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(Circulation. 2000;101:e193.)
© 2000 American Heart Association, Inc.

Circulation Electronic Pages

Possible Different Involvement of Interleukin-1 Receptor Antagonist Gene Polymorphism in Coronary Single Vessel Disease and Myocardial Infarction

Licia Iacoviello, MD, PhD; Maria Benedetta Donati, MD, PhD

"Angela Valenti" Laboratory of Genetic and Environmental Risk Factors for Thrombotic Disease, Department of Vascular Medicine and Pharmacology, Istituto di Ricerche Farmacologiche Mario Negri, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy

Marinella Gattone, MD

Fondazione Salvatore Maugeri Clinica del Lavoro e della Riabilitazione, IRCCS, Veruno, Italy

	Introduction

 
To the Editor:

Francis et al¹ recently reported that a polymorphism in the gene of the interleukin-1 receptor antagonist (IL-1Ra) is associated with the risk of single, but not multiple, vessel disease in a sample of Sheffield patients undergoing coronary angiography. The authors assume a true genetic distinction between the different expressions of vascular disease. However, a different pathogenetic involvement of the IL-1Ra gene in the mechanisms of atherosclerosis and thrombosis can also be suggested, with thrombosis being more frequent in the presence of multiple vessel disease. No data were, however, presented on patients with acute myocardial infarction (AMI).

We studied the IL-1RA gene in 158 Italian patients (129 men and 29 women) with AMI who were younger than 45 years (men) or 50 years (women) of age and who were frequency-matched for age and sex with 153 controls selected from a list of general practitioners in the same area. After amplification, 3 different alleles were identified: A1 (4 repeats) at 412 bp, A2 (2 repeats) at 240 bp, and A4 (5 repeats) at 498 bp.

Genotype distribution was in Hardy-Weinberg equilibrium in cases and controls (²=0.73, P=0.3 and ²=0.85, P=0.3, respectively). The frequency of alleles 1 and 2 in controls was 0.73 (95% confidence interval [CI], 0.67 to 0.68) and 0.25 (95% CI, 0.21 to 0.30), respectively, which is similar to the frequencies described by Francis et al. The frequency of allele 4, which was not found in the UK population, was lower (0.02; 95% CI, . . . [Full Text of this Article]

D. C. Crossman, MD, Professor; Sheila E. Francis, PhD; Nicola J. Camp, PhD; Rachael M. Dewberry, BSc; Julian Gunn, MRCP; David C. Cumberland, FRCR; Gordon W. Duff, FRCP

Divisions of Clinical Sciences and Molecular and Genetic Medicine, University of Sheffield, Sheffield, UK

Petros Syrris, PhD; Nicholas D. Carter, PhD; Stephen Jeffery, PhD; Juan Carlos Kaski, MD

Departments of Medical Genetics and Cardiological Sciences, St George’s Hospital Medical School, London, UK