Role of Single Nucleotide Polymorphism L55M in the Paraoxonase 1 Gene as a Risk and Prognostic Factor in Acute...

The aim of the current study is to explore the possible role of L55M, (rs 854560, 163T > A) SNP as a predisposing factor for acute coronary syndrome (ACS) and to assess its potency as a prognostic biomarker for short (1 year) survival and for median (5 years) and 9-year long patients’ outcome. Methods: The current work is a prospective case-control study with 77 patients with acute coronary syndrome (53 with ST-elevation myocardial infarction, STEMI, 14 with non-ST-elevation myocardial infarction, NSTEMI and 10 with unstable angina, UA) and 122 control individuals. Patients were followed-up for 9 years. The genotyping for PON1 L55M SNP was carried on by PCR-RFLP method. Results: The results of the genotyping for PON1 L55M SNP showed a statistically significant difference (p = 0.023) between the controls and the whole group of patients with acute coronary syndrome, as the individuals with genotype with at least one variant M allele had about 2.5-fold higher risk for developing ACS than those which are homozygous of the wild-type L allele (LL genotype). In patients with variant M allele genotypes (LM + MM) which suffer from non-ST-segment elevation ACS (NSTEACS, i.e., UA or NSTEMI), the serum levels of total cholesterol (TC) and triacylglycerols (TAG) are significantly higher than in NSTEACS patients with LL genotype (p = 0.022 for TC and p = 0.015 for TAG). There was no significant difference in the survival rate at the 1st, 5th and 9th year of follow-up between ACS patients with different genotypes, although it is worth to note that in the subgroup of NSTEACS, all patients (n = 13) with variant M allele genotypes (LM + MM) were alive at the end of the first year, while 2 of the patients with LL genotype (18.2%) were dead. Conclusions: The results of our current study suggest that the variant M allele and the M allele genotypes (LM + MM) of the PON1 L55M polymorphism are risk factors for acute coronary syndrome, especially for patients with STEMI, but do not support the possible effect of this polymorphism on the clinical progression and outcome of the patients with ACS either in short or long follow-up periods.