Abstract
Objectives Premature myocardial infarction (PMI) is an uncommon disease, and its incidence varies between 2% and 10%, rising, depending on genetic susceptibility under the influence of lifestyle. The purpose of this study was to investigate the association between SIRT1 single nucleotide polymorphisms (SNPs), SIRT1, and eNOS (endothelial nitric oxide synthase) protein expressions, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) in young patients with premature ST-elevation myocardial infarction (STEMI). Methods Genotyping of the three single-nucleotide polymorphisms (rs7895833 A > G in the promoter region, rs7069102 C > G in intron 4, and rs2273773 C > T in exon 5) in SIRT1 gene was performed in 108 consecutive patients (87.0% were men with a mean age of 40.74 ± 3.82 years) suffering from ST-elevation myocardial infarction at the age of ≤45 and 91 control subjects. Results The risk for myocardial infarction was increased by 2.31 times in carriers of CC or CG genotypes. SIRT1 protein levels were enhanced and endothelial nitric oxide synthase levels were diminished in ST-elevation myocardial infarction patients regardless of the underlying gene variant. There was no correlation between SIRT1 expression and the amount of endothelial nitric oxide synthase, total antioxidant status, total oxidant status, and oxidative stress index levels in patients and in the control group either. Conclusions SIRT1 single-nucleotide polymorphisms were associated with premature myocardial infarction, which affected the SIRT1 and endothelial nitric oxide synthase protein expression, irrespective of the underlying SIRT1 genotype.
Highlights
Myocardial infarction (MI) is an atypical disease in young individuals with a varying prevalence between 2% and 10% [1,2,3,4,5,6].An increasing prevalence of risk factors for coronary artery disease (CAD), such as impaired glucose tolerance and obesity in adolescence, is counteracting for the protection featured by young age [7]. us, in this population, an early recognition and a risk factor modification is of key importance [8].Pathogenesis of myocardial infarction in young people is likely to be different from those in an older population [9]
Patients included in this study presented with a history of premature myocardial infarction (PMI) to the Departments of Cardiology of the Bezmialem Vakif University Hospital and Mehmet Akif Ersoy Heart Hospital between January 2012 and May 2015
Patients’ Demographic and Biochemical Analysis. e clinical characteristics of the study groups are given in Patients suffering from premature ST-elevation myocardial infarction were more likely to be overweight (BMI >25 : 79.1% vs 45.1%, p 0.001), with a higher rate of smokers (87.1% vs 58.0%, p 0.001), and had dyslipidemia (73.1% vs 12.1%, p < 0.001) compared to the control group
Summary
Myocardial infarction (MI) is an atypical disease in young individuals with a varying prevalence between 2% and 10% [1,2,3,4,5,6].An increasing prevalence of risk factors for coronary artery disease (CAD), such as impaired glucose tolerance and obesity in adolescence, is counteracting for the protection featured by young age [7]. us, in this population, an early recognition and a risk factor modification is of key importance [8].Pathogenesis of myocardial infarction in young people is likely to be different from those in an older population [9]. Myocardial infarction (MI) is an atypical disease in young individuals with a varying prevalence between 2% and 10% [1,2,3,4,5,6]. An increasing prevalence of risk factors for coronary artery disease (CAD), such as impaired glucose tolerance and obesity in adolescence, is counteracting for the protection featured by young age [7]. Pathogenesis of myocardial infarction in young people is likely to be different from those in an older population [9]. Identifying the effect of these possible genetic modifiers on disease phenotype might be of great interest to detect young people at risk very early
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