Clinical Chemistry
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Clinical Chemistry 43: 990-995, 1997;
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(Clinical Chemistry. 1997;43:990-995.)
© 1997 American Association for Clinical Chemistry, Inc.

Articles

Cardiac troponin I and T alterations in hearts with severe left ventricular remodeling

Vincent Ricchiuti1, Jianyi Zhang2 and Fred S. Apple1,a

1 Departments of Laboratory Medicine and Pathology and
2 Medicine, Hennepin County Medical Center and the University of Minnesota, Minneapolis, MN 55415.
a Author for correspondence, at: Hennepin County Medical Center, Clinical Labs MC 812, 701 Park Ave., Minneapolis, MN 55415. Fax 612-904-4229; e-mail fred.apple{at}co.hennepin.mn.us

Cardiac troponin T (cTnT) and troponin I (cTnI) have been suggested as new, more specific markers of myocardial cellular damage. The objective of this study was to examine how the distributions of cTnI and cTnT were affected in postinfarction left ventricular remodeled (LVR) myocardium. At 2 months postinfarct in a porcine heart failure model, both Western blot and biochemical assay analyses were performed on left ventricular myocardium remote from the infarct zone in ligation animals (n = 8). Results were compared with data from the left ventricular myocardium from similar sized healthy (control) pigs (n = 7). Autoradiograms from Western blot analysis showed that the protein mass for cTnI and cTnT in LVR hearts decreased 80% (P <0.001) and 40% (P <0.02), respectively, when compared with nondiseased tissue. Similarly, the concentrations for cTnI and cTnT in LVR hearts decreased 42% (P <0.05) and 70% (P <0.001), respectively, compared with nondiseased normal tissue. The clinical assumption is that the appearance of cTnI and cTnT in the blood is proportional to chronic loss of cTnI and cTnT from injured myocardium associated with left ventricular remodeling.


Key Words: indexing terms: heart disorders • animal models of disease • Western blot analysis • immunoassays




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