Independent Risk Factor For Acute Myocardial Infarction Research Articles

Elevated Circulatory Levels of UL16 Binding Protein 1 Positive Microparticles Are Associated With Acute Myocardial Infarction and its Severity.

Atherosclerosis is a vascular inflammatory disease characterized by the activation and stress of various inflammatory cells, leading to the development of coronary artery disease and subsequently acute myocardial infarction (AMI). Among AMI cases, ST-segment elevation myocardial infarction (STEMI) is typically more severe than non-STEMI (NSTEMI). UL16-binding proteins (ULBPs), which are NKG2D ligands, can be expressed on the surface of stressed and activated cells, prompting these cells to generate microparticles (MPs). Consequently, MPs carrying ULBPs, particularly ULBP1 (ULBP1+ MPs), may be released into the bloodstream. This study aimed to investigate the association between ULBP1+ MPs and the presence of AMI and its severity. We recruited 58 AMI patients and 45 age-matched control subjects. Levels of ULBP1+ MPs and ULBP1+ MPs originating from T lymphocytes (ULBP1+ TMPs) were measured using flow cytometry. Both ULBP1+ MP and ULBP1+ TMP levels were significantly elevated in AMI patients compared to controls. Elevated levels of these MPs were independent risk factors for AMI with odds ratios (OR) of 4.3 (95%CI=1.5-12.3) for ULBP1+ MPs and 5.8 (95%CI=2.0-17.0) for ULBP1+ TMPs. Additionally, ULBP1+ TMP levels were significantly higher in STEMI patients compared to NSTEMI patients, with an independent association observed between ULBP1+ TMPs and STEMI (OR=3.9; 95%CI=1.2-12.8). Elevated levels of ULBP1+ MPs and ULBP1+ TMPs are associated with AMI and its severity. These biomarkers could serve as indicators of vulnerable plaques that lead to AMI.

Aldehyde Dehydrogenase 2 rs671 G/A and a/A Genotypes are Associated with the Risk of Acute Myocardial Infarction.

Aldehyde dehydrogenase 2 (ALDH2) is a key catalytic enzyme involved in the aldehyde metabolism that plays an important role in the occurrence and development of acute myocardial infarction (AMI). However, the relationship of ALDH2 polymorphism and susceptibility to AMI may differ among different regions and populations, and it has not yet been reported in Hakka population. The purpose of the present study was to investigate it in this population. Four hundred and nineteen AMI patients and 636 individuals without AMI were included in the present study. The ALDH2 rs671 polymorphism was genotyped using polymerase chain reaction (PCR)-microarray. Differences in ALDH2 rs671 genotypes and alleles between patients and controls were compared, and the relationship between ALDH2 rs671 genotypes and AMI risk was analyzed. Patients with AMI had a lower frequency of ALDH2 rs671 G/G genotype (43.2% vs 52.7%, p=0.003), and a higher G/A genotype (45.6% vs 38.5%, p=0.025) than controls. And AMI patients had a lower frequency of ALDH2 rs671 G allele (66.0% vs 71.9%), and a higher A allele (34.0% vs 28.1%) (p=0.004) than controls. Logistic regression analysis showed that overweight (body mass index (BMI)≥24.0 kg/m2 vs BMI 18.5-23.9 kg/m2: odds ratio (OR) 2.046, 95% confidence interval (CI): 1.520-2.754, p<0.001), history of hypertension (yes vs no: OR 3.464, 95% CI: 2.515-4.770, p<0.001), ALDH2 rs671 G/A genotype (G/A vs G/G: OR 1.476, 95% CI: 1.102-1.976, p=0.009), and A/A genotype (A/A vs G/G: OR 1.656, 95% CI: 1.027-2.668, p=0.038) maybe the independent risk factors for AMI. Overweight (BMI≥24.0 kg/m2), a history of hypertension, and ALDH2 rs671 G/A or A/A genotypes increased the risk of developing AMI in Hakka population.

Low expression of Notch1 may be associated with acute myocardial infarction.

The transmembrane protein Notch1 is associated with cell growth, development, differentiation, proliferation, apoptosis, adhesion, and the epithelial mesenchymal transition. Proteomics, as a research method, uses a series of sequencing techniques to study the composition, expression levels, and modifications of proteins. Here, the association between Notch1 and acute myocardial infarction (AMI) was investigated using proteomics, to assess the possibility of using Notch1 as a biomarker for the disease. Fifty-five eligible patients with AMI and 74 with chronic coronary syndrome (CCS) were enrolled, representing the experimental and control groups, respectively. The mRNA levels were assessed using RT-qPCR and proteins were measured using ELISA, and the results were compared and analyzed. Notch1 mRNA levels were 0.52 times higher in the peripheral blood mononuclear cells of the AMI group relative to the CCS group (p < 0.05) while Notch1 protein levels were 0.63 times higher in peripheral blood plasma in AMI patients (p < 0.05). Notch1 levels were not associated with older age, hypertension, smoking, high abdominal-blood glucose, high total cholesterol, and high LDL in AMI. Logistic regression indicated associations between AMI and reduced Notch1 expression, hypertension, smoking, and high fasting glucose. Notch1 expression was reduced in the peripheral blood of patients with AMI relative to those with CCS. The low expression of Notch1 was found to be an independent risk factor for AMI and may thus be an indicator of the disease.

FSTL3 partially mediates the association of increased nonalcoholic fatty liver disease fibrosis risk with acute myocardial infarction in patients with type 2 diabetes mellitus

BackgroundThe study aimed to investigate an association of increased liver fibrosis with acute myocardial infarction (AMI), and to investigate the mediating effect of serum follistatin-like protein 3 (FSTL3) on the association in patients with type 2 diabetes mellitus (T2DM).MethodA total of 1424 participants were included in this study, and were firstly divided into two groups: 429 T2DM patients and 995 T2DM patients with NAFLD to assess the association of NAFLD and AMI. Then 995 T2DM co-existent NAFLD patients were categorized by NAFLD fibrosis risk to explore the association between NAFLD fibrosis risk and AMI. Immunohistochemistry staining and semi-quantitative analysis of liver FSTL3 were performed in 60 patients with NAFLD. There were 323 individuals (191 without AMI and 132 with AMI) in T2DM co-existent NAFLD patients who had serum samples, and serum FSTL3 was tested and mediation effect of FSTL3 in association of NAFLD fibrosis and AMI was performed.ResultsFirst, increased NAFLD fibrosis risk was an independent risk factor for AMI in patients with T2DM and co-existent NAFLD. In addition, analysis of Gene Expression Omnibus (GEO) database and immunohistochemical staining confirmed the increased expression of FSTL3 in the liver of NAFLD patients with fibrosis. Serum FSTL3 significantly increased in patients with high NAFLD fibrosis risk and AMI, and closely associated with NAFLD fibrosis and AMI severity in T2DM patients with co-existent NAFLD. Most importantly, analysis of the level of mediation revealed that increased serum FSTL3 partially mediated the association of increased NAFLD fibrosis risk with AMI in T2DM patients with co-existent NAFLD.ConclusionsNAFLD fibrosis was closely associated with AMI in T2DM patients. FSTL3 expression was enriched in the liver of NAFLD patients with significant and advanced fibrosis, and serum FSTL3 partially mediated the association of increased liver fibrosis risk with AMI in T2DM patients.

The usability of MCP-1, fetuin-A, TAS, and TOS levels in the diagnosis of acute myocardial infarction.

Our aims were to determine whether the levels of plasma monocyte chemotactic protein-1 (MCP-1), fetuin-A, serum total antioxidant status (TAS), and serum total oxidant status (TOS) are cardiac biomarkers and to clarify their relationship with each other in acute myocardial infarction (AMI). The study included 90 participants: 60 patients with AMI [30 with and 30 without ST-segment elevation myocardial infarction (STEMI)] and 30 cardiac patients without AMI. The diagnostic values of serum Hs-cTnT, MCP-1, fetuin-A, TAS, and TOS levels in predicting AMI were evaluated statistically. Median levels of MCP-1 [120.10 ng/L (interquartile range: 76.94-230.54 ng/L)] and TOS [2.89 U/MI (IQR: 2.31-3.94 U/Ml)] were statistically higher, and median levels of fetuin-A [433.52 mg/L (IQR: 387.89-584.49 mg/L)] and TAS (3.10 ± 0.86 U/mL) were lower in patients with AMI than in controls. The parameter with the area under the curve (0.815), sensitivity (73.3%), and specificity (66.7%) closest to those of Hs-cTnT was fetuin-A, followed by MCP-1, TOS, and TAS, respectively. A one-unit increase in MCP-1 levels increased the probability of AMI by 1.023 times (p = 0.002). A one-unit increase in fetuin-A levels decreased the probability of AMI by 0.995 times (p = 0.003). A one-unit increase in serum TOS levels was 1.29 times more characteristic of STEMI than of NSTEMI (p = 0.044). MCP-1, oxidative stress parameters, and fetuin-A might support Hs-cTnT levels in the early diagnosis of AMI. Fetuin-A and MCP-1 levels may be independent risk factors for AMI, whereas TOS could be used to distinguish STEMI from NSTEMI.

Correlation Between Low THBS3 Expression in Peripheral Blood and Acute Myocardial Infarction.

Thrombospondin (THBS) 3 is an adhesive glycoprotein involved in cell-cell and cell-matrix interactions. The purpose of this study is to determine whether THBS3 expression in peripheral blood can be used as a biomarker to predict the risk of acute myocardial infarction (AMI). The peripheral blood of 111 patients with stable coronary artery disease (SCAD) and 112 patients with AMI was obtained. The experimental and the control cohorts were the AMI and SCAD groups, respectively. The expression of THBS3 mRNA and protein in both groups was determined using reverse-transcription polymerase chain reaction and enzyme-linked immunosorbent assay. THBS3 expression (range) in the peripheral plasma of patients in the AMI group was lower than that of patients in the SCAD group (4.526 (3.748-5.521), 5.511 (4.726-6.334), respectively), which was 0.82 times lower than the control (p < 0.001). Furthermore, THBS3 mRNA level in the peripheral blood mononuclear cells of patients with AMI was 0.47 times lower than that in patients with SCAD (p < 0.05). AMI was associated with fasting blood glucose levels, platelet counts and low THBS3 expression. Logistic regression analysis revealed that decreased expression of THBS3 protein increased the probability of AMI by 4.076 times (p < 0.01). Additionally, high fasting blood glucose and high platelet counts increased the risk of AMI by 2.819 and 6.515 times, respectively (p < 0.05). THBS3 mRNA and protein levels in the peripheral blood of patients in the AMI group were much lower compared with those of patients in the SCAD group. Low THBS3 expression in peripheral blood was related to AMI and was an independent risk factor for AMI. Thus, low THBS3 expression in peripheral blood may be a novel, suitable molecular marker for the early detection of AMI.

Association of functional variant of aldehyde dehydrogenase 2 with acute myocardial infarction of Chinese patients

BackgroundThe variant of ALDH2 was thought to be associated with Acute Myocardial Infarction (AMI) due to the consumption of alcohol. This study focused on how ALDH2 variant acts as an independent risk factor for AMI, regardless of alcohol consumption.Methods and resultsWe used the case–control INTERHEART-China study which took place at 25 centres in 17 cities in mainland China. Cases were patients with AMI and matched by age, sex, and site to controls. Information about alcohol consumption and genotype were collected. We divided cases and controls by alcohol consumption: alcohol intake group and no alcohol intake group. Then, calculated the Odd Ratio (OR) value with confidence interval (CI) at 95% level to find the association between ALDH2 variant and AMI. Results were then adjusted by sex, age, BMI, and other common risk factors of AMI. The study involves a total of 2660 controls and 2322 AMI patients. The no drink intake group showed that there was a correlation between the ALDH2 variant and AMI (OR = 1.236, 95% CI = 1.090–1.401, p = 0.00092). After adjustment of different risk factors this association remained (OR = 1.247, 95% CI = 1.099–1.415, p = 0.00062). Similar results were also obtained from the no alcohol intake group (OR = 1.196, 95% CI = 0.993–1.440, p = 0.05963), however, due to the limited sample size, the result was not significant enough statistically.ConclusionFrom our results, ALDH2 variant is associated with the risk of AMI even in population that has no alcohol consumption. This suggests that ALDH2 variant may act as an independent risk factor for AMI.

Association between genetic variations of mitochondrial isocitrate dehydrogenase (IDH2) and acute myocardial infarction

PurposeMitochondrial isocitrate dehydrogenase (IDH2) is a major contributor to cellular redox control. The aim of this study was to preliminary link IDH2 genetic variations to redox imbalance, atherogenesis and risk of acute myocardial infarction (AMI). MethodsThis case-control study included 120 AMI patients and 120 healthy controls. IDH2 genetic variations were tested using direct sequencing. IDH2 enzyme activity was measured spectrophotometrically. Malondialdehyde (MDA) and Oxidized low density lipoproteins (ox-LDL) concentrations, as biomarkers of oxidative stress, were quantitated using ELISA. ResultsFour missense heterozygous mutations were detected within IDH2 gene. The variant forms of the enzyme showed a markedly reduced enzymatic activity (2.22 ± 0.56 mU/mL in wild type compared to 0.65 ± 0.35 mU/mL in mutant enzyme). IDH2 enzyme activity correlated negatively with MDA and ox-LDL concentrations (r = −80.875 and −0.891 respectively). There was a strong association between IDH2 mutations and elevated MDA and ox-LDL (rpb = 0.764 and 0.652, both p < 0.001). After adjustment of other risk factors, IDH2 genetic variations showed to be an independent risk factor for AMI (ß=1.792, p = 0.019). ConclusionsThe study proved that IDH2 genetic variations lead to impaired enzyme activity, redox imbalance, accumulation of lipid-peroxides and coronary atherogenesis. However, because such gene association has not been studied before, further studies are recommended.

Expression of ATP-binding cassette subfamily B member 1 gene in peripheral blood of patients with acute myocardial infarction

ABSTRACT This study aimed to determine the amount of expression of the ATP-binding cassette subfamily B member 1 (ABCB1) gene chip as a prospective diagnostic marker for acute myocardial infarction (AMI) in a wide population . In the AMI and control groups, 113 patients with AMI and 83 persons with non-coronary artery disease were selected for peripheral venous leukocyte collection. Western blot and real-time polymerase chain reaction (RT-PCR) were employed to detect relative ABCB1 expression in both groups. The results showed that the ABCB1 transcription and protein levels in the AMI group were higher than in the control. The relative mRNA expression of ABCB1 was 0.26 (0.03–0.79) in the AMI group and 0.13 (0.01–0.52) in the control group (P < 0.05). The expression of the ABCB1 gene at the protein level in the AMI group was 1.65 times that in the control (P < 0.05). Further, the subjects in the AMI group were older (P < 0.001), had lower levels of high-density lipoprotein cholesterol (P = 0.038), and had higher incidence of type II diabetes mellitus (P = 0.003) compared with the control. Logistic regression analysis showed that the expression of ABCB1 in peripheral blood was correlated with the occurrence of AMI (P = 0.003). High ABCB1 expression, type II diabetes, and advanced age were found to serve as potential independent risk factors for AMI, with a 4.88-fold, 2.99-fold, and 2.63-fold increased risk of AMI. Overall, the high expression of ABCB1 in peripheral blood might be related to the occurrence of AMI.

Contribution of glutathione peroxidase 1 (Pro200Leu) single nucleotide polymorphism and serum homocysteine levels in the risk of acute myocardial infarction in Egyptians

BackgroundOxidative stress is among the most common risk factors in the pathogenesis of acute myocardial infarction (AMI). Glutathione peroxidase 1 enzyme coded by the GPX1 gene plays an essential role in reducing oxidative stress. Previous studies correlated the GPX1 (Pro200Leu) single nucleotide polymorphism (SNP) with AMI incidence. Elevated homocysteine (Hcy) levels induce oxidative stress and are considered an independent risk factor for AMI. Evidence showed a complex relationship between Hcy and GPx-1 activity. This study examined the association of the common (Pro200Leu) SNP in GPX1 with AMI incidence in an Egyptian population. This study is the first to check this association in an Egyptian population. Moreover, the association between serum Hcy and the incidence of AMI was checked, and the novelty was to statistically correlate GPX1 Pro200Leu genotypes with serum Hcy levels in patients and control subjects. Hundred control subjects and hundred and twenty AMI patients were genotyped using PCR-RFLP analysis. An ELISA was used to measure serum Hcy levels. ResultsThe GPX1 (Pro200Leu) genotype distribution and allele frequency were not significantly different between patients and control subjects (P = 0.60 and P = 0.62, respectively). Serum levels of Hcy were significantly elevated in patients compared to control subjects (P ≤ 0.0001). However, no significant difference was observed in serum Hcy levels among different GPX1 genotypes in neither patients nor control subjects. ConclusionsThe minor T allele of GPX1 Pro200Leu is not associated with AMI risk in this Egyptian population. However, high homocysteine serum levels might contribute independently to the risk of AMI. Finally, Hcy levels were not significantly different in homozygous minor TT compared to homozygous wild CC.

Low ZCCHC9 Gene Expression in Peripheral Blood May Be an Acute Myocardial Infarction Genetic Molecular Marker in Patients with Stable Coronary Atherosclerotic Disease.

PurposeZCCHC9 is a zinc finger protein with a CCHC zinc finger structure and has important roles in several cellular processes. This study was conducted on an expanded number of samples to evaluate The usefulness of ZCCHC9 gene expression in peripheral blood as a molecular marker for the prediction of AMI (acute myocardial infarction) risk.Patients and MethodsPeripheral blood samples were collected from 117 patients with stable CAD (coronary atherosclerotic disease) and 126 patients with AMI. The mRNA level of the ZCCHC9 gene was assessed by qRT-PCR, and its protein level was determined by Western blotting.ResultsThe AMI group exhibited reduced expression of the ZCCHC9 gene, at both transcript and protein levels, than the stable CAD group. The low expression of the ZCCHC9 gene was not related to blood glucose level (P=0.635), blood lipid level, and troponin level (P=0.715), and may cause AMI through the MAPK signaling pathway. Compared with other patients, patients with low ZCCHC9 gene expression in their peripheral blood have a 2.597-fold higher risk of AMI.ConclusionZCCHC9 gene expression in peripheral blood was significantly lower in patients with AMI than in stable CAD patients. Individuals with low expression of ZCCHC9 in peripheral blood have higher a probability to develop AMI than those with stable CAD. Thus, lowered ZCCHC9 gene expression can act as an independent risk factor for AMI.

High retinoic acid receptor-related orphan receptor A gene expression in peripheral blood leukocytes may be related to acute myocardial infarction.

ObjectiveThis study aimed to investigate whether differential expression of the retinoic acid receptor-related orphan receptor A (RORA) gene is related to occurrence of acute myocardial infarction (AMI).MethodsThis was a retrospective study. White blood cells of 93 patients with acute myocardial infarction and 74 patients with stable coronary artery disease were collected. Reverse transcription quantitative polymerase chain reaction and western blotting were used to measure RORA mRNA and protein expression, respectively.ResultsRORA mRNA expression levels in peripheral blood leukocytes in patients with AMI were 1.57 times higher than those in patients with stable coronary artery disease. Protein RORA levels in peripheral blood of patients with AMI were increased. Binary logistic regression analysis showed that high expression of RORA was an independent risk factor for AMI, and it increased the risk of AMI by 2.990 times.ConclusionRORA expression levels in patients with AMI is significantly higher than that in patients with stable coronary artery disease. High expression of RORA is related to AMI and it may be an independent risk factor for AMI.

Low G0S2 gene expression levels in peripheral blood may be a genetic marker of acute myocardial infarction in patients with stable coronary atherosclerotic disease: A retrospective clinical study.

Background:The G0/G1 switch 2 (G0S2) gene is closely related to lipolysis, cell proliferation, apoptosis, oxidative phosphorylation, and the development of a variety of tumors. The aim of the present study was to expand the sample size to confirm the relationship between the expression of the G0S2 gene in peripheral blood and acute myocardial infarction (AMI) based on previous gene chip results.Methods:Three hundred patients were initially selected, of which 133 were excluded in accordance with the exclusion criteria. Peripheral blood leukocytes were collected from 92 patients with AMI and 75 patients with stable coronary atherosclerotic disease (CAD). mRNA expression levels of G0S2 in peripheral blood leukocytes was measured by RT-PCR, and protein expression levels by Western blot analysis. The results of these assays in the 2 groups were compared.Results:mRNA expression levels of GOS2 in the peripheral blood leukocytes of patients with AMI were 0.41-fold lower than those of patients with stable CAD (P < .05), and GOS2 protein expression levels were 0.45-fold lower. Multivariate logistic regression analysis indicated that low expression levels of the G0S2 gene increased the risk of AMI by 2.08-fold in stable CAD patients.Conclusions:G0S2 gene expression in the peripheral blood leukocytes of AMI patients was lower than that of stable CAD patients. Low G0S2 gene expression in peripheral blood leukocytes is an independent risk factor for AMI in stable CAD patients.

Significance of plasma free fatty acid level for assessing and diagnosing acute myocardial infarction.

Aim: To clarify the diagnostic value of the circulating free fatty acid (FFA) level for acute myocardial infarction (AMI) in coronary heart disease patients. Methods & results: A total of 1776 patients were screened by coronary angiography from October 2014 to February 2016. The plasma FFA level was significantly higher in coronary heart disease patients with lesions in three or more vessels than those with lesions in one or two vessels. Moreover, an elevated FFA level was identified as an independent risk factor for AMI on multivariate regression analysis and shown to be a sensitive and specific indicator for AMI diagnosis by receiver operating characteristic curve analysis. Conclusion: An elevated FFA level is an independent risk factor and independent diagnostic marker for AMI.

Low Expression of FFAR2 in Peripheral White Blood Cells May Be a Genetic Marker for Early Diagnosis of Acute Myocardial Infarction.

Objective To find molecular markers for the diagnosis of acute myocardial infarction (AMI), this research further verified the relationship between the expression level of FFAR2 gene and AMI by expanding the sample size based on the previous gene chip results. Methods Peripheral venous leukocytes were collected from 113 patients with AMI and 94 patients with noncoronary artery disease as the experimental group and the control group, respectively. Real-time fluorescence quantitative polymerase chain reaction was used to detect the expression of the FFAR2 gene. Western blot analysis was applied to detect the relative expression of the FFAR2 gene at the level of protein. Furthermore, the relationship between gene expression and clinical data was also analyzed and compared. Results The level of expression of FFAR2 gene in peripheral blood of patients with AMI was significantly lower than that of the control group (0.33 [0.04–1.08], 0.62 [0.07–1.86], respectively; p < 0.05), which was 0.53 times that of the control group. Western blot results presented that the FFAR2 protein level in the peripheral blood of the AMI group was lower than that of the control group (0.114; p=0.004). Analyzing clinical data of the subjects indicated that the average age of the AMI group was significantly higher than the age of control group (p < 0.01). Also, the fasting blood glucose level was higher (p < 0.01), and the high-density lipoprotein cholesterol (HDL-C) level was lower (p=0.03). The FFAR2 mRNA level correlated positively with the HDL-C level (p < 0.01). Logistic regression analysis suggested that the low expression of the FFAR2 gene in peripheral blood may be a risk factor for AMI independent of age, family history of diabetes, fasting blood glucose level, and HDL-C level (p=0.025). Compared with the high FFAR2 expression group, the risk of AMI in the low FFAR2 expression group was 6.308 times higher. Conclusion The expression level of the FFAR2 gene in peripheral blood of patients with AMI was significantly lower than that in the control group. Low expression of the FFAR2 gene in peripheral blood is an independent risk factor for AMI. Hence, it may also be a potential biomarker to predict AMI.

Low expression of PIK3C2A gene: A potential biomarker to predict the risk of acute myocardial infarction.

Aims:Phosphoinositide 3-kinases (PI3Ks) are a family of enzymes that phosphorylate the 3′-OH of inositol ring of phosphatidylinositol (PI) and regulate a broad range of signaling pathways. PIK3C2A is structurally distinct from the other members of this class and is expressed in endothelial cells, vascular endothelium, and smooth muscle. In ischemic cardiovascular diseases, such as coronary artery disease, pathology is associated with endothelial damage and inflammation, downregulation of the EPC cell population and function, and impaired angiogenesis. This study aims to make an assessment on whether expression of PIK3C2A gene can be used as a biomarker for predicting the risk of acute myocardial infarction (AMI).Methods:We collected peripheral blood from 84 subjects with non-coronary heart disease and 70 patients with AMI. The real-time quantitative PCR test was applied to measure levels of PIK3C2A gene expression at mRNA level in peripheral blood.Results:Our results indicated that the level of PIK3C2A gene expression in peripheral blood of AMI patients was significantly lower than one in the non-coronary heart disease subjects. Binary logistic regression analysis showed that low expression of PIK3C2A gene was an independent risk factor of AMI and increased the risk of AMI by 2.231 folds. Moreover, it was found that low expression of PIK3C2A gene was not associated with level of fasting blood glucose, platelet count, Gensini score of coronary artery, and quantity of cardiac troponin.Conclusion:The level of PIK3C2A gene expression in patients with AMI is significantly lower than that of healthy people. Low expression of PIK3C2A gene is an independent risk factor of AMI. Low expression of PIK3C2A could serve as a potential biomarker to predict risk of AMI.

Association of Thrombospondin-1 (N700S) and Thrombospondin-4 (A387P) Gene Polymorphisms with the Incidence of Acute Myocardial Infarction in Egyptians

Thrombospondin (TSP) 1 and 4 are extracellular matrix glycoproteins that me- diate cell proliferation, platelet aggregation and inflammatory response. Conflicting data addressed the possible contribution of TSP-1 and TSP-4 gene polymorphisms to acute myocardial infarction (AMI). Our study aimed to examine the association of TSP-1 (N700S) and TSP-4 (A387P) genetic variants with the incidence of AMI in Egyptians. It also correlated TSP-1 variants to TSP-1 and TNF-α serum concentrations while TSP-4 variants to IL-8 concentration identifying TSPs' contribution to vascular inflammation. Genotyping was done in 214 subjects; 114 AMI patients and 100 controls using PCR-RFLP analysis. Serum Tsp-1, TNF-α and IL-8 levels were measured by ELISA assay. For TSP-4, (GC and CC) genotype distribution and the (C) allele frequency were significantly higher in AMI patients than controls (p = 0.0186), (p = 0.0117) respectively. In contrast, TSP-1 genotypes and allele frequencies showed no significant difference between AMI and controls (p = 0.7124 and p = 0.7201, respectively). Serum TSP-1, TNF-α and IL-8 concentrations were significantly elevated in AMI compared to controls (p = 0.0146, p < 0.0001 and p = 0.0057) respectively. Serum IL-8 levels had a significant difference among TSP-4 genotypes (p= 0.0368), being highest in the mutant C allele. Serum TSP-1 and TNF-α concentrations showed no significant difference among TSP-1 genotypes, but there was a positive correlation between both concentrations in AMI patients (p = 0.0014), (r = 0.4125). TSP-4 A387P polymorphism, but not TSP-1 polymorphism, is an independent risk factor for AMI in the Egyptians.

Matrix Metalloproteinase Mediated Type I Collagen Degradation is an Independent Predictor of Increased Risk of Acute Myocardial Infarction in Postmenopausal Women

Acute myocardial infarction (AMI) is often underdiagnosed in women. It is therefore of interest to identify biomarkers that indicate increased risk of AMI and thereby help clinicians to have additional focus on the difficult AMI diagnosis. Type I Collagen, a component of the cardiac extracellular matrix, is cleaved by matrix metalloproteinases (MMPs) generating the neo-epitope C1M. We investigated the association between serum-C1M and AMI and evaluated whether C1M is a prognostic marker for outcome following AMI. This study is based on The Prospective Epidemiological Risk Factor (PERF) Study including postmenopausal women. 316 out of 5,450 women developed AMI within the follow-up period (14 years, median). A multivariate Cox analysis assessed association between serum-C1M and AMI, and re-infaction or death subsequent to AMI. The risk of AMI increased by 18% (p = 0.03) when serum-C1M was doubled and women in the highest quartile had a 33% increased risk compared to those in the low quartiles (p = 0.025). Serum-C1M was, however not related to reinfarction or death subsequent to AMI. In this study C1M was be an independent risk factor for AMI. Measuring MMP degraded type I collagen could be useful for prediction of increased risk of AMI if replicated in other cohorts.

High expression of long chain acyl-coenzyme A synthetase 1 in peripheral blood may be a molecular marker for assessing the risk of acute myocardial infarction.

The current study aimed to investigate whether the increased expression of long chain acyl-coenzymeA synthetase 1 (ACSL1) in peripheral blood leukocytes (PBL) may be a molecular marker for the genetic evaluation of acute myocardial infarction (AMI). The mechanism of action of ACSL1 in the pathogenesis of AMI was also investigated. A total of 75 patients with AMI and 70 individuals without coronary heart disease were selected to participate in the present study. The demographic and clinical information of the enrolled subjects was recorded. Reverse transcription quantitative polymerase chain reaction and western blot analysis were applied to measure the expression of ACSL1 at the mRNA and protein levels. It was demonstrated that the expression of ACSL1 mRNA and protein in PBL was increased in patients with AMI compared with controls. Logistic regression analysis indicated that ACSL1 expression in PBL was an independent risk factor of AMI. There was a significant positive association between the level of ACSL1 expression and the degree of atherosclerosis in the coronary artery. Furthermore, patients with AMI exhibited an increased risk of atherosclerosis due to increased fasting blood glucose, total cholesterol, triglyceride and lipoprotein levels and decreased high-density lipoprotein levels, compared with controls. Therefore, the current study demonstrated that ACSL1 expression was increased in the PBLs of patients with AMI. The elevated expression of ACSL1 acts an independent risk factor of AMI and may act as a potential biomarker when determining the risk of AMI.

Acute myocardial infarction in patients with atrial fibrillation with a CHA2DS2-VASc score of 0 or 1: a nationwide cohort study.

The risk of acute myocardial infarction (AMI) in patients with atrial fibrillation (AF) with a CHA2DS2-VASc score of 0 (for men) or 1 (for women) has not been previously investigated. The objective of the present study was to compare the risk of AMI in AF and non-AF subjects with a low (0 or 1) CHA2DS2-VASc score. By using the National Health Insurance Research Database in Taiwan, we identified 7254 men with AF (with a CHA2DS2-VASc score of 0) and 4860 women with AF (with a CHA2DS2-VASc score of 1). For each study patient, 1 age-, sex-, and CHA2DS2-VASc score-matched subject without AF was randomly selected to constitute the control group (n = 12,114). The clinical end point was the occurrence of AMI. During a mean follow-up period of 5.7 ± 3.6 years, 258 patients (1.1%) suffered an AMI, with an annual incidence of 0.29% and 0.10% for patients with and without AF. AF was an independent risk factor of AMI, with an adjusted hazard ratio (HR) of 2.93 (95% confidence interval 2.21-3.87; P < .001). The risk of AMI was higher in men with AF than in women with AF, with a hazard ratio of 2.24 (95% confidence interval 1.61-3.11; P < .001) after adjustment for age and other comorbidities. In patients with a CHA2DS2-VASc score of 0 or 1, AF was an independent risk factor of AMI. The risk of AMI was higher in men with AF than in women with AF. Cardiovascular risk prevention should be performed as part of the holistic management of AF to minimize the risks of AMI associated with AF.