Paraoxonase 1 (Q192R) gene polymorphism, coronary heart disease and the risk of a new acute coronary event

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• 作者：Efr&eacute ; n Mart&iacute ; nez-Quintana^a ; ^{efrencardio@gmail.com} ; Fayna Rodr&iacute ; guez-Gonz&aacute ; lez^b ; Jos&eacute ; Mar&iacute ; a Medina-Gil^a ; Paloma Garay-S&aacute ; nchez^c ; Antonio Tugores^c
• 关键词：Paraoxonase 1 ; Polymorphism ; Acute coronary event ; Coronary artery disease
• 刊名：Clínica e Investigación en Arteriosclerosis
• 出版年：2017
• 出版时间：January-February 2017
• 年：2017
• 卷：29
• 期：1
• 页码：1-6
• 全文大小：704 K
• 卷排序：29

文摘

Paraoxonase 1 (PON1) plays a major role in the oxidation of low density lipoprotein and in the prevention of coronary atherogenesis. In this context, coding region polymorphisms of PON1 gene, responsible for the enzyme activity, has become of interest as a marker for atherogenesis.MethodsA study and follow-up was conducted on 529 patients with an acute coronary event in order to assess the association between the PON1 Q192R (rs662;A/G) polymorphism, the type of acute coronary syndrome, cardiovascular risk factors (arterial hypertension, diabetes mellitus, dyslipidaemia, and smoking), the extent and severity of coronary atherosclerosis, and the medium-term clinical follow-up.ResultsThe QQ genotype was found in 245 (46.3%) patients, with 218 (41.2%) patients showing the QR genotype, and 66 (14.5%) patients had the RR genotype. No significant differences were found between the QQ and QR/RR genotypes as regards the clinical characteristics, the analytical data, and the angiographic variables. Similarly, Kaplan–Meier survival analysis showed no significant differences in presenting with a new acute coronary event (p = 0.598), cardiac mortality (p = 0.701), stent thrombosis (p = 0.508), or stent re-stenosis (p = 0.598) between QQ and QR/RR genotypes during the follow-up period (3.3 ± 2.2 years).ConclusionsIn patients with an acute coronary syndrome, the PON1 Q192R genotypes did not influence the risk of suffering a new acute coronary event during the medium-term follow-up.