Protective role of Lipoprotein-Associated Phospholipase A2 Gene (A379V) Polymorphism against Myocardial Infarction among Egyptians

Background: Oxidation of low density lipoproteins is an initial step of atherogenesis that generates pro-inflammatory phospholipids, including platelet-activating factor (PAF) and its analogs. Platelet-activating factor is degraded by lipoprotein associated phospholipase A2 (Lp-PLA2), also known as platelet-activating factor-acetylhydrolase (PAF-AH), a circulating enzyme having both pro and anti-inflammatory activities. Lipoprotein associated phospholipase A2 activity has been postulated to be a risk factor for acute coronary syndrome (ACS); however, whether Lp-PLA2 has a causal or protective role is still unclear. A large number of single nucleotide polymorphisms (SNPs) that affect Lp-PLA2 mass and activity in plasma have been described. Aim: The aim of the present work is to determine the prevalence of Lp-PLA2 gene A379V single nucleotide polymorphism (SNP) in Egyptians suffering from myocardial infarction (MI) in comparison to healthy controls and to correlate this genetic variant with different cardiovascular risk factors. Methods: Lp-PLA2 gene A379V polymorphism (rs1051931) was investigated in fifty patients having MI and fifty age and sex matched healthy controls using real-time PCR. Results: The homozygous CC genotype, coding for alanine at position 379 of Lp-PLA2 protein, had the highest frequency among patients (72%) compared with controls (46%) while heterozygous CT genotype had the highest frequency among controls (46%) compared with patients (24%) with a significant difference (p=0.033). The major “C” allele had the highest frequency among patients (84%) compared with controls (69%) while the minor “T” allele, coding for valine at the same position, had the highest frequency among controls (31%) compared with patients (16%) with a significant difference (p=0.012). Conclusion: The Lp-PLA2 A379V gene polymorphism was found to be less frequent in MI patients presented with ACS than in healthy controls, suggesting that this SNP might be protective against the development of MI.