2004
DOI: 10.1002/clc.4960270312
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Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events

Abstract: 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.

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Cited by 30 publications
(27 citation statements)
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References 27 publications
(25 reference statements)
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“…41 In the present study, echocardiographic imaging was a sensitive tool for diagnosis of IE, with a sensitivity of 87.5%, compared with necropsy, which was used as the gold standard for diagnosis. When coagulation testing was performed, results were nearly always abnormal; therefore, consideration should be given to testing all dogs with IE for coagulation function.…”
Section: Discussionmentioning
confidence: 65%
“…41 In the present study, echocardiographic imaging was a sensitive tool for diagnosis of IE, with a sensitivity of 87.5%, compared with necropsy, which was used as the gold standard for diagnosis. When coagulation testing was performed, results were nearly always abnormal; therefore, consideration should be given to testing all dogs with IE for coagulation function.…”
Section: Discussionmentioning
confidence: 65%
“…The plasma level of PF4 is proportional to the extent and duration of platelet activation and of PF4 turnover, depending to a large extent on the underlying clinical status of each patient [38]. Increased PF4 levels are observed in inflammatory or infectious disease [39,40], diabetes [41], cardiovascular and renal disease [42-44], atherosclerosis [45] and other conditions affecting vascular health [41,46-48] or in response to traumatic medical procedures [49-51] or cardiopulmonary bypass [52]. Upon release from activated platelets, PF4 rapidly associates with heparan sulfate on endothelial cells and can be brought back into circulation by heparin, for which it has a higher affinity [30,31,53].…”
Section: Reviewmentioning
confidence: 99%
“…5 In turn, endocarditis may cause thrombocytopenia through shearing forces over the damaged valve. 6 The adherence of S aureus to platelets leads to platelet activation and aggregation. 7 When this occurs in a localized manner, it may result in formation of a thrombus; if the interaction occurs diffusely in the bloodstream, it may result in consumption of platelets, leading to thrombocytopenia.…”
Section: © 2011 Mayo Foundation For Medical Education and Researchmentioning
confidence: 99%