Linked Life Data

12633799

Source:http://linkedlifedata.com/resource/pubmed/id/12633799

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-3-13
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9149
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
689-92
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12633799-Adolescent, pubmed-meshheading:12633799-Adult, pubmed-meshheading:12633799-Antithrombin III, pubmed-meshheading:12633799-Blood Coagulation, pubmed-meshheading:12633799-Child, pubmed-meshheading:12633799-Coagulants, pubmed-meshheading:12633799-Embolism, pubmed-meshheading:12633799-Endocarditis, Bacterial, pubmed-meshheading:12633799-Female, pubmed-meshheading:12633799-Fibrinolysis, pubmed-meshheading:12633799-Humans, pubmed-meshheading:12633799-Male, pubmed-meshheading:12633799-Middle Aged, pubmed-meshheading:12633799-Peptide Hydrolases, pubmed-meshheading:12633799-Plasminogen Activator Inhibitor 1, pubmed-meshheading:12633799-Platelet Activation, pubmed-meshheading:12633799-Platelet Factor 4, pubmed-meshheading:12633799-Prothrombin, pubmed-meshheading:12633799-Serine Proteinase Inhibitors, pubmed-meshheading:12633799-beta-Thromboglobulin
pubmed:year
2003
pubmed:articleTitle
Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events.
pubmed:affiliation
Department of Cardiology, Türkiye Yüksek Ihtisas Hastanesi, Ankara, Turkey. maraspoli2000@yahoo.com
pubmed:publicationType
Journal Article, Comparative Study