Neutrophils in human myocardial infarction with rupture of the free wall.
BACKGROUND
Experimental studies have shown that neutrophils might play an important role in the pathogenesis of ischemic and reperfusion injury in myocardial infarction (MI). Our aim was to compare histologic characteristics of MI with and without rupture of the free wall (RFW), with emphasis on the density of interstitial neutrophil infiltration.


METHODS
Autopsy samples of infarcted heart tissue from 110 patients with MI (50 with and 60 without RFW) were included. On the basis of histologic changes and clinical data, all cases were divided into three groups according to the duration of MI (<or=1 day, 1--7 days, and 1--4 weeks). Neutrophils were stained immunohistochemically with antibodies against CD 15. The intensity of interstitial neutrophil infiltration was determined on the basis of percentage of the infiltrated myocardial area using an image analysis system.


RESULTS
In MI that were less than 1 day or more than 7 days old, we did not observe any differences in histologic characteristics between cases with and those without RFW. In MI that were more than 1 day and less than 7 days old, we observed a significantly more intensive interstitial neutrophil infiltration in cases with RFW than in those without RFW. However, there were no significant differences in neutrophil infiltration between patients who received reperfusion treatment and those who did not.


CONCLUSIONS
Our results suggest that intensive interstitial neutrophil infiltration in human MI might increase the risk of the RFW between the 2nd and the 7th days when the density of neutrophil infiltration is believed to reach a peak. We failed to confirm the hypothesis based on experimental studies that reperfusion treatment contributes significantly to the density of neutrophil infiltration.
Zidar
Nina
N
Institute of Pathology, Medical Faculty, 1000 Ljubljana, Slovenia. nina.zidar@mf.uni-lj.si
Jeruc
Jera
J
Balazic
Joze
J
Stajer
Dusan
D
D000368:Aged; D005260:Female; D006342:Heart Rupture, Post-Infarction / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D016256:Lewis X Antigen / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000276:immunology* / Q000473:pathology; D020556:Neutrophil Infiltration / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology
D016256:Lewis X Antigen