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CLINICAL STUDIES

Immune system activation follows inflammation in unstable angina: pathogenetic implications

^a Department of Cardiology, Catholic University, Rome, Italy

Manuscript received December 23, 1997; revised manuscript received June 22, 1998, accepted July 9, 1998.

Address for correspondence: Dr. Giuseppina Caligiuri, CMM L8:03, Cardiovascular Research Unit, Karolinska Hospital, 171 76 Stockholm, Sweden
giuseppina.caligiuri{at}cmm.ki.se

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.

Abbreviations and Acronyms   Cp = Chlamydia pneumoniae   CRP = C-reactive protein   CSA = chronic stable angina   IL = interleukin   UA = unstable angina

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