Basic Research in Cardiology

, Volume 104, Issue 3, pp 341–351

Beta2-integrin activation on T cell subsets is an independent prognostic factor in unstable angina pectoris

  • Mathias H. Konstandin
  • Hülya Aksoy
  • Guido H. Wabnitz
  • Christian Volz
  • Christian Erbel
  • Henning Kirchgessner
  • Evangelos Giannitsis
  • Hugo A. Katus
  • Yvonne Samstag
  • Thomas J. Dengler
ORIGINAL CONTRIBUTION

DOI: 10.1007/s00395-008-0770-8

Cite this article as:
Konstandin, M.H., Aksoy, H., Wabnitz, G.H. et al. Basic Res Cardiol (2009) 104: 341. doi:10.1007/s00395-008-0770-8

Abstract

Background

Cardiac troponins provide excellent risk stratification in unstable angina (UA), but no reliable markers are available in troponin-negative patients. Beta2-integrin mediated T cell recruitment plays a pivotal role in coronary atherosclerotic plaque rupture. The present study investigates beta2-integrin activation on T cell subsets as a risk marker in UA.

Methods

Functional activation (affinity/avidity) of beta2-integrins on T cells was measured using a flow cytometry-based whole blood assay in 87 patients with UA.

Results

Beta2-integrin activation was significantly higher in patients with severe coronary artery disease (sC) and myocardial infarction (MI) compared to patients with no/minimal coronary atherosclerosis (no/mC), irrespective of troponin status. Adjusted for cardiovascular risk factors, medication, left ventricular function, MI at enrollment and high sensitivity C-reactive protein (hsCRP), beta2-integrin activation was independently associated with incidence of revascularization, hospitalization and all major cardiovascular events during 9 months of follow-up after index investigation. The highest prognostic value of beta2-integrin activation was seen in troponin-and hsCRP-negative patients.

Conclusion

Quantitative assessment of T cell beta2-integrin activation allows to identify high risk patients with UA and sC without established MI; furthermore, it is associated with incidence of future cardiovascular events independent of conventional risk factors (troponin, hsCRP).

Keywords

acute coronary syndromeT cellinflammationintegrinatherosclerosis

Supplementary material

395_2008_770_MOESM1_ESM.doc (30 kb)
(DOC 29.5 kb)

Copyright information

© Steinkopff Verlag Darmstadt 2009

Authors and Affiliations

  • Mathias H. Konstandin
    • 1
  • Hülya Aksoy
    • 1
  • Guido H. Wabnitz
    • 2
  • Christian Volz
    • 1
  • Christian Erbel
    • 1
  • Henning Kirchgessner
    • 2
  • Evangelos Giannitsis
    • 1
  • Hugo A. Katus
    • 1
  • Yvonne Samstag
    • 2
  • Thomas J. Dengler
    • 1
  1. 1.Dept. of CardiologyRuprecht-Karls-UniversityHeidelbergGermany
  2. 2.Institute for ImmunologyRuprecht-Karls-UniversityHeidelbergGermany