Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events.
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.
Ileri
Mehmet
M
Department of Cardiology, Türkiye Yüksek Ihtisas Hastanesi, Ankara, Turkey. maraspoli2000@yahoo.com
Alper
Aysin
A
Senen
Kubilay
K
Durmaz
Tahir
T
Atak
Ramazan
R
Hisar
Ismet
I
Yetkin
Ertan
E
Turhan
Hasan
H
Demirkan
Deniz
D
D000293:Adolescent; D000328:Adult; D000990:Antithrombin III / Q000032:analysis; D001777:Blood Coagulation / Q000502:physiology*; D002648:Child; D003029:Coagulants / Q000097:blood; D004617:Embolism / Q000097:blood* / Q000150:complications / Q000503:physiopathology*; D004697:Endocarditis, Bacterial / Q000097:blood* / Q000150:complications / Q000503:physiopathology*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D015539:Platelet Activation / Q000502:physiology*; D010978:Platelet Factor 4 / Q000032:analysis; D011516:Prothrombin / Q000032:analysis; D015842:Serine Proteinase Inhibitors / Q000097:blood; D001620:beta-Thromboglobulin / Q000032:analysis
D003029:Coagulants; D017395:Plasminogen Activator Inhibitor 1; D015842:Serine Proteinase Inhibitors; C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; D010978:Platelet Factor 4; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases