Elevated white cell count in acute coronary syndromes: relationship to variants in inflammatory and thrombotic genes

doi:10.1186/1471-2350-5-13

BMC Medical Genetics

Volume 5

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Research article

Elevated white cell count in acute coronary syndromes: relationship to variants in inflammatory and thrombotic genes

Connie E Byrne¹^,3^* , Anthony Fitzgerald²^,3^* , Christopher P Cannon⁴ , Desmond J Fitzgerald¹^,3 and Denis C Shields¹^,3^,5

¹Department of Clinical Pharmacology, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland

²Department of Epidemiology, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland

³Institute of Biopharmaceutical Sciences, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland

⁴TIMI Study Group, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA USA

⁵Surgen Ltd., Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland

author email corresponding author email* Contributed equally

BMC Medical Genetics 2004, 5:13doi:10.1186/1471-2350-5-13


Published:	1 June 2004

Abstract

Background

Elevated white blood cell counts (WBC) in acute coronary syndromes (ACS) increase the risk of recurrent events, but it is not known if this is exacerbated by pro-inflammatory factors. We sought to identify whether pro-inflammatory genetic variants contributed to alterations in WBC and C-reactive protein (CRP) in an ACS population.

Methods

WBC and genotype of interleukin 6 (IL-6 G-174C) and of interleukin-1 receptor antagonist (IL1RN intronic repeat polymorphism) were investigated in 732 Caucasian patients with ACS in the OPUS-TIMI-16 trial. Samples for measurement of WBC and inflammatory factors were taken at baseline, i.e. Within 72 hours of an acute myocardial infarction or an unstable angina event.

Results

An increased white blood cell count (WBC) was associated with an increased C-reactive protein (r = 0.23, p < 0.001) and there was also a positive correlation between levels of β-fibrinogen and C-reactive protein (r = 0.42, p < 0.0001). IL1RN and IL6 genotypes had no significant impact upon WBC. The difference in median WBC between the two homozygote IL6 genotypes was 0.21/mm³(95% CI = -0.41, 0.77), and -0.03/mm³(95% CI = -0.55, 0.86) for IL1RN. Moreover, the composite endpoint was not significantly affected by an interaction between WBC and the IL1 (p = 0.61) or IL6 (p = 0.48) genotype.

Conclusions

Cytokine pro-inflammatory genetic variants do not influence the increased inflammatory profile of ACS patients.