Background: Atherosclerosis plays an important role in the pathophysiology of acute coronary syndrome (ACS). CD36 is a scavenger receptor involved in lipid metabolism. Some single-nucleotide variants in the non-coding region could indirectly alter the expression and the function of the protein. Objective:The aim of this study was to investigate the gene and protein expression associated with CD36 variants (rs1194182;C > G; rs1049654;C > A, rs1334512;G > T, and rs3211892;G > A) in ACS patients from the western Mexican population. Methods:We recruited 310 ACS patients and 308 subjects in the control group (CG).Genotyping was determined by TaqMan SNP genotyping assays. CD36 expression at the mRNA level was quantified by TaqMan gene expression assays. Soluble CD36 (sCD36) was measured by enzyme-linked immunosorbent assay. Results:We show that rs1194182G > C variant provides a protective effect with a 1.7-fold lower susceptibility to develop ACS (p = 0.03); however, this association was masked by diabetes and dyslipidemia. We observed a higher sCD36 concentration in patient with ST-segment elevation myocardial infarction (STEMI) compared with patients with unstable angina (UA) (p = 0.038). Likewise, in diabetic patients versus non-diabetic (p < 0.001). We observed in patients an increase in CD36 mRNA expression (1.91 times higher) than in the CG (p = 0.02). Conclusion:The rs1194182 seems to be associated with diabetes in a risky manner, in ACS patients and protective for dyslipidemia in both groups. The concentration of sCD36 seems to be associated with the clinical spectrum of the ACS patients and the presence of diabetes, since patients with STEMI present significantly elevated level compared with UA.

Apolipoprotein B (APOB) is associated with the development of atherosclerosis and consequently in the acute coronary syndrome (ACS) physiopathology. Single number variants (SNVs) in apolipoprotein B gene (APOB) influence over the susceptibility for this syndrome. The aim of this study was to determine the impact of the rs1469513, rs673548, rs676210, and rs1042034 SNVs and serum levels of APOB in the risk of ACS in a population from western Mexico. We included 300 patients in the group of cases (ACSG) and 300 individuals in the control group (CG). APOB levels were evaluated by immunonephelometry, and SNVs were genotyped with TaqMan probes. We found significant allelic and genotypic differences between groups for rs673548 and rs676210 (OR = 1.33, p = 0.030 , OR = 2.69, p < 0.001 ) and rs1042034 (OR = 0.50, p = 0.037 ) SNVs. We found a risk haplotype TAGT (OR: 2.14, IC 1.50–3.04, p < 0.001 ). Our findings support a significant risk association between rs673548 and rs676210 variants for ACS; meanwhile, rs1042034 could be considered protective factor in a western Mexican population. Also, in this population, haplotype TAGT may confer 2.14 times a higher risk. APOB serum levels were compared by genotype variants in both groups without any significant statistical difference.

Acute coronary syndrome (ACS) can be triggered by the presence of inflammatory factors which promote the activation of immune cells by costimulatory molecules such as CD40 and its ligand CD40L. Environmental and genetic factors are involved in the etiology of the ACS. The aim of this study was to explore the gene and protein expression associated with CD40 and CD40L genetic variants in ACS patients from the western Mexican population. A total of 620 individuals from western Mexico were recruited: 320 ACS patients and 300 individuals without a history of ischemic cardiopathy were evaluated. The genotype was determined using TaqMan SNP genotyping assays. CD40 and CD40L expressions at the mRNA level were quantified using TaqMan Gene Expression Assays. Soluble protein isoforms were measured by enzyme-linked immunosorbent assay. We did not find evidence of association between CD40 (rs1883832, rs4810485, and rs11086998) and CD40L (rs3092952 and rs3092920) genetic variants and susceptibility to ACS, although rs1883832 and rs4810485 were significantly associated with high sCD40 plasma levels. Plasma levels of sCD40L can be affected by gender and the clinical spectrum of acute coronary syndrome. Our results do not suggest a functional role of CD40 and CD40L genetic variants in ACS. However, they could reflect the inflammatory process and platelet activation in ACS patients, even when they are under pharmacological therapy. Due to the important roles of the CD40-CD40L system in the pathogenesis of ACS, longitudinal studies are required to determine if soluble levels of CD40 and CD40L could be clinically useful markers of a recurrent cardiovascular event after an ACS.

IntroductionThe increased risk of myocardial infarction (MI) in T2DM is well documented. Polymorphisms in APOA1 and APOB genes allow us to identify new genetic markers in Mexican population with T2DM and MI.Material and methodsWe studied 135 patients with DMT2 and MI (DI); another 85 non-infarcted diabetic individuals with DMT2 but without previous ischemic events (NID) and 242 Healthy subjects (HS), all three groups were selected with the aim to investigate the association between the polymorphisms and infarction when T2DM is present or absent.Results-75 G>A polymorphism: differences were found in genotype distribution between DI and NID individuals (OR: 2.01, CI:1.117-3.623, p= 0.019) with an increased risk for A in the dominant model (OR: 1.77, CI: 1.020-3.084, p= 0.042); also concentrations of ApoA-I for A/A were lower in comparison with G/A (p = 0.038) and LDL-C and HDL-C levels were lower in G/A respecting to G/G carriers. 83 C> T polymorphism of APOA1: for DI individuals: HDL-C was lower in T/T respecting to C/C and triglyceride levels were lower in C/T respect to C/C carriers.ConclusionsThe -75 G>A APOA1 polymorphism could be considered as a susceptibility factor for Myocardial Infarction in individuals with T2DM and 2488 C>T APOB polymorphism is associated with changes in HDL-C and LDL-C and triglycerides in the same group.roup.

Acute coronary syndrome (ACS) belongs to the clinical entities characterized by obstruction of a coronary artery. In its etiology, inflammation contributes significantly trough the activation of immune cells by co-stimulatory molecules as CD40 and CD40L. The purpose of this work was to explore the changes of mRNA and circulating soluble levels of CD40-CD40L in ACS patients and association with genetic variants in a western Mexican population. 320 ACS patients and 300 individuals with similar age than cases without ischemic cardiopathy were recruited. Genotype determination was made using TaqMan SNP genotyping assays. CD40 and CD40L mRNA expression in whole blood samples were quantified using TaqMan Gene Expression Assays. Soluble levels were measured in plasma by enzyme-linked immunosorbent assay. We did not find evidence of association between on CD40 (rs1883832, rs4810485 and rs11086998) and CD40L (rs3092952 and rs3092920) genetic variants and susceptibility to ACS nor changes in their mRNA expression (p&gt;0.05), although rs1883832 and rs4810485 affected significantly sCD40 circulating levels (p=0.005; p=0.015, respectively). Circulating soluble levels were higher in ACS patients; specifically sCD40L was higher in male patients with unstable angina compared to female patients (p=0.016). Our results showed genetic variants affect soluble levels of CD40 although the CD40 and CD40L polymorphisms are not associated with susceptibility to ACS in western Mexican population. CD40L mRNA expression, sCD40 and sCD40L plasma levels were higher in ACS patients even when they are under pharmacological treatment, which suggests an active role of the CD40-CD40L system in the immunopathogenesis of acute coronary syndrome.