Comparative study of high sensitivity troponin T and heart-type fatty acid-binding protein in STEMI patients

AbstractAim and backgroundHeart-type fatty acid-binding proteins (H-FABP) which are detected within 2–3h of acute myocardial infarction are involved in uptake of free fatty acids in the myocardium. Our aim in the present study is to compare window periods of H-FABP to high sensitivity troponin T (hs-Trop T) in acute ST elevation myocardial infarction (STEMI).Methods160 STEMI diagnosed patient’s serum samples are analyzed for hs-Trop T and H-FABP. Different window periods of chest pain onset (<3h, 3–6h and >6h) are compared with complications, in-hospital mortality and statistically analyzed.ResultsFrom 160 patients, 53 (33%) cases are presented in <3h, 75 (47%) in 3–6, and 32 (20%) after >6h respectively. Accordingly sensitivity of hs-Trop T was 92%, 94% and 97% while H-FABP was 75%, 88% and 84%, respectively. Overall sensitivity was 94% and 82% respectively. Statistically significant difference between mean hs-Trop T values with respect to window period <3, 3–6 and >6h was 0.21, 0.35 and 0.80ng/ml respectively, p value<0.0001. No significant difference in H-FABP values was observed.Hs-Trop T positively correlated with age (r=0.153, P=0.05), window period (r=0.363, P<0.0001), TIMI score (r=0.208, P=0.008), ejection fraction (r=0.191, P=0.008), serum H-FABP (r=0.229, P=0.004), and serum hs-CRP (r=0.326, p<0.001). There was a statistically significant difference of mean hs-Trop T values with or without in hospital mortality (0.35 vs. 0.85ng/ml, respectively, p=0.008).No significant correlation to age, TIMI score, ejection fraction and hs-CRP values for H-FABP was observed.ConclusionIt appears that hs-Trop T is a more sensitive marker than H-FABP in early hours of AMI and higher hs-Trop T predicts increase in-hospital mortality

LDLR rs688 TT Genotype and T Allele Are Associated with Increased Susceptibility to Coronary Artery Disease—A Case-Control Study

Purpose: The low-density lipoprotein receptor is responsible for the binding and uptake of plasma LDL particles and plays a critical role in maintaining cellular cholesterol homeostasis. LDLR gene SNP rs688 has been reported to be associated with increased plasma total and LDL cholesterol in several populations and can lead to elevated plasma LDL levels, resulting in an increased risk for atherosclerosis and coronary artery disease. This study aimed to explore genetic LDLR variant rs688 for its potential roles in coronary artery disease. Methodology: This study recruited 200 coronary artery disease patients and 200 healthy individuals. Genotyping of LDLR-rs688C &gt; T gene variations was performed using the allele specific PCR method. Correlation of LDLR-rs688C &gt; T gene variants with different clinicopathological features of coronary artery disease patients was performed. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were applied to evaluate the correlation of this microRNA polymorphism with coronary artery disease risk. Results: A significant difference was observed in genotype distribution among the coronary artery disease and matched healthy controls (p = 0.003). The frequencies of all three genotypes CC, CT, TT reported in the patient samples were 14%, 65% and 21% and in the healthy controls samples were 18%, 73% and 9%, respectively. The increased risk of developing CAD in Indian patients was found to be associated with LDLR rs688 TT genotype (OR = 3.0, 95% CI, 1.43 &times; 6.2; p = 0.003) RR 1.87 (1.20&ndash;2.91) p = 0.0037) and also the increased risk of developing CAD was reported to be associated with LDLR rs688 T allele (OR = 0.74, 95% CI, 1.57&ndash;0.97; p = 0.03) RR 0.85 (0.73&ndash;0.99) p = 0.03) compared to the C allele. Therefore, it was observed that more than a 3.0- and 0.74-fold increase risk of developing CAD was associated with TT genotype and T allele in Indian coronary artery disease patients. Conclusion: The findings indicated that LDLR rs688 TT genotype and T allele are associated with an increased susceptibility to coronary artery disease patients. LDLR-rs688C &gt; T gene variation can be used as a predisposing genetic marker for coronary artery disease. Further studies with larger sample sizes are necessary to confirm our findings

LDLR Gene Polymorphisms (rs5925 and rs1529729) Are Associated with Susceptibility to Coronary Artery Disease in a South Indian Population

Cardiovascular diseases (CVD) are a major cause of death in India and worldwide. Atherosclerosis is caused by the interaction of environmental and genetic factors. Hypercholesterolemia is an example of a classical risk factor for CVD. The low-density lipoprotein receptor (LDLR) is one of the regulating mechanisms the liver uses for cholesterol homeostasis. Gene variations in the LDLR have been reported to cause hypercholesterolemia and consequently CVD. We investigated the association of polymorphisms in the LDLR (rs5925 and rs1529729) with coronary artery disease (CAD) in 200 coronary artery disease patients and 200 matched healthy controls using allele-specific PCR (AS-PCR). The results indicated that the CT genotype of the rs1529729 polymorphism was associated a decreased susceptibility to CAD with an odds ratio (OR) = 0.42 (95% confidence interval (CI), 0.23&ndash;0.77), risk ratio (RR) = 0.59 (0.39&ndash;0.89), P = 0.0047. The TT genotype of the rs1529729 polymorphism was also associated with decreased susceptibility to CAD with an OR = 0.19 (95% CI, 0.076&ndash;0.47), RR = 0.57 (0.47&ndash;0.69), P = 0.0003. The GA genotype of the rs5925 polymorphism was associated with decreased susceptibility to CAD with an OR = 0.45 (95% CI, 0.27&ndash;0.75), RR = 0.65 (0.47&ndash;0.88), P = 0.002. We concluded that the CT and TT genotypes of the rs1529729 polymorphism and the GA genotype of the rs5925 polymorphism are probably associated with decreased susceptibility to CAD. The simplicity of AS-PCR makes it particularly suitable for the rapid, large-scale screening of gene variabilities in the LDLR. AS-PCR could provide significant benefits in clinical applications with its ability to amplify a lower quantity of samples in a cost-saving manner. Nevertheless, these findings need to be validated in well-designed studies with larger sample sizes and in different populations

Reply to Comment: Evaluation of the Association of Omentin 1 rs2274907 A &gt; T and rs2274908 G &gt; A Gene Polymorphisms with Coronary Artery Disease in Indian Population: A Case–Control Study

Coronary artery disease (CAD) is a major cause of death all over the world. CAD is caused by atherosclerosis which is induced by the interaction of genetic factors and environmental factors. Genome-wide association studies have revealed the association of certain gene polymorphisms with susceptibility to CAD. Omentin 1 is an adipokine secreted by the visceral adipose tissues and has been reported to have anti-inflammatory, cardioprotective, and enhances insulin sensitivity. In this study, we examined the role of omentin-1 common single nucleotide polymorphisms (SNPs) (rs2274907 A &gt; T and rs2274908 G &gt; A) in CAD. We conclude that the AT genotype and the T allele of the rs2274907 A &gt; T is associated with Cad in the south Indian population. Our results indicated that the rs2274907 SNP may be associated with CAD in this population. This finding needs further validation in well-designed and large-sample size studies before being introduced in clinical settings