Patients with unstable angina pectoris show an increased frequency of the Fc gamma RIIa R131 allele

Abstract

Patients with Systemic Lupus Erythematosus (SLE) carry an increased risk for the development of coronary artery disease (CAD). The R131 allele of the Fc gamma receptor IIa (FcγRIIa) is associated with SLE incidence and disease severity but also with CAD. Compared to stable angina pectoris (SAP) the unstable angina (UAP), as a manifestation of destabilizing CAD, is associated with increased risk of persistent instability, myocardial infarction, and death. Identification of clinically relevant determinants for unstable angina promises reduction of UAP-associated mortality in patients with SLE. We conducted a clinical study among 553 consecutive patients with stable angina pectoris (n = 330) and unstable angina pectoris (n = 223). All patients were genotyped for a frequent functional variant at position 131 of the mature FcγRIIa. UAP, but not SAP was significantly associated with the R/R131 genotype (P < 0.001). In troponin-negative patients with angina carrying the R/R131 genotype the odds ratio for suffering from UAP was 4.02 (95% confidence interval, 2.52–6.41) compared to those with non-R/R131 genotypes. In a multivariable analysis, the R/R131 genotype independently predicted the risk for development of UAP in a model adjusted for classical atherogenic risk factors. Our data imply that risk stratification of SLE- and other high risk patients with troponin-negative angina could be significantly improved by FcγRIIa genotyping.

Keywords::

• SLE
• stable
• unstable angina pectoris
• coronary disease
• Fc gamma receptor IIa
• allele R131

Acknowledgement

The authors are thankful to Monika Kallmünzer, Julia Ertner, Melanie Dümmler, Simon Roth, Nur Erdem, and Miranda Blokland for expert technical assistance.

Declaration of interests: This work was supported by the Interdisciplinary Center for Clinical Research (IZKF) grant to D.R.S. (Rotationsstipendium), by an intramural grant of the University Hospital Erlangen, University of Erlangen-Nuremberg to L.E.M. (ELAN M3-09.03.18.1), by the K. und R. Wucherpfennigstiftung to M.H. The authors declare no competing financial interests and are responsible for the content and writing of this paper.