Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events.
BACKGROUND
Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE).


OBJECTIVE
The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in patients with IE with and without embolic events by measuring the plasma levels of prothrombin fragment 1+2 (PF1+2), thrombin-antithrombin III complex (TAT), plasminogen activator inhibitor-1 (PAI-1), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF4), respectively.


METHODS
The study included 76 consecutive patients (female = 55, male = 21, mean age 26 years, range 8-64 years) with definite IE according to the Duke criteria; of these, 13 (17.1%) had embolic events.


RESULTS
Plasma concentrations of PF1+2 (3.2 +/- 1.3 vs. 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/l, p < 0.001, respectively) and TAT (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 patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-TG (63.3 +/- 10.9 vs. 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p < 0.001, respectively) and PF4 (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 PAI-1 levels than 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).


CONCLUSIONS
Patients with IE and with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state, which contributes to the increased risk of thromboembolic events in this particular group.
Buyukasýk
N Semnur
NS
Department of Internal Medicine, Ankara Numune Hospital, Ankara, Turkey.
Ileri
Mehmet
M
Alper
Aysin
A
Senen
Kubilay
K
Atak
Ramazan
R
Hisar
Ismet
I
Yetkin
Ertan
E
Turhan
Hasan
H
Demirkan
Deniz
D
D000293:Adolescent; D000328:Adult; D000990:Antithrombin III; D001777:Blood Coagulation / Q000502:physiology*; D002648:Child; D004697:Endocarditis, Bacterial / Q000097:blood* / Q000503:physiopathology; D005260:Female; 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; D018709:Statistics, Nonparametric; D013923:Thromboembolism / Q000097:blood* / Q000503:physiopathology; D001620:beta-Thromboglobulin / Q000032:analysis
D017395:Plasminogen Activator Inhibitor 1; C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; D010978:Platelet Factor 4; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases