The aim of this study was to explore the role of variants of the gene encoding arachidonate 5-lipoxygenase-activating protein (ALOX5AP) as possible susceptibility factors for coronary artery disease(CAD) and myocardial infarction (MI) in patients with or without angiographically proven CAD. A total of1431 patients with or without angiographically documented CAD were examined simultaneously for sevenALOX5AP single-nucleotide polymorphisms, allowing reconstruction of the at-risk haplotypes (HapA andHapB) previously identified in the Icelandic and British populations. Using a haplotype-based approach,HapA was not associated with either CAD or MI. On the other hand, HapB and another haplotype withinthe same region (that we named HapC) were significantly more represented in CAD versus CAD-freepatients, and these associations remained significant after adjustment for traditional cardiovascular riskfactors by logistic regression (HapB: odds ratio (OR) 1.67, 95% confidence interval (CI) 1.04–2.67;P¼0.032; HapC: OR 2.41, 95% CI 1.09–5.32; P¼0.030). No difference in haplotype distributions wasobserved between CAD subjects with or without a previously documented MI. Our angiography-basedstudy suggests a possible modest role of ALOX5AP in the development of the atheroma rather than in itslate thrombotic complications such as MI.

ALOX5AP gene variants and risk of coronary artery disease: an angiography-based study

GIRELLI, Domenico
;
MARTINELLI, Nicola;TRABETTI, Elisabetta;OLIVIERI, Oliviero;CAVALLARI, Ugo Antonio Aristide;MALERBA, Giovanni;BUSTI, Fabiana;FRISO, Simonetta;PIZZOLO, Francesca;PIGNATTI, Pierfranco;CORROCHER, Roberto
2007

Abstract

The aim of this study was to explore the role of variants of the gene encoding arachidonate 5-lipoxygenase-activating protein (ALOX5AP) as possible susceptibility factors for coronary artery disease(CAD) and myocardial infarction (MI) in patients with or without angiographically proven CAD. A total of1431 patients with or without angiographically documented CAD were examined simultaneously for sevenALOX5AP single-nucleotide polymorphisms, allowing reconstruction of the at-risk haplotypes (HapA andHapB) previously identified in the Icelandic and British populations. Using a haplotype-based approach,HapA was not associated with either CAD or MI. On the other hand, HapB and another haplotype withinthe same region (that we named HapC) were significantly more represented in CAD versus CAD-freepatients, and these associations remained significant after adjustment for traditional cardiovascular riskfactors by logistic regression (HapB: odds ratio (OR) 1.67, 95% confidence interval (CI) 1.04–2.67;P¼0.032; HapC: OR 2.41, 95% CI 1.09–5.32; P¼0.030). No difference in haplotype distributions wasobserved between CAD subjects with or without a previously documented MI. Our angiography-basedstudy suggests a possible modest role of ALOX5AP in the development of the atheroma rather than in itslate thrombotic complications such as MI.
ALOX5AP; coronary artery disease; myocardial infarction
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/311258
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