Abstract
Matrix metalloproteinase 9 (MMP9) is functionally implicated in the process of infarct healing. Several genetic variation of the MMP9 gene have been described, among which the MMP9 Arg668Gln polymorphism. In the present study, we assessed whether this polymorphism influences outcome after acute myocardial infarction (MI). One thousand forty-nine patients undergoing coronary angiography were genotyped for the MMP9 Arg668Gln polymorphism by TaqMan allelic discrimination assay. This population included 154 controls, 161 patients with non ST-elevation MI (NSTEMI), 504 patients with ST-elevation MI (STEMI), and 230 patients with angina. Frequency of the MMP9 Arg668Gln polymorphism in the global population was 25.1%, and was comparable between all groups. STEMI patients had higher creatine phosphokinase (CPK), troponin T (TnT) and MMP9 plasma levels and had lower ejection fraction (EF) than NSTEMI patients. However, the polymorphism was not associated with infarct severity as determined by peak CPK and TnT levels, nor with LV remodeling and outcome as assessed by 1-month EF and NYHA class, as well as 2- year mortality. In silico molecular modeling simulations predicted that the MMP9 polymorphism may decrease MMP9 activity, but this could not be verified by plasma determinations. This study investigated for the first time the association between the MMP9 Arg668Gln polymorphism and clinical outcome after acute MI. Our results indicate that the polymorphism does not seem to be associated with clinical outcome and in particular with the development of left ventricular dysfunction and heart failure.
Highlights
Left ventricular (LV) remodeling following myocardial infarction (MI), culminating in the development of heart failureFrancisco Azuaje,[1] Yvan Devaux,[1] Daniel R
Wagner[1,3] (HF), is a complex phenomenon involving sev- Key words: matrix metalloproteinase 9, myocardial eral biological processes such as the turnover infarction, polymorphism, ventricular function
Performed conforming to the Helsinki molecular dynamics, by means of an equilibra- We investigated whether the frequencies of Declaration and approved by the local ethics tion phase of 2.1 ns rising temperature from 0 MMP9 polymorphism differed between concommittee
Summary
Left ventricular (LV) remodeling following myocardial infarction (MI), culminating in the development of heart failure. Francisco Azuaje,[1] Yvan Devaux,[1] Daniel R. Wagner[1,3]. (HF), is a complex phenomenon involving sev- Key words: matrix metalloproteinase 9, myocardial eral biological processes such as the turnover infarction, polymorphism, ventricular function. Of the extracellular matrix (ECM) and inflam-
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