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Article: Effects of atrioventricular asynchrony on platelet activation: Implication of thromboembolism in paced patients

TitleEffects of atrioventricular asynchrony on platelet activation: Implication of thromboembolism in paced patients
Authors
KeywordsPacing
Platelet activation
Thromboembolism
Issue Date1997
PublisherB M J Publishing Group. The Journal's web site is located at http://heart.bmjjournals.com/
Citation
Heart, 1997, v. 78 n. 4, p. 358-363 How to Cite?
AbstractObjective - To investigate the platelet activation in different modes of pacing in patients implanted with dual chamber rate adaptive pacemaker (DDDR) for bradyarrhythmias, and to explore the possible underlying mechanism of the higher thromboembolic incidence in single chamber ventricular rate adaptive (VVIR) pacing. Design - Platelet activation was determined in chronically paced patients during three different pacing modes (VVIR, DDD, and DDDR) in a randomized crossover fashion. Setting - Pacemaker clinic at a university teaching hospital. Patients - 15 patients with complete heart block, mean (SD) age 63 (10) years, and 12 patients with sick sinus syndrome, mean age 68 (9) years, implanted with DDDR pacemakers. Main outcome measures - Platelet activation was assessed by measuring the plasma concentrations of platelet factor 4 (PF4) and β thromboglobulin using an enzyme linked immunosorbent assay (ELISA). Mean log plasma PF4 and β thromboglobulin values were compared in paced patients during different pacing modes and with control. Results - Compared with controls, patients paced in DDDR, DDD, and VVIR modes had higher mean log plasma concentrations of PF4 (0.90 (0.32), 0.92 (0.29), and 1.12 (0.33) v 0.61 (0.29) log IU/ml, all p < 0.05, respectively) and β thromboglobulin (1.55 (0.20), 1.59 (0.16), and 1.71 (0.18) v 1.40 (0.12) log IU/ml, all p < 0.05, respectively). In paced patients, VVIR pacing was associated with higher plasma concentrations of PF4 and β thromboglobulin than either DDDR or DDD pacing (all p < 0.05). There was no significant difference in plasma PF4 and β thromboglobulin between patients with complete heart block and sick sinus syndrome in the corresponding pacing mode. Holter monitoring showed no difference in mean pacing rate and occurrence of cardiac arrhythmias to account for the increased platelet activation during VVIR pacing. There was no relation between the percentage of ventricular pacing on Holter during DDDR, DDD, and VVIR modes and the log mean plasma concentrations of PF4 (r = 0.002, 0.001, and 0.001, respectively, all p > 0.05) and β thromboglobulin (r = 0.007, 0.01, and 0.001, respectively, all p > 0.05). Conclusions - Single chamber ventricular pacing was associated with enhanced spontaneous systemic platelet activation compared with physiological dual chamber pacing. This was related to the loss of atrioventricular synchrony rather than to the underlying cause of bradycardia, lack of rate response, or coexisting arrhythmia. This abnormality may be associated with increased thromboembolism and was correctable by an appropriate pacing mode prescription and possibly antiplatelet treatment.
Persistent Identifierhttp://hdl.handle.net/10722/42412
ISSN
2015 Impact Factor: 5.693
2015 SCImago Journal Rankings: 2.647
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLau, CPen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorCheng, Gen_HK
dc.date.accessioned2007-01-29T08:49:21Z-
dc.date.available2007-01-29T08:49:21Z-
dc.date.issued1997en_HK
dc.identifier.citationHeart, 1997, v. 78 n. 4, p. 358-363en_HK
dc.identifier.issn1355-6037en_HK
dc.identifier.urihttp://hdl.handle.net/10722/42412-
dc.description.abstractObjective - To investigate the platelet activation in different modes of pacing in patients implanted with dual chamber rate adaptive pacemaker (DDDR) for bradyarrhythmias, and to explore the possible underlying mechanism of the higher thromboembolic incidence in single chamber ventricular rate adaptive (VVIR) pacing. Design - Platelet activation was determined in chronically paced patients during three different pacing modes (VVIR, DDD, and DDDR) in a randomized crossover fashion. Setting - Pacemaker clinic at a university teaching hospital. Patients - 15 patients with complete heart block, mean (SD) age 63 (10) years, and 12 patients with sick sinus syndrome, mean age 68 (9) years, implanted with DDDR pacemakers. Main outcome measures - Platelet activation was assessed by measuring the plasma concentrations of platelet factor 4 (PF4) and β thromboglobulin using an enzyme linked immunosorbent assay (ELISA). Mean log plasma PF4 and β thromboglobulin values were compared in paced patients during different pacing modes and with control. Results - Compared with controls, patients paced in DDDR, DDD, and VVIR modes had higher mean log plasma concentrations of PF4 (0.90 (0.32), 0.92 (0.29), and 1.12 (0.33) v 0.61 (0.29) log IU/ml, all p < 0.05, respectively) and β thromboglobulin (1.55 (0.20), 1.59 (0.16), and 1.71 (0.18) v 1.40 (0.12) log IU/ml, all p < 0.05, respectively). In paced patients, VVIR pacing was associated with higher plasma concentrations of PF4 and β thromboglobulin than either DDDR or DDD pacing (all p < 0.05). There was no significant difference in plasma PF4 and β thromboglobulin between patients with complete heart block and sick sinus syndrome in the corresponding pacing mode. Holter monitoring showed no difference in mean pacing rate and occurrence of cardiac arrhythmias to account for the increased platelet activation during VVIR pacing. There was no relation between the percentage of ventricular pacing on Holter during DDDR, DDD, and VVIR modes and the log mean plasma concentrations of PF4 (r = 0.002, 0.001, and 0.001, respectively, all p > 0.05) and β thromboglobulin (r = 0.007, 0.01, and 0.001, respectively, all p > 0.05). Conclusions - Single chamber ventricular pacing was associated with enhanced spontaneous systemic platelet activation compared with physiological dual chamber pacing. This was related to the loss of atrioventricular synchrony rather than to the underlying cause of bradycardia, lack of rate response, or coexisting arrhythmia. This abnormality may be associated with increased thromboembolism and was correctable by an appropriate pacing mode prescription and possibly antiplatelet treatment.en_HK
dc.format.extent664125 bytes-
dc.format.extent27136 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.languageengen_HK
dc.publisherB M J Publishing Group. The Journal's web site is located at http://heart.bmjjournals.com/en_HK
dc.relation.ispartofHearten_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsHeart. Copyright © B M J Publishing Group.en_HK
dc.subjectPacingen_HK
dc.subjectPlatelet activationen_HK
dc.subjectThromboembolismen_HK
dc.subject.meshCardiac pacing, artificial - adverse effectsen_HK
dc.subject.meshElectrocardiography, ambulatoryen_HK
dc.subject.meshHeart block - blood - physiopathology - therapyen_HK
dc.subject.meshPlatelet activationen_HK
dc.subject.meshThromboembolism - etiologyen_HK
dc.titleEffects of atrioventricular asynchrony on platelet activation: Implication of thromboembolism in paced patientsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1355-6037&volume=78&issue=4&spage=358&epage=363&date=1997&atitle=Effects+of+atrioventricular+asynchrony+on+platelet+activation:+Implication+of+thromboembolism+in+paced+patientsen_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid9404251-
dc.identifier.pmcidPMC1892270-
dc.identifier.scopuseid_2-s2.0-0030690047en_HK
dc.identifier.hkuros28862-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030690047&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume78en_HK
dc.identifier.issue4en_HK
dc.identifier.spage358en_HK
dc.identifier.epage363en_HK
dc.identifier.isiWOS:A1997YC55200013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLau, CP=35275317200en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridCheng, G=35313354500en_HK

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