Upregulation of ICAM-1 on cardiomyocytes in jeopardized human myocardium during infarction

Objective: Impaired perfusion of the myocardium induces a local inflammator y response. In animal models, there is ample evidence that polymorphonuclea r leucocytes (PMNs) infiltrating infarcted myocardium contribute significan tly to infarct size. Methods: To explore a possible role for PMNs in the ti ssue 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 depositi on of complement in tissue specimens of infarcted and healthy parts of the heart obtained from 20 patients, who had died following acute myocardial in farction. Results: ICAM-1 was transiently expressed by endothelium and for a longer period (few days) on myofibers of infarcted myocardium. This expre ssion only occurred in parts that stained positive for complement. PMN infi ltration exclusively occurred in areas with ICAM-1 expression, but not ever y ICAM-1-positive area contained PMN infiltrates. CD66b was found in PMNs b ut was also fixed to the plasma membrane of myofibers that stained positive for complement and ICAM-1. Conclusion: These findings indicate that, in in farcted human myocardium, PMNs are degranulated, possibly upon interaction with ICAM-I and activated complement. (C) 1999 Elsevier Science B.V. All ri ghts reserved.