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Article: Relation between mitral regurgitation and platelet activation

TitleRelation between mitral regurgitation and platelet activation
Authors
Issue Date1997
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jac
Citation
Journal Of The American College Of Cardiology, 1997, v. 30 n. 7, p. 1813-1818 How to Cite?
AbstractObjectives. This study sought to examine the effect of mitral regurgitation (MR) on platelet activation in patients with mitral valve prolapse (MVP) or rheumatic MR. Background. MVP and rheumatic MR are associated with an increased incidence of thromboembolic events. Although the underlying causes are not clear, increased platelet activation has been suggested as one of the pathogenic mechanisms. Results of previous studies that have investigated the relation between MVP and platelet activation are controversial. Whether the presence of MR in patients with mitral valve disease is associated with platelet activation remains unclear. Methods. We studied platelet activation by measuring the plasma level of platelet factor 4 (PF4) and beta-thromboglobulin (BTG) in 16 patients with MVP, 12 patients with rheumatic MR and 25 control subjects. A detailed echocardiographic examination, including M-mode measurement and color Doppler flow mapping to detect the presence and severity of MR was performed. Results. Patients and control subjects were matched for gender, age and left ventricular ejection fraction. Eight (50%) of 16 patients with MVP had MR. Patients with MVP and MR and patients with rheumatic MR had a significantly larger left atrial diameter. Mean log plasma levels of PF4 and BTG were significantly higher in patients with MVP and MR and patients with rheumatic MR than in control subjects (1.17 ± 0.22 and 0.93 ± 0.23 IU/ml vs. 0.52 ± 0.34 IU/ml, p < 0.01; 1.70 ± 0.21 and 1.53 ± 0.15 IU ml vs. 1.37 ± 0.15 IU/ml, p < 0.05, respectively) but were comparable in patients with MVP and no MR and control subjects. Plasma levels of PF4 and BTG were positively correlated with the severity of MR, as assessed by a semiquantitative method (r = 0.59, p = 0.0001; r = 0.60, p = 0.0001, respectively). Increasing age and left atrial enlargement were not related to platelet activation. Conclusions. MR in mitral valve disease was associated with systemic platelet activation. MVP itself was not associated with increased platelet activation. The degree of platelet activation was positively correlated with the severity of MR and was independent of the underlying etiology of mitral valve disease, age and left atrial size. The possibility of a higher incidence of thromboembolism and the role of antiplatelet agents in such patients will require further studies to determine.
Persistent Identifierhttp://hdl.handle.net/10722/78247
ISSN
2015 Impact Factor: 17.759
2015 SCImago Journal Rankings: 10.097
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorCheng, Gen_HK
dc.date.accessioned2010-09-06T07:40:46Z-
dc.date.available2010-09-06T07:40:46Z-
dc.date.issued1997en_HK
dc.identifier.citationJournal Of The American College Of Cardiology, 1997, v. 30 n. 7, p. 1813-1818en_HK
dc.identifier.issn0735-1097en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78247-
dc.description.abstractObjectives. This study sought to examine the effect of mitral regurgitation (MR) on platelet activation in patients with mitral valve prolapse (MVP) or rheumatic MR. Background. MVP and rheumatic MR are associated with an increased incidence of thromboembolic events. Although the underlying causes are not clear, increased platelet activation has been suggested as one of the pathogenic mechanisms. Results of previous studies that have investigated the relation between MVP and platelet activation are controversial. Whether the presence of MR in patients with mitral valve disease is associated with platelet activation remains unclear. Methods. We studied platelet activation by measuring the plasma level of platelet factor 4 (PF4) and beta-thromboglobulin (BTG) in 16 patients with MVP, 12 patients with rheumatic MR and 25 control subjects. A detailed echocardiographic examination, including M-mode measurement and color Doppler flow mapping to detect the presence and severity of MR was performed. Results. Patients and control subjects were matched for gender, age and left ventricular ejection fraction. Eight (50%) of 16 patients with MVP had MR. Patients with MVP and MR and patients with rheumatic MR had a significantly larger left atrial diameter. Mean log plasma levels of PF4 and BTG were significantly higher in patients with MVP and MR and patients with rheumatic MR than in control subjects (1.17 ± 0.22 and 0.93 ± 0.23 IU/ml vs. 0.52 ± 0.34 IU/ml, p < 0.01; 1.70 ± 0.21 and 1.53 ± 0.15 IU ml vs. 1.37 ± 0.15 IU/ml, p < 0.05, respectively) but were comparable in patients with MVP and no MR and control subjects. Plasma levels of PF4 and BTG were positively correlated with the severity of MR, as assessed by a semiquantitative method (r = 0.59, p = 0.0001; r = 0.60, p = 0.0001, respectively). Increasing age and left atrial enlargement were not related to platelet activation. Conclusions. MR in mitral valve disease was associated with systemic platelet activation. MVP itself was not associated with increased platelet activation. The degree of platelet activation was positively correlated with the severity of MR and was independent of the underlying etiology of mitral valve disease, age and left atrial size. The possibility of a higher incidence of thromboembolism and the role of antiplatelet agents in such patients will require further studies to determine.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/jacen_HK
dc.relation.ispartofJournal of the American College of Cardiologyen_HK
dc.rightsJournal of American College of Cardiology. Copyright © Elsevier Inc.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshEchocardiographyen_HK
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMitral Valve Insufficiency - blood - complications - ultrasonographyen_HK
dc.subject.meshMitral Valve Prolapse - blood - complications - ultrasonographyen_HK
dc.subject.meshPlatelet Activationen_HK
dc.subject.meshPlatelet Factor 4 - analysisen_HK
dc.subject.meshRheumatic Heart Disease - blood - complications - ultrasonographyen_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshThromboembolism - epidemiology - etiologyen_HK
dc.subject.meshbeta-Thromboglobulin - analysisen_HK
dc.titleRelation between mitral regurgitation and platelet activationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0735-1097&volume=30 &issue=7&spage=1813&epage=&date=1997&atitle=Relation+between+mitral+regurgitation+and+platelet+activationen_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0735-1097(97)00380-Xen_HK
dc.identifier.pmid9385912-
dc.identifier.scopuseid_2-s2.0-0031539405en_HK
dc.identifier.hkuros31837en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031539405&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1813en_HK
dc.identifier.epage1818en_HK
dc.identifier.isiWOS:A1997YH37900032-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridCheng, G=35313354500en_HK

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