.001, respectively) were elevated in patients with embolic events compared with both patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-thromboglobulin (63.3 +/- 10.9 vs 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p <0.001, respectively) and platelet factor 4 (106.0 +/- 28.7 vs 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p <0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher plasminogen activator inhibitor-1 levels than both nonembolic patients and healthy subjects (14.4 +/- 6.4 vs 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). In conclusion, IE patients with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state that may contribute to the increased risk of thromboembolic events in this particular group.
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PMID:Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events. 1263 99