CD4+CD28− lymphocytes and cerebral ischaemic stroke. Part II: CD4+CD28− lymphocytes and carotid artery atherosclerotic plaque characteristics

Abstract

Background and purpose

CD4+CD28− lymphocytes can directly contribute to the instability of atherosclerotic plaque. This paper attempts to answer the question of the potential influence of the CD4+CD28− lymphocyte population on the ultrasound image of atherosclerotic plaque in the common carotid artery (CCA) wall.

Material and methods

The study involved a group of 109 patients, aged 45 to 65 years, including 42 patients with first-ever ischaemic stroke, experiencing symptoms resulting from disturbances of the anterior area of cerebral circulation, arterial hypertension and/or type 2 diabetes mellitus (group 1). Group 2 consisted of 34 patients with mentioned risk factors, without ischaemic stroke. The control group comprised 33 healthy individuals. The percentage of CD4+CD28− lymphocytes was assessed with flow cytometry.

Results

A significant difference in the incidence of heterogeneous plaques was noted between groups 1 and 3 (p = = 0.0023) as well as between group 2 and 3 (p = 0.0005), whereas groups 1 and 2 did not differ from each other. The proportion of CD4+CD28− lymphocytes was similar in groups 1 and 2 (p = 0.97), but it differed between groups 1 and 3 (p < 0.0001) and between groups 2 and 3 (p < 0.001). A correlation was found between the proportion of CD4+CD28− lymphocytes in the blood and the number of CCA atherosclerotic plaques (Rs = 0.191, p = 0.046). The proportion of CD4+CD28− lymphocytes in peripheral blood did not correlate with the ultrasound types of atherosclerotic plaques. No correlation between the proportion of CD4+CD28− lymphocytes and the area of atherosclerotic plaques was found.

Conclusions

The correlation between the proportion of CD4+CD28− lymphocytes and the number of atherosclerotic plaques within the CCA suggests that the cells are involved in the mechanism of carotid plaque formation. There is no proof of the involvement of the above-mentioned cells in the mechanism of plaque destabilization in those arteries.