4.3 Article

Neutrophils in human myocardial infarction with rupture of the free wall

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CARDIOVASCULAR PATHOLOGY
卷 14, 期 5, 页码 247-250

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ELSEVIER SCIENCE INC
DOI: 10.1016/j.carpath.2005.04.002

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myocardial infarction; heart rupture; histology; neutrophils; pathogenesis

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Introduction: Experimental studies have shown that neutrophils might play an important role in the pathogenesis of ischemic and reperfusion injury in myocardial infarction (NIT). 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 (<= day, 1-7 days, and 1-4 weeks). Neutrophils were stained immumohistochemically with antibodies against CD15. 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 I 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 neutropbil 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. (c) 2005 Elsevier Inc. All rights reserved.

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