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https://hdl.handle.net/2440/99633
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dc.contributor.author | Procter, N. | - |
dc.contributor.author | Ball, J. | - |
dc.contributor.author | Ngo, D. | - |
dc.contributor.author | Chirkov, Y. | - |
dc.contributor.author | Isenberg, J. | - |
dc.contributor.author | Hylek, E. | - |
dc.contributor.author | Stewart, S. | - |
dc.contributor.author | Horowitz, J. | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | Herz: Cardiovascular Diseases, 2016; 41(1):57-62 | - |
dc.identifier.issn | 0340-9937 | - |
dc.identifier.issn | 1615-6692 | - |
dc.identifier.uri | http://hdl.handle.net/2440/99633 | - |
dc.description.abstract | Objective: Atrial fibrillation (AF) is a condition where platelet hyperaggregability is commonly present. We examined potential physiological bases for platelet hyperaggregability in a cohort of patients with acute and chronic AF. In particular, we sought to identify the impact of inflammation [myeloperoxidase (MPO) and C-reactive protein (CRP)] and impaired nitric oxide (NO) signaling. Methods: Clinical and biochemical determinants of adenosine diphosphate (ADP)-induced platelet aggregation were sought in patients (n = 106) hospitalized with AF via univariate and multivariate analysis. Results: Hyper-responsiveness of platelets to ADP was directly (r = 0.254, p < 0.01) correlated with plasma concentrations of thrombospondin-1 (TSP-1), a matricellular protein that impairs NO responses and contributes to development of oxidative stress. In turn, plasma TSP-1 concentrations were directly correlated with MPO concentrations (r = 0.221, p < 0.05), while MPO concentrations correlated with those of asymmetric dimethylarginine (ADMA, r = 0.220, p < 0.05), and its structural isomer symmetric dimethylarginine (SDMA, r = 0.192, p = 0.05). Multivariate analysis identified TSP-1 (β = 0.276, p < 0.05) concentrations, as well as female sex (β = 0.199, p < 0.05), as direct correlates of platelet aggregability, and SDMA concentrations (β = − 0.292, p < 0.05) as an inverse correlate. Conclusion: We conclude that platelet hyperaggregability, where present in the context of AF, may be engendered by impaired availability of NO, as well as via MPO-related inflammatory activation. | - |
dc.description.statementofresponsibility | Nathan E.K. Procter, Jocasta Ball, Doan T.M. Ngo, Yuliy Y. Chirkov, Jeffrey S. Isenberg, Elaine M. Hylek, Simon Stewart, John D. Horowitz | - |
dc.language.iso | en | - |
dc.publisher | Urban & Vogel | - |
dc.rights | © Urban & Vogel 2015 | - |
dc.source.uri | http://dx.doi.org/10.1007/s00059-015-4335-y | - |
dc.subject | Atrial fibrillation | - |
dc.subject | thrombospondin-1 | - |
dc.subject | myeloperoxidase | - |
dc.subject | asymmetric dimethylarginine | - |
dc.subject | platelet aggregation | - |
dc.title | Platelet hyperaggregability in patients with atrial fibrillation: Evidence of a background proinflammatory milieu | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1007/s00059-015-4335-y | - |
dc.relation.grant | NHMRC | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Stewart, S. [0000-0001-9032-8998] | - |
dc.identifier.orcid | Horowitz, J. [0000-0001-6883-0703] | - |
Appears in Collections: | Aurora harvest 7 Medicine publications |
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