title: Potential mechanisms of the acute coronary syndrome presentation in patients with the coronary slow flow phenomenon - insight from a plasma proteomic approach.
abstract: OBJECTIVE
  The coronary slow flow phenomenon [CSFP] is a coronary microvascular disorder, characterized by delayed distal vessel opacification despite the absence of obstructive coronary artery disease. Patients frequently present with an acute coronary syndrome [ACS] although the pathophysiological mechanisms responsible are unknown. The aim of this study was to identify potential mechanisms for the ACS presentation associated with the CSFP using a plasma proteomic profiling approach.
  
  
  RESULTS
  Plasma samples from nine CSFP subjects [56 ± 11years] were assayed for high sensitivity C-reactive protein [hsCRP], troponin T [TnT], creatine kinase [CK], and proteomic analyses (n=6), during an ACS presentation and one month later [chronic phase]. Proteomic analysis involved chromatographic depletion of 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 spectrometry and two differentially expressed proteins were selected for validation via Western blotting. During the ACS presentation, hsCRP was elevated [ACS=14.9 ± 3.9 mg/L vs chronic=4.23 ± 1.37 mg/L, p=0.05] but TnT and CK levels were unchanged. Proteomic analysis identified six proteins that were significantly different in abundance between the acute and chronic samples. During the ACS presentation there was a 1.6 ± 0.13 fold 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 by Western blotting [1.33 ± 0.17 OD acute/chronic ratio, p=0.05].
  
  
  CONCLUSIONS
  The findings from this novel detailed approach, implicate an inflammatory/oxidative stress process in the pathogenesis of the ACS presentation associated with the CSFP. Future studies should further elucidate these mechanisms.
authors.affiliation: Cardiology Unit, The Queen Elizabeth Hospital, Discipline of Medicine, University of Adelaide, South Australia, Australia.
authors.forename: Victoria A
authors.initials: VA
authors.lastname: Kopetz
authors.forename: Megan A S
authors.initials: MA
authors.lastname: Penno
authors.forename: Peter
authors.initials: P
authors.lastname: Hoffmann
authors.forename: David P
authors.initials: DP
authors.lastname: Wilson
authors.forename: John F
authors.initials: JF
authors.lastname: Beltrame
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000175:diagnosis* / Q000453:epidemiology; D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D054318:No-Reflow Phenomenon / Q000097:blood* / Q000175:diagnosis* / Q000453:epidemiology; D018384:Oxidative Stress; D011446:Prospective Studies; D040901:Proteomics / Q000379:methods*
chemical_list: D001798:Blood Proteins