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Article: Relation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary Intervention

TitleRelation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary Intervention
Authors
Issue Date2005
PublisherExcerpta Medica, Inc.. The Journal's web site is located at http://www.ajconline.org/
Citation
American Journal Of Cardiology, 2005, v. 96 n. 6, p. 760-763 How to Cite?
AbstractPrevious studies have shown that more complete platelet inhibition improves the coronary flow reserve (CFR), a measure of microvascular integrity, in patients undergoing percutaneous coronary intervention (PCI). We hypothesized that patients with aspirin resistance would have impaired CFR after elective PCI. We used VerifyNow Aspirin to determine the response to aspirin in 117 consecutive patients who underwent elective single-lesion PCI. The assay results are expressed quantitatively in Aspirin Reaction Units based on the degree of platelet aggregation. All patients received a 300-mg loading dose of clopidogrel >12 hours before and a 75-mg maintenance dose the morning of PCI. CFR was estimated using the Thrombolysis In Myocardial Infarction frame count method. Of the 117 patients, 22 (18.8%) were aspirin resistant. The clinical, angiographic, and procedural characteristics of the aspirin-sensitive and -resistant patients were balanced. All patients underwent successful PCI with <50% residual diameter stenosis and Thrombolysis In Myocardial Infarction grade 3 flow after PCI. Aspirin-resistant patients had a lower CFR than the aspirin-sensitive patients (1.42 ± 0.35 vs 1.80 ± 0.64, p = 0.018). Univariate correlates of CFR included the Aspirin Reaction Unit (r = -0.227, p = 0.014) and post-PCI creatine kinase-MB elevation (p = 0.048). Multivariate linear regression analysis revealed the Aspirin Reaction Unit to be the only independent determinant of CFR after PCI (r2 = 0.051, p = 0.014). Thus, aspirin resistance was associated with impaired CFR in patients who underwent elective PCI, implicating insufficient aspirin-induced platelet inhibition as a cause of microvascular dysfunction by distal atherothrombotic embolization and/or spasm. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78272
ISSN
2015 Impact Factor: 3.154
2015 SCImago Journal Rankings: 2.063
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, WHen_HK
dc.contributor.authorLee, PYen_HK
dc.contributor.authorNg, Wen_HK
dc.contributor.authorKwok, JYYen_HK
dc.contributor.authorCheng, Xen_HK
dc.contributor.authorLee, SWLen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLau, CPen_HK
dc.date.accessioned2010-09-06T07:41:03Z-
dc.date.available2010-09-06T07:41:03Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Cardiology, 2005, v. 96 n. 6, p. 760-763en_HK
dc.identifier.issn0002-9149en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78272-
dc.description.abstractPrevious studies have shown that more complete platelet inhibition improves the coronary flow reserve (CFR), a measure of microvascular integrity, in patients undergoing percutaneous coronary intervention (PCI). We hypothesized that patients with aspirin resistance would have impaired CFR after elective PCI. We used VerifyNow Aspirin to determine the response to aspirin in 117 consecutive patients who underwent elective single-lesion PCI. The assay results are expressed quantitatively in Aspirin Reaction Units based on the degree of platelet aggregation. All patients received a 300-mg loading dose of clopidogrel >12 hours before and a 75-mg maintenance dose the morning of PCI. CFR was estimated using the Thrombolysis In Myocardial Infarction frame count method. Of the 117 patients, 22 (18.8%) were aspirin resistant. The clinical, angiographic, and procedural characteristics of the aspirin-sensitive and -resistant patients were balanced. All patients underwent successful PCI with <50% residual diameter stenosis and Thrombolysis In Myocardial Infarction grade 3 flow after PCI. Aspirin-resistant patients had a lower CFR than the aspirin-sensitive patients (1.42 ± 0.35 vs 1.80 ± 0.64, p = 0.018). Univariate correlates of CFR included the Aspirin Reaction Unit (r = -0.227, p = 0.014) and post-PCI creatine kinase-MB elevation (p = 0.048). Multivariate linear regression analysis revealed the Aspirin Reaction Unit to be the only independent determinant of CFR after PCI (r2 = 0.051, p = 0.014). Thus, aspirin resistance was associated with impaired CFR in patients who underwent elective PCI, implicating insufficient aspirin-induced platelet inhibition as a cause of microvascular dysfunction by distal atherothrombotic embolization and/or spasm. © 2005 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherExcerpta Medica, Inc.. The Journal's web site is located at http://www.ajconline.org/en_HK
dc.relation.ispartofAmerican Journal of Cardiologyen_HK
dc.subject.meshAgeden_HK
dc.subject.meshAngioplasty, Balloon, Coronaryen_HK
dc.subject.meshAspirin - pharmacologyen_HK
dc.subject.meshCoronary Circulation - drug effectsen_HK
dc.subject.meshDrug Resistanceen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLinear Modelsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPlatelet Aggregation Inhibitors - pharmacologyen_HK
dc.subject.meshTiclopidine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshTreatment Outcomeen_HK
dc.titleRelation of aspirin resistance to coronary flow reserve in patients undergoing elective percutaneous coronary Interventionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9149&volume=96&issue=6&spage=760&epage=3&date=2005&atitle=Relation+of+aspirin+resistance+to+coronary+flow+reserve+in+patients+undergoing+elective+percutaneous+coronary+interventionen_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/j.amjcard.2005.04.056en_HK
dc.identifier.pmid16169354-
dc.identifier.scopuseid_2-s2.0-24944525789en_HK
dc.identifier.hkuros113797en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-24944525789&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume96en_HK
dc.identifier.issue6en_HK
dc.identifier.spage760en_HK
dc.identifier.epage763en_HK
dc.identifier.isiWOS:000232096700005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, WH=7409637978en_HK
dc.identifier.scopusauthoridLee, PY=8933949600en_HK
dc.identifier.scopusauthoridNg, W=7401613562en_HK
dc.identifier.scopusauthoridKwok, JYY=8933949800en_HK
dc.identifier.scopusauthoridCheng, X=37044433500en_HK
dc.identifier.scopusauthoridLee, SWL=23990967700en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK

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