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