• J. Card. Fail. · Mar 2005

    Plasma monitoring of the myocardial specific tissue inhibitor of metalloproteinase-4 after alcohol septal ablation in hypertrophic obstructive cardiomyopathy.

    • Robert E Stroud, Anne M Deschamps, Abigail S Lowry, Amy E Hardin, Rupak Mukherjee, Merry L Lindsey, Sammanda Ramamoorthy, Michael R Zile, William H Spencer, and Francis G Spinale.
    • Division of Cardiothoracic Surgery Medical University of South Carolina, Charleston, South Carolina 29403, USA.
    • J. Card. Fail. 2005 Mar 1; 11 (2): 124-30.

    BackgroundThe overall goal of this study was to develop an assay procedure for measuring the relative abundance of tissue inhibitor of metalloproteinase (TIMP)-4 in plasma, and then use this approach to determine dynamic changes of TIMP-4 levels in hypertrophic obstructive cardiomyopathic (HOCM) patients after an acute myocardial infarction (MI). Matrix metalloproteinases (MMPs) contribute to tissue remodeling and are regulated by the endogenous TIMPs. TIMP-4 is observed to be expressed in higher abundance in the myocardium when compared with other types of tissues. Recent clinical studies have measured changes in TIMP-4 levels; however, these studies have been limited to measuring this protein from myocardial tissue samples. To date, no studies have monitored TIMP-4 levels in plasma samples.Methods And ResultsPlasma TIMP-4 levels were examined (by semiquantitative immunoblotting) in normal (n=18) and HOCM (n=16) patients after alcohol-induced MI. Serial measurements of plasma TIMP-4 levels were examined up to 60 hours after alcohol-induced MI in patients with HOCM. Unglycosylated plasma TIMP-4 levels increased 250% in the HOCM patients when compared with normal controls. Total plasma TIMP-4 levels decreased by 20% at 30 hours after alcohol-induced MI.ConclusionsThe unique results demonstrated that an induction of a controlled MI, specifically through alcohol ablation, caused a reduction in plasma TIMP-4 levels in HOCM patients after alcohol-induced MI that would facilitate myocardial remodeling in the early post-MI setting.

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