Circulating Stromelysin‐1 (MMP‐3): A novel predictor of LV dysfunction, remodelling and all‐cause mortality after acute myocardial infarction

Changes to cardiac matrix are central to ventricular remodelling after acute MI and matrix metalloproteinase expression is implicated in this process. We investigated the temporal profile of MMP‐3 and its relationship to LV dysfunction and prognosis following AMI.

[1]  E. Ohlstein,et al.  Matrix metalloproteinase expression in cardiac myocytes following myocardial infarction in the rabbit. , 2001, Life sciences.

[2]  P. Libby,et al.  Matrix metalloproteinase inhibition attenuates early left ventricular enlargement after experimental myocardial infarction in mice. , 1999, Circulation.

[3]  P. Amouyel,et al.  Prognostic impact of matrix metalloproteinase gene polymorphisms in patients with heart failure according to the aetiology of left ventricular systolic dysfunction. , 2003, European heart journal.

[4]  A. Hamsten,et al.  Lower serum concentration of matrix metalloproteinase‐3 in the acute stage of myocardial infarction , 2006, Journal of internal medicine.

[5]  N. Doll,et al.  Regression of Left Ventricular Hypertrophy After Surgical Therapy for Aortic Stenosis Is Associated With Changes in Extracellular Matrix Gene Expression , 2001, Circulation.

[6]  R M Whitlock,et al.  Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. , 1987, Circulation.

[7]  N. Ozdemir,et al.  Contribution of plasma matrix metalloproteinases to development of left ventricular hypertrophy and diastolic dysfunction in hypertensive subjects. , 2006, The Tohoku journal of experimental medicine.

[8]  Leslie L. Clark,et al.  Specific Temporal Profile of Matrix Metalloproteinase Release Occurs in Patients After Myocardial Infarction: Relation to Left Ventricular Remodeling , 2006, Circulation.

[9]  M. Pfeffer,et al.  Ventricular Remodeling After Myocardial Infarction: Experimental Observations and Clinical Implications , 1990, Circulation.

[10]  G. Keren,et al.  Circulating matrix metalloproteinase-2 but not matrix metalloproteinase-3, matrix metalloproteinase-9, or tissue inhibitor of metalloproteinase-1 predicts outcome in patients with congestive heart failure. , 2005, American heart journal.

[11]  Leong L Ng,et al.  Plasma matrix metalloproteinase-9 and left ventricular remodelling after acute myocardial infarction in man: a prospective cohort study. , 2007, European heart journal.

[12]  E. Maltezos,et al.  Comparison of levels of matrix metalloproteinase-2 and -3 in patients with ischemic cardiomyopathy versus nonischemic cardiomyopathy. , 2005, The American journal of cardiology.

[13]  V. Regitz-Zagrosek,et al.  Regulation of matrix metalloproteinases and their inhibitors in the left ventricular myocardium of patients with aortic stenosis , 2004, Journal of Molecular Medicine.

[14]  F. Spinale,et al.  Time-dependent changes in matrix metalloproteinase activity and expression during the progression of congestive heart failure: relation to ventricular and myocyte function. , 1998, Circulation research.

[15]  Mario J. Garcia,et al.  Effects of selective matrix metalloproteinase inhibitor (PG-116800) to prevent ventricular remodeling after myocardial infarction: results of the PREMIER (Prevention of Myocardial Infarction Early Remodeling) trial. , 2006, Journal of the American College of Cardiology.

[16]  Richard T. Lee,et al.  Selective Matrix Metalloproteinase Inhibition Reduces Left Ventricular Remodeling but Does Not Inhibit Angiogenesis After Myocardial Infarction , 2002, Circulation.

[17]  G. Gibson,et al.  Differential expression of MMPs and TIMPs in moderate and severe heart failure in a transgenic model. , 2006, Journal of cardiac failure.

[18]  M. Zile,et al.  Matrix metalloproteinase inhibition during the development of congestive heart failure : effects on left ventricular dimensions and function. , 1999, Circulation research.

[19]  P. Libby,et al.  Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. , 2000, The Journal of clinical investigation.

[20]  Leong L Ng,et al.  Plasma MMP-9 and MMP-2 following acute myocardial infarction in man: correlation with echocardiographic and neurohumoral parameters of left ventricular dysfunction. , 2004, Journal of cardiac failure.