Chemokine receptor 5 polymorphism in myocardial infarction patients from Luxembourg.

Sophie Rodius, Christine Lambert, Carole Devaux, Jean-Claude Schmit, Yvan Devaux, Daniel R Wagner
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Abstract

Background: The CC-chemokine receptor 5 (CCR5) is regulating inflammatory pathways and may thus be implicated in the development and progression of heart failure (HF). A 32 base pair deletion of the ccr5 gene, called CCR5delta32, prevents the expression of CCR5 at the cell surface. We analyzed the association between the CCR5delta32 deletion and the risk and severity of myocardial infarction (MI) in a cohort of patients from Luxembourg.

Methods: Using TaqMan allelic discrimination assay, we genotyped a total of 1080 patients undergoing coronary angiography. This population contained 3 groups of patients: controls with atypical chest pain, abnormal stress testing but normal coronary angiography (n = 154), patients with angina who underwent uncomplicated primary coronary intervention (n = 230), and patients with acute MI (n = 696). In MI patients, left ventricular ejection fraction (LVEF) was determined 1-month after MI with echocardiography.

Results: The frequency of the CCR5delta32 deletion was 16.3% in the global population, and was similar between controls, patients with angina and MI patients. The deletion was not associated with variations of plasma levels of creatine phosphokinase and troponin T, nor it was associated with LVEF, New York Heart Association class or 2-year mortality. The frequency of the deletion was comparable between MI patients with LV dysfunction (EF < or = 40%, n = 82) and no LV dysfunction (EF > 40%, n = 402).

Conclusions: The frequency of the CCR5delta32 deletion in Luxembourg is similar to that observed in other European countries and is not associated with the risk of developing MI and LV dysfunction.

卢森堡心肌梗死患者趋化因子受体5多态性
背景:cc趋化因子受体5 (CCR5)调节炎症途径,因此可能与心力衰竭(HF)的发生和进展有关。ccr5基因的32个碱基对缺失,被称为CCR5delta32,阻止了ccr5在细胞表面的表达。我们分析了来自卢森堡的一组患者CCR5delta32缺失与心肌梗死(MI)风险和严重程度之间的关系。方法:采用TaqMan等位基因鉴别法对1080例冠状动脉造影患者进行基因分型。该人群包含3组患者:非典型胸痛、应激试验异常但冠状动脉造影正常的对照组(n = 154)、心绞痛患者(n = 230)和急性心肌梗死患者(n = 696)。心肌梗死患者在心肌梗死后1个月用超声心动图测定左心室射血分数(LVEF)。结果:CCR5delta32缺失的频率在全球人群中为16.3%,在对照组、心绞痛患者和心肌梗死患者之间相似。缺失与血浆肌酸磷酸激酶和肌钙蛋白T水平的变化无关,也与LVEF、纽约心脏协会分级或2年死亡率无关。有左室功能障碍的心肌梗死患者(EF <或= 40%,n = 82)和无左室功能障碍的心肌梗死患者(EF > 40%, n = 402)的基因缺失频率相当。结论:卢森堡CCR5delta32缺失的频率与其他欧洲国家相似,与发生心肌梗死和左室功能障碍的风险无关。
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