The utility of C4d, C9, and troponin T immunohistochemistry in acute myocardial infarction.

Published

Journal Article

CONTEXT: Full activation and involvement of the complement pathway follows acute myocardial infarction. Complement fragment C4d is a stable, covalently bound marker of complement activation. Troponin T is specific for cardiomyocytes. OBJECTIVES: To determine the specificity of C4d, C9, and troponin T immunoreactivity in necrotic myocytes and to establish whether they can be used to delineate acute myocardial infarction. DESIGN: Twenty-six autopsy cases with a total of 54 myocardium areas of infarction were reviewed retrospectively. Immunohistochemistry for C4d, C9, and troponin T was used on paraffin sections of formalin-fixed tissue. Controls consisted of 5 cases without evidence of infarction, and histologically normal myocardium functioned as an internal control. RESULTS: C4d and C9 antibodies reacted strongly and diffusely with necrotic myocytes in all samples of infarctions for up to 2 days (19 of 19; 100%). Adjacent histologically normal myocytes were nonreactive, resulting in a clear delineation between damaged and viable myocardium. Reactivity declined with increased duration and was absent in scars. Troponin T showed loss of staining in preinflammatory lesions (8 of 13; 62%); however, nonspecific patchy loss of staining was present in negative controls and in viable myocardium. Immunostains provided new diagnoses in 2 cases, including evidence of reinfarction and a newly diagnosed acute myocardial infarction. CONCLUSIONS: C4d and C9 have comparable reactivity and specificity for necrotic myocytes. C4d and C9 staining of necrotic myocytes is apparent before the influx of inflammatory cells, demonstrating utility in early myocardial infarction. Patchy loss of Troponin T in some cases of histologically normal myocardium limited its usefulness as a sole marker of infarction.

Full Text

Duke Authors

Cited Authors

  • Jenkins, CP; Cardona, DM; Bowers, JN; Oliai, BR; Allan, RW; Normann, SJ

Published Date

  • February 2010

Published In

Volume / Issue

  • 134 / 2

Start / End Page

  • 256 - 263

PubMed ID

  • 20121615

Pubmed Central ID

  • 20121615

Electronic International Standard Serial Number (EISSN)

  • 1543-2165

Digital Object Identifier (DOI)

  • 10.1043/1543-2165-134.2.256

Language

  • eng

Conference Location

  • United States