Please click here to obtain permission to reproduce this image.
Click on image to view larger version.
Figure 2 Distribution of inflammatory cells in the coronary plaques (data are presented as means ± standard error of the mean). (A) Inflammatory cells in the acute myocardial infarction (AMI) group were significantly higher than those in the chronic stable angina (SA) and control (CTRL) groups, independently of the type of plaque observed (statistical analysis: A vs. B: p = 0.001; A vs. C: p = 0.001; B vs. C: p = not significant). (B) In the AMI group, no significant difference was observed between infarct-related coronary arteries (IRAs) and non-IRAs, independently of the type of plaque observed. (C) Both culprit and vulnerable plaques in the AMI group showed significantly more inflammatory infiltrates, compared with those observed in the stable plaques of the same group of patients (A vs. C: p = 0.006; B vs. C: p = 0.04). No statistically significant differences were observed between culprit and vulnerable plaques (p = 0.21). However, stable plaques in AMI patients had three-fold greater inflammation than stable and vulnerable coronary plaques of SA patients, and about four-fold of that measured in CTRL patients (C vs. D: p = 0.001; C vs. E: p = 0.001). (D) Immunohistochemical characterization of the various cytotypes in the coronary plaques. Significantly fewer CD68- and CD3-positive cells were found in stable and vulnerable plaques from SA and CTRL groups compared with those from AMI patients (AMI vs. SA and CTRL: actin p = 0.01; CD68: p = 0.01; CD3: p = 0.01).
|
