© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Upregulation of ICAM-1 on cardiomyocytes in jeopardized human myocardium during infarction
aDepartment of Pathology, Free University Hospital, De Boelelaan 1117, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands
bDepartment of Cardiology, Free University Hospital, De Boelelaan 1117, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands
cDepartment of Internal Medicine, Free University Hospital, De Boelelaan 1117, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands
dCentral Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands
* Corresponding author. Tel.: +31-20-444-4028; Fax: +31-20-44402964; E-mail:pathol@azvu.nl
Objective: Impaired perfusion of the myocardium induces a local inflammatory response. In animal models, there is ample evidence that polymorphonuclear leucocytes (PMNs) infiltrating infarcted myocardium contribute significantly to infarct size. Methods: To explore a possible role for PMNs in the tissue damage of human myocardial infarction, we investigated localization of intercellular adhesion molecule-1 (ICAM-1) and CD66b (previously clustered as CD67), a marker of degranulation of human PMNs, in relation to deposition of complement in tissue specimens of infarcted and healthy parts of the heart obtained from 20 patients, who had died following acute myocardial infarction. Results: ICAM-1 was transiently expressed by endothelium and for a longer period (few days) on myofibers of infarcted myocardium. This expression only occurred in parts that stained positive for complement. PMN infiltration exclusively occurred in areas with ICAM-1 expression, but not every ICAM-1-positive area contained PMN infiltrates. CD66b was found in PMNs but was also fixed to the plasma membrane of myofibers that stained positive for complement and ICAM-1. Conclusion: These findings indicate that, in infarcted human myocardium, PMNs are degranulated, possibly upon interaction with ICAM-1 and activated complement.
KEYWORDS Infarction; Complement activation; Inflammation; Leukocytes; Human
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