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. 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. 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). 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.
|Number of pages||10|
|Journal||Bulletin de la Société des Sciences Médicales du Grand-Duché de Luxembourg|
|Publication status||Published - 2011|