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Thromb Haemost 2005; 94(06): 1251-1256
DOI: 10.1160/TH05-06-0417
Wound Healing and Inflammation/Infection
Schattauer GmbH

Fractalkine receptor polymorphisms V249I and T280M as genetic risk factors for restenosis

Alexander Niessner
1   Department of Internal Medicine II, Division of Cardiology
3   Department of Medicine, Lowance Center for Human Immunology, Emory University, Atlanta, Georgia, USA
,
Rodrig Marculescu
2   Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Austria
,
Heda Kvakan
1   Department of Internal Medicine II, Division of Cardiology
,
Arvand Haschemi
2   Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Austria
,
Georg Endler
2   Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Austria
,
Cornelia M. Weyand
3   Department of Medicine, Lowance Center for Human Immunology, Emory University, Atlanta, Georgia, USA
,
Gerald Maurer
1   Department of Internal Medicine II, Division of Cardiology
,
Christine Mannhalter
2   Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Austria
,
Johann Wojta
1   Department of Internal Medicine II, Division of Cardiology
,
Oswald Wagner
2   Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Austria
,
Kurt Huber
4   3 rd Department of Medicine, Cardiology and Emergency Medicine, Wilhelminen-Hospital, Vienna, Austria
› Author AffiliationsGrant support: The work of Dr. Alexander Niessner was supported by a “Schrödinger” grant from the “Fonds zur Förderung der wissenschaftlichen Forschung”. This study was supported by grants from the “Hans und Blanca Moser-Stiftung zur Förderung der Ausbildung von Krebs- und Herzspezialisten” and the “Österreichische Kardiologische Gesellschaft” to Dr. Rodrig Marculescu.
Further Information

Publication History

Received 15 June 2005

Accepted after revision 08 August 2005

Publication Date:
07 December 2017 (online)

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Summary

The chemokine fractalkine (FKN) recruits leukocytes into lesions of the arterial wall, which may lead to restenosis after stenting. FKN also regulates proliferation of smooth muscle cells, another mechanism pivotal to neointimal thickening. We assessed the hypothesis that functionally important polymorphisms of the FKN receptor CX3CR1 influence restenosis after coronary stenting. Three hundred and sixty-five patients undergoing coronary stenting were genotyped for the CX3CR1 polymorphisms V249I and T280M. Restenosis occurred in 25% of patients, and recurrent (> 1) restenosis at the target lesion in 8%.The allele I249 was associated with an increased risk of restenosis (adjusted odds ratio 2.4, 95% confidence interval: 1.3–4.2,P = 0.003) and recurrent restenosis (odds ratio 2.7,95% confidence interval:1.3–5.9,P = 0.011).Particularly, patients with I249 lacking the allele M280 were at an elevated risk of restenosis (P = 0.006) and, accordingly, the haplotype containing I249 but not M280 was more frequent in patients with restenosis (P = 0.001). In conclusion, the CX3CR1 I249 allele is associated with an increased risk of restenosis while the CX3CR1 M280 allele might counteract the harmful influence of I249.These findings show the importance of the chemokine FKN and genetic variations of its receptor for restenosis after coronary stenting. Recognition of these inherited risk modifiers may help to individualize treatment of coronary stenosis.

Keywords

Restenosis - stent - chemotaxis - fractalkine - single nucleotide - polymorphism
 

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