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Monocyte chemoattractant protein-1: A dichotomous role in cardiac remodeling following acute myocardial infarction in man?

Authors :
Weir, Robin A.P.
Murphy, Charles Aengus
Petrie, Colin J.
Martin, Thomas N.
Clements, Suzanne
Steedman, Tracey
Wagner, Galen S.
McMurray, John J.V.
Dargie, Henry J.
Source :
Cytokine. May2010, Vol. 50 Issue 2, p158-162. 5p.
Publication Year :
2010

Abstract

Abstract: Introduction: Monocyte chemoattractant protein-1 (MCP-1) is elevated after acute myocardial infarction (AMI), and potentiates left ventricular (LV) remodeling in murine models of AMI. We examined the relationships between serum MCP-1, change in LV function and biomarkers related to remodeling in a cohort of AMI patients. Methods: Serum MCP-1 concentrations were measured in 100 patients (age 58.9±12.0years, 77% male) admitted with AMI and LV dysfunction, at baseline (mean 46h), 12 and 24weeks; cardiac magnetic resonance imaging and measurement of matrix metalloproteinase-2 (MMP-2), MMP-3 and MMP-9 occurred at each time-point. Results: MCP-1 increased significantly from 697 [483, 997]pg/mL at baseline to 878 [678, 1130]pg/mL at 24weeks (p <0.001). MMP-3 concentration increased while MMP-9 decreased significantly over time; MMP-2 concentration did not change significantly. Baseline MCP-1 correlated with change in (Δ) LV end-systolic volume index (ΔLVESVI; r =-0.48, p =0.01) and with ΔLV ejection fraction (ΔLVEF; r =0.50, p =0.02). However, ΔMCP-1 correlated positively with ΔLVESVI (r =0.40, p =0.006) and negatively with ΔLVEF (r =−0.36, p =0.004). MCP-1 had no relationship with any MMP. Conclusions: MCP-1 may have a dichotomous role following AMI, aiding early infarct healing but potentiating later remodeling, which merits further study before any therapeutic trials of MCP-1 modulation in humans. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
10434666
Volume :
50
Issue :
2
Database :
Academic Search Index
Journal :
Cytokine
Publication Type :
Academic Journal
Accession number :
49123565
Full Text :
https://doi.org/10.1016/j.cyto.2010.02.020