Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/7879
Title: Tissue plasminogen activator antigen predicts medium-term left ventricular end-systolic volume after acute myocardial infarction
Authors: Weir, R.A.
Balmain, S.
Steedman, T.
Ng, L.L.
Squire, I.B.
Rumley, A.
Dargie, H.J.
Lowe, G.D.
First Published: Aug-2009
Publisher: Springer Verlag
Citation: J Thromb Thrombolysis. DOI 10.1007/s11239-009-0383-6. Tissue plasminogen activator antigen predicts medium-term left ventricular end-systolic volume after acute myocardial infarction
Abstract: Von Willebrand factor (VWF) and tissue plasminogen activator (t-PA) predict adverse cardiovascular outcome following acute myocardial infarction (AMI) and are weakly associated with pre-discharge left ventricular ejection fraction (LVEF). We examined the relationships between VWF, t-PA antigen, matrix metalloproteinase (MMP)-2,-3, and -9, and B-type natriuretic peptide (BNP), and their predictive effect on serial change in LV volumes in a cohort of patients admitted with AMI. Plasma VWF, t-PA antigen, MMP-2,-3,-9, and BNP were measured at a mean 46 h after AMI in 100 patients (mean age 58.9 ± 12 years, 77% male) with depressed LVEF. Cardiac magnetic resonance (CMR) imaging was then performed. Biomarker measurement and CMR were repeated at 12 and 24 weeks. Plasma concentrations of VWF, BNP and MMP-9 were elevated while t-PA antigen concentration was at the upper limits of normal; over 24 weeks VWF, t-PA antigen, MMP-9 and BNP decreased significantly. Baseline VWF correlated with BNP (r = 0.35, P < 0.001) and MMP-3 (r = 0.24, P = 0.019) as did t-PA antigen (r = 0.27, P = 0.007 for BNP; r = 0.40, P < 0.001 for MMP-3). t-PA antigen, VWF, MMP-3 and BNP were univariate predictors of LV end-systolic volume at 24 weeks; tPA antigen and BNP remained significant independent predictors on multivariate analysis. t-PA antigen and VWF are related to medium-term LV volumes after AMI, and to MMP-3. This novel link between the coagulation-fibrinolysis system and matrix turnover merits further study in understanding the pathophysiology of adverse ventricular remodeling after AMI.
ISSN: 0929-5305 (Print)
1573-742X (Online)
Links: http://dx.doi.org/10.1007/s11239-009-0383-6
http://hdl.handle.net/2381/7879
Type: Article
Description: Metadata. Full text of this item is not currently available on the LRA.
Appears in Collections:Published Articles, Dept. of Cardiovascular Sciences

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