Abstract

Myocardial infarction (MI) is a leading cause of the development of congestive heart failure, which results from progressive remodeling of the left ventricle (LV). Understanding the transition from physiological wound healing to adverse LV remodeling may help to identify at an earlier stage those post-MI patients who are most likely to develop heart failure. Accordingly, the purpose of this study was to evaluate post-MI plasma samples for potential candidate markers of adverse remodeling. Plasma samples from unoperated male C57BL/6J mice (n=6) and 7 day post-MI male C57BL/6J mice (n=6) were evaluated using multi-analyte profile testing to perform quantitative immunoassays on 67 antigens. Infarct size was 47±5% for the MI group. LV mass to body weight ratio increased from 3.23±0.04 mg/g in the unoperated group to 4.26±0.29 mg/g in the MI group (p<0.01). Of the 67 antigens evaluated, four analytes were significantly elevated in the MI samples. Monocyte chemotactic protein-1 (MCP-1) doubled from 77±6 pg/mL in control plasma to 149±25 pg/mL in MI plasma (p=0.018). Matrix metalloproteinase-9 (MMP-9) increased from 39±2 ng/mL in control plasma to 48±3 ng/mL in MI plasma (p=0.045). Myoglobin increased from 46±7 ng/mL in control plasma to 167±53 ng/mL in MI plasma (p=0.035). Levels of von Willebrand factor (vWF) increased from 523±62 ng/mL in control plasma to 775±37 ng/mL in MI plasma (p<0.01). All four of these factors have been previously associated with MI and/or myocardial injury. The pattern of sustained elevation of MCP-1, MMP-9, myoglobin, and vWF at 7 days post-MI suggests that these factors may play a role in continued adverse remodeling. In conclusion, multi-analyte profiling of post-MI samples allows the rapid evaluation of multiple factors to determine which factors may be predictive and/or causative of adverse LV remodeling.

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