Immune system activation follows inflammation in unstable angina: Pathogenetic implications

Objectives. The aim of this study was to assess the relations between inflammation, specific immune response and clinical course in unstable angina (UA), Background. Several studies suggest that either inflammation and/or T-cell activation might have a pathogenetic role in UA, but neither their potential reciprocal connection nor their relation to the clinical course is known. Methods. Serum levels of C-reactive protein (CRP) (inflammation), IgG, IgA, IgM, C3, C4 (humoral immunity), IL-2 and the percentage of CD4+, CD8+ and CD3+/DR+ T-cells (cell-mediated immunity) were measured in 35 patients with UA and 35 patients with chronic stable angina (CSA) during a period of 6 months. Results. The CRP levels and the main specific immune markers (CD4+ and CD3+/DR+ cells, IL-2 and IgM) were higher in unstable than in stable angina. In UA, the serum levels of IgM and IL-2 and the percentage of double positive CD3+/DR+ significantly increased at 7 to 15 days, and returned to baseline at 6 months. The increment of circulating activated T cells (CD3+/DR+) in UA was inversely related to the admission levels of CRP (r = -0.63, p = 0.003) and associated with a better outcome. Conclusions. Our data suggest that the inflammatory component systemically detectable in UA may be antigen-related and that the magnitude of the immune response correlates with the clinical outcome of instability. (C) 1998 by the American College of Cardiology.