Potential mechanisms of the acute coronary syndrome presentation in patients with the coronary slow flow phenomenon ?Insight from a plasma proteomic approach

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• 作者：Victoria A. Kopetz^a ; Megan A.S. Penno^b ; Peter Hoffmann^b ; David P. Wilson^c ; John F. Beltrame^a ; ^{john.beltrame@adelaide.edu.au}
• 关键词：CSFP ; coronary slow flow phenomenon ; 2D-DIGE ; two-dimensional difference gel electrophoresis ; ACS ; acute coronary syndrome ; TnT ; troponin T ; CK ; creatine kinase ; hsCRP ; high-sensitivity C-reactive protein ; AAT ; alpha-1 anti-trypsin ; ACT ; alpha-1 anti-chym
• 刊名：International Journal of Cardiology
• 出版年：2012
• 出版时间：5 April, 2012
• 年：2012
• 卷：156
• 期：1
• 页码：84-91
• 全文大小：689 K

文摘

Aims

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.

Methods and results

Plasma samples from nine CSFP subjects [56 ¡À 11 years] 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 ¡À 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 ¡À 3.9 mg/L vs chronic = 4.23 ¡À 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 ¡À 0.13 fold increase in the anti-oxidant enzyme paraoxonase-1 and an increase in inflammatory proteins alpha-1-antichymotrypsin [1.65 ¡À 0.13 fold] and alpha-1-antitrypsin [2.5 ¡À 0.34 fold]. The latter was confirmed by Western blotting [1.33 ¡À 0.17 OD acute/chronic ratio, p = 0.05].

Conclusion

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.