Abstract

Both experimental and pathological studies suggest that immune response and inflammation may play an important role in the pathogenesis of coronary spasm. To elucidate the role of systemic immune and inflammatory responses in the pathogenesis of coronary spasm, we studied circulating T-lymphocyte activation in variant angina patients (VAPs), stable effort angina patients (EAPs) and in control participants. Twenty documented VAPs, 13 EAPs and 20 control participants were studied. To evaluate T-lymphocyte activation, T-lymphocyte surface antigen expression, including CD3, CD4, CD8 and HLA-DR, was measured by two-colour flow cytometric analysis. Serum-soluble interleukin-2 receptor (sIL-2R) and C-reactive protein (CRP) were also measured by enzyme-linked immunosorbent assay. We restudied 10 of the VAPs to investigate the relationship between the disease activity of variant angina and T-lymphocyte activation. The percentage of CD3+/DR+ T-lymphocytes in VAPs (14.8%) was significantly higher than in EAPs (10.7%, P < 0.05) and control participants (9.7%, P < 0.005); however, levels of sIL-2R were the same among the three groups. Levels of CRP were within normal range in all VAPs. The percentage of CD8+/DR+ T-lymphocytes was significantly higher in VAPs (9.5%, P < 0.005) than in EAPs (5.5%) and control participants (5.9%), whereas the percentage of CD4+/DR+ T-lymphocytes was similar among the three groups. The percentage of activated T-lymphocytes in VAPs was unchanged during the follow-up period (mean intervals, 10 months). These results indicate that the chronic activation of T-lymphocytes, especially CD8+ T-lymphocytes, may be involved in the pathogenesis of coronary spasm.

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