antibodies against myc-associated zinc finger protein: an independent marker in acute coronary syndrome?

antibodies against myc-associated zinc finger protein: an independent marker in acute coronary syndrome?

;Diana Ernst;Christian Widera;Niklas T. Baerlecken;Wolfgang Schlumberger;Cornelia Daehnrich;Reinhold E. Schmidt;Katja Gabrysch;Lars Wallentin;Torsten Witte
sudebno-meditsinskaia ekspertiza 2017 Vol. 8 pp. -
141
ernst2017frontiersantibodies

Abstract

IntroductionAtherosclerosis is considered the pathophysiology underlying cardiovascular (CVD), cerebrovascular, and peripheral vascular diseases. Evidence supporting an autoimmune component is emerging, with imaging studies correlating MYC-associated zinc finger protein antibody (MAZ-Ab) optical density (OD) with plaque activity. This study compares MAZ-Ab OD on ELISA testing among patients presenting with acute coronary syndromes (ACSs) to healthy controls and investigates the association of MAZ-Ab to traditional CVD risk factors.MethodsPatients admitted with ACSs between August 2007 and July 2011 were included. Serum samples taken at presentation were retrospectively tested for MAZ-Ab and compared with serum from healthy volunteers with no CVD risk factors. Large-scale assessment of post-ACS prognostic relevance was performed using the established PLATO cohort.ResultsIn total 174 ACS patients and 96 controls were included. Among ACS patients, median MAZ-Ab OD was higher compared with controls (0.46 vs. 0.27; p = 0.001). Although the majority of ACS patients (116/174; 67%) had suffered from a ST-elevation myocardial infarction, no significant differences in MAZ-Ab titers were evident between ACS subtypes (p = 0.682). No associations between MAZ-Ab OD and conventional CVD risk factors were identified. Large-scale testing revealed no prognostic stratification regarding reinfarction (OR 1.04 [95% CI: 0.94–1.16]; p = 0.436).ConclusionMAZ-Ab OD was higher or all ACS phenotypes compared with controls. Given current understanding of MAZ-Ab function, these findings support an autoimmune component to CVD independent of conventional risk factors and indeed the extent of end-organ damage.

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238805
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10.3389/fimmu.2017.01595
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