title: Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Ankara Numune Hospital, Ankara, Turkey.
authors.forename: N Semnur
authors.initials: NS
authors.lastname: Buyukasýk
authors.forename: Mehmet
authors.initials: M
authors.lastname: Ileri
authors.forename: Aysin
authors.initials: A
authors.lastname: Alper
authors.forename: Kubilay
authors.initials: K
authors.lastname: Senen
authors.forename: Ramazan
authors.initials: R
authors.lastname: Atak
authors.forename: Ismet
authors.initials: I
authors.lastname: Hisar
authors.forename: Ertan
authors.initials: E
authors.lastname: Yetkin
authors.forename: Hasan
authors.initials: H
authors.lastname: Turhan
authors.forename: Deniz
authors.initials: D
authors.lastname: Demirkan
mesh_terms: 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
chemical_list: 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