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

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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).

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Correspondence to Mathias H. Konstandin.

Additional information

Returned for 1. Revision: 15 October 2008 1. Revision received: 23 October 2008

Returned for 2. Revision: 30 October 2008 2. Revision received: 31 October 2008

Y. Samstag and T.J. Dengler contributed equally.

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Konstandin, M.H., Aksoy, H., Wabnitz, G.H. et al. Beta2-integrin activation on T cell subsets is an independent prognostic factor in unstable angina pectoris. Basic Res Cardiol 104, 341–351 (2009). https://doi.org/10.1007/s00395-008-0770-8

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