Potential mechanisms of the acute coronary syndrome presentation in patients with the coronary slow flow phenomenon - Insight from a plasma proteomic approach
Date
2012
Authors
Kopetz, V.
Penno, M.
Hoffmann, P.
Wilson, D.
Beltrame, J.
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Journal article
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International Journal of Cardiology, 2012; 156(1):84-91
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Victoria A. Kopetz, Megan A.S. Penno, Peter Hoffmann, David P. Wilson and John F. Beltrame
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Abstract
Aims: The coronary slow flow phenomenon [CSFP] is a coronary microvascular disorder, characterized bydelayed distal vessel opacification despite the absence of obstructive coronary artery disease. Patients frequentlypresent with an acute coronary syndrome [ACS] although the pathophysiological mechanismsresponsible are unknown. The aim of this study was to identify potential mechanisms for the ACS presentationassociated with the CSFP using a plasma proteomic profiling approach.
Methods and results: Plasma samples from nine CSFP subjects [56± 11 years] were assayed for high sensitivityC-reactive protein [hsCRP], troponin T [TnT], creatine kinase [CK], and proteomic analyses (n= 6), duringan ACS presentation and one month later [chronic phase]. Proteomic analysis involved chromatographic depletionof abundant plasma proteins followed by two-dimensional differential gel electrophoresis [2-D DIGE].Protein spots demonstrating ±1.5-fold change relative to the control were identified by mass spectrometryand two differentially expressed proteins were selected for validation via Western blotting. During the ACSpresentation, hsCRP was elevated [ACS= 14.9± 3.9 mg/L vs chronic= 4.23± 1.37 mg/L, p= 0.05] but TnTand CK levels were unchanged. Proteomic analysis identified six proteins that were significantly differentin abundance between the acute and chronic samples. During the ACS presentation there was a 1.6± 0.13fold increase in the anti-oxidant enzyme paraoxonase-1 and an increase in inflammatory proteins alpha-1-antichymotrypsin [1.65± 0.13 fold] and alpha-1-antitrypsin [2.5± 0.34 fold]. The latter was confirmed byWestern blotting [1.33± 0.17 OD acute/chronic ratio, p= 0.05].
Conclusion: The findings from this novel detailed approach, implicate an inflammatory/oxidative stress processin the pathogenesis of the ACS presentation associated with the CSFP. Future studies should further elucidatethese mechanisms.
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© 2011 Elsevier Ireland Ltd. All rights reserved.