Lymphotoxin-alpha gene and risk of myocardial infarction in 6,928 cases and 2,712 controls in the ISIS case-control study.
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ABSTRACT:
SUBMITTER: Clarke R
PROVIDER: S-EPMC1487176 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Peripheral blood samples of patients with acute myocardial infarction were matched with those of control patients to identify possible differences in corresponding gene expression profiles. The controls were matched to cases based on gender, age, status of diabetes mellitus and smoking status. Six months cardiovascular survival status of the cases was used to identify two distinct subgroups among the cases. Linear models for microarray data (‘limma’) were employed to identify differential gene expression. Shrunken centroids technique helped in identifying the subsets of differentially expressed genes with predictive properties in independent samples. Predictive properties were evaluated using bootstrap sampling. Using the limma modeling with the log-fold change threshold of one (clinical significance) and Storey’s q-value approach (statistical significance), sixty transcripts were found to be both clinically and statistically differentially expressed among the cases not surviving the follow-up period relative to controls, while no such transcripts were observed among other surviving cases. The two subgroups of cases exhibited fourteen differentially expressed transcripts. Predictive modeling indicated sixteen out of sixty transcripts to best discriminate between the controls and cases who died during the follow-up period from cardiovascular causes, while for the surviving cases the already non-significant set of transcripts could not be further reduced. Eleven out of fourteen transcripts were found to best discriminate between the two groups of cases using shrunken centroids. The study identified genes, which were differentially expressed during the acute myocardial infarction, including those associated with short-term fatality of the cases.
2014-12-05 | GSE34198 | GEO
Project description:Peripheral blood samples of patients with acute myocardial infarction were matched with those of control patients to identify possible differences in corresponding gene expression profiles. The controls were matched to cases based on gender, age, status of diabetes mellitus and smoking status. Six months cardiovascular survival status of the cases was used to identify two distinct subgroups among the cases. Linear models for microarray data (M-bM-^@M-^XlimmaM-bM-^@M-^Y) were employed to identify differential gene expression. Shrunken centroids technique helped in identifying the subsets of differentially expressed genes with predictive properties in independent samples. Predictive properties were evaluated using bootstrap sampling. Using the limma modeling with the log-fold change threshold of one (clinical significance) and StoreyM-bM-^@M-^Ys q-value approach (statistical significance), sixty transcripts were found to be both clinically and statistically differentially expressed among the cases not surviving the follow-up period relative to controls, while no such transcripts were observed among other surviving cases. The two subgroups of cases exhibited fourteen differentially expressed transcripts. Predictive modeling indicated sixteen out of sixty transcripts to best discriminate between the controls and cases who died during the follow-up period from cardiovascular causes, while for the surviving cases the already non-significant set of transcripts could not be further reduced. Eleven out of fourteen transcripts were found to best discriminate between the two groups of cases using shrunken centroids. The study identified genes, which were differentially expressed during the acute myocardial infarction, including those associated with short-term fatality of the cases. The genome-wide study used matched case-control design, with 97 samples of 90 patients in three disease groups. Matched control samples were used and several (7) technical replicates were performed.
2014-12-05 | E-GEOD-34198 | biostudies-arrayexpress
Project description:Certain non-steroidal anti-inflammatory drugs (NSAIDs) have been associated with an increased risk of myocardial infarction (MI), a risk linked to cyclo-oxygenase-2 inhibition. There are limited studies assessing the risk of MI associated with meloxicam, an increasingly popular drug with COX-2 inhibiting properties. A nested matched case-control study using The Health Improvement Network, a UK population-based database was conducted. NSAID users between 35 and 89 years of age with at least 1 year enrollment in the cohort were included. Incident MI cases were matched on age, sex, practice and event date with up to 4 controls. NSAID exposure was categorized as remote (between 60 days and 1 year), recent (between 1 and 60 days) or current relative to the event date. Current users were further classified as naproxen (negative control), diclofenac (positive control), meloxicam or other NSAID users. Multivariable conditional logistic regression was conducted to determine the risk of MI for each NSAID use categories compared with that of remote users. 9291 MI cases were matched with 30,676 controls. The cases had a higher prevalence of traditional cardiac risk factors, chronic kidney disease and inflammatory arthritis and cardioprotective drug utilization. The adjusted odds ratio of MI for current user compared to remote users were: meloxicam 1.38 (1.17-1.63), naproxen 1.12 (0.96-1.30) and diclofenac 1.37 (1.25-1.50). In this large population-based study, meloxicam increased the risk of MI by 38%. This study warrants cautious use of this increasingly popular drug.
| S-EPMC8143590 | biostudies-literature
Project description:Previous studies have shown an association between acute myocardial infarction and preceding respiratory infection. Contradictory evidence exists on the influence of influenza vaccination and pneumococcal vaccination in preventing cardiovascular disease. We aimed to investigate the possible association of influenza vaccination and pneumococcal vaccination with acute myocardial infarction.We used a matched case-control design with data from the United Kingdom General Practice Research Database. Cases were patients who were at least 40 years of age at diagnosis of first acute myocardial infarction recorded from Nov.1, 2001, to May 31, 2007, and were matched for sex, general practice, age and calendar time (i.e., month corresponding to index date of acute myocardial infarction), with up to four controls each. Data were analyzed using conditional logistic regression, adjusted for vaccination target groups, cardiovascular risk factors, treatment medications and attendances at a general practice.We included 78 706 patients, of whom 16 012 were cases and 62 694 were matched controls. Influenza vaccination had been received in the previous year by 8472 cases (52.9%) and 32 081 controls (51.2%) and was associated with a 19% reduction in the rate of acute myocardial infarction (adjusted odds ratio [OR] 0.81, 95% confidence interval [CI] 0.77-0.85). Early seasonal influenza vaccination was associated with a lower rate of acute myocardial infarction (adjusted OR 0.79, 95% CI 0.75-0.83) than vaccination after mid-November (adjusted OR 0.88, 95% CI 0.79-0.97). Pneumococcal vaccination was not associated with a reduction in the rate of acute myocardial infarction (adjusted OR 0.96, 95% CI 0.91-1.02).Influenza vaccination but not pneumococcal vaccination is associated with a reduced rate of first acute myocardial infarction. This association and the potential benefit of early seasonal vaccination need to be considered in future experimental studies.
| S-EPMC2952008 | biostudies-other
Project description:BackgroundAlthough epidemiological evidence for the beneficial effect of low alcohol consumption on myocardial infarction is strong, the impact of heavy drinking episodes is less clear.ObjectivesThe aim of this study was to investigate a possible association between the risk for acute myocardial infarction occurrence and alcohol consumption.MethodsOur hospital-based case-control study comprised 374 participants (187 newly diagnosed patients with myocardial infarction and 187 controls, individually matched by gender, age, and place of residence). This study was performed in Kragujevac (a city in Serbia) during 2010. Logistic regression analysis was used to determine odds ratio (OR) with 95% confidence intervals (95% CI).ResultsThe history of alcohol consumption in patients with acute myocardial infarction and their controls did not differ significantly: the percentage of those that were consuming alcohol was slightly higher in cases (54.5%) than in controls (50.3%). The habit of binge drinking during the previous 12 months was significantly more common in cases (25.1%) than in controls (12.8%): adjusted OR = 2.2 (95%CI = 1.2-4.2, p = 0.017), p for trend = 0.015. Analysis of binge drinking by age, gender and place of residence revealed that the increase in risk for acute myocardial infarction was associated with older age (adjusted OR = 5.1, 95%CI = 1.7-15.1, p for trend = 0.010), male gender (adjusted OR = 2.3, 95%CI = 1.1-5.2, p for trend = 0.028) and rural place of residence (adjusted OR = 4.8, 95%CI = 1.3-18.5, p for trend = 0.033).ConclusionOur results suggest that binge drinking is associated with twice the risk for myocardial infarction compared to not drinking. Since consumption of alcohol is very common in the Serbian population, the effect of binge drinking on myocardial infarction should be considered an important public health issue.
| S-EPMC5986147 | biostudies-literature
Project description:ObjectivesThe tumor necrosis factor-alpha (TNF-α) gene may play an important role in coronary heart disease (CHD) and myocardial infarction (MI) risk. Recently, controversial results regarding the association of the G-308 A (rs1800629)polymorphism of the TNF-α gene with CHD/MI have been reported. We herein examine a possible association between the G-308 A (rs1800629)polymorphism of the TNF-α gene and CHD/MI in a sample of the Chinese Han population.Materials and methodsWe determined the genotypes of TNF-α G-308 A (rs1800629) in 535 unrelated Chinese patients with CHD, 420 patients with MI, and 1020 coronary artery disease-free controls. Additionally, a meta-analysis of all previous studies on the TNF-α G-308 A polymorphism and the risk of CHD and MI was performed.ResultsAA genotypes in the G-308 A (rs1800629)polymorphism of the TNF-α gene did not occur more frequently in CHD/MI patients than in controls; odds ratios (95% confidence intervals) were 1.743 (0.325 to 1.423) for CHD and 1.731 (0.442 to 1.526) for MI, after adjusting for conventional risk factors. Further stratification for age, gender, and other cardiovascular risk factors did not alter the prior negative findings. Pooled meta-analysis of 23 studies also found no statistically significant associations between the TNF-α polymorphism and CHD/MI risk in the genetic additive, dominant, and recessive models. Subgroup analyses showed no association between the TNF-α polymorphism and CHD/MI in Asian and Caucasian populations.ConclusionOur study showed no association between the G-308 A (rs1800629) polymorphism of the TNF-α gene (presence of A allele) and CHD/MI in the Chinese Han population. There was no evidence of a difference in risk effects of rs1800629 between Caucasians and Asians.
| S-EPMC3354475 | biostudies-literature
Project description:ObjectiveTo test the hypothesis that the use of chondroitin sulfate (CS) or glucosamine reduces the risk of acute myocardial infarction (AMI).DesignCase-control study nested in a primary cohort of patients aged 40 to 99 years, using the database BIFAP during the 2002-2015 study period. From this cohort, we identified incident cases of AMI and randomly selected five controls per case, matched by exact age, gender, and index date. Adjusted odds ratios (AOR) and 95% confidence interval (CI) were computed through a conditional logistic regression. Only new users of CS or glucosamine were considered.ResultsA total of 23,585 incident cases of AMI and 117,405 controls were included. Of them, 89 cases (0.38%) and 757 controls (0.64%) were current users of CS at index date, yielding an AOR of 0.57 (95%CI: 0.46-0.72). The reduced risk among current users was observed in both short-term (<365 days, AOR = 0.58; 95%CI: 0.45-0.75) and long-term users (>364 days AOR = 0.56; 95%CI:0.36-0.87), in both sexes (men, AOR = 0.52; 95%CI:0.38-0.70; women, AOR = 0.65; 95%CI:0.46-0.91), in individuals over or under 70 years of age (AOR = 0.54; 95%CI:0.38-0.77, and AOR = 0.61; 95%CI:0.45-0.82, respectively) and in individuals at intermediate (AOR = 0.65; 95%CI:0.48-0.91) and high cardiovascular risk (AOR = 0.48; 95%CI:0.27-0.83), but not in those at low risk (AOR = 1.11; 95%CI:0.48-2.56). In contrast, the current use of glucosamine was not associated with either increased or decreased risk of AMI (AOR = 0.86; 95%CI:0.66-1.08).ConclusionsOur results support a cardioprotective effect of CS, while glucosamine seems to be neutral. The protection was remarkable among subgroups at high cardiovascular risk.
| S-EPMC8274913 | biostudies-literature
Project description:The primary objective of this study was to investigate the association between antidepressants use and the risk of acute myocardial infarction (AMI).MethodsWe conducted a nested case-control study using a primary care database over the period 2002-2015. From a cohort of patients aged 40-99 years, we identified incident AMI cases and randomly selected 5 controls per case, matched to cases for exact age, sex and index date. Exposure to antidepressants were categorised as current, recent, past and nonusers. Adjusted odds ratio (AOR) and 95% confidence interval (CI) were computed using conditional logistic regression to assess the association between the current use of different antidepressants subgroups and AMI as compared to nonuse. Dose and duration effects were explored.ResultsTotals of 24 155 incident AMI cases and 120 775 controls were included. The current use of antidepressants as a group was associated with a reduced risk (AOR = 0.86; 95% CI: 0.81-0.91), but mainly driven by selective serotonin reuptake inhibitors (AOR = 0.86; 95% CI:0.81-0.93). A reduced risk was also observed with trazodone (AOR = 0.76;95% CI: 0.64-0.91), and clomipramine (AOR = 0.62; 95% CI: 0.40-0.96), whereas no significant effect was observed with other antidepressants. A duration-dependent effect was suggested for selective serotonin reuptake inhibitors, trazodone and clomipramine, while there was no clear dose-dependency.ConclusionThis study suggests that current use of antidepressants interfering selectively with the reuptake of serotonin, and those antagonizing the 5-HT2A receptor, are associated with a decrease in AMI risk and should be the antidepressants of choice in patients at cardiovascular risk.
| S-EPMC7495291 | biostudies-literature
Project description:BACKGROUND: Lymphotoxin-alpha (LTA) is a pro-inflammatory cytokine with anti-tumor activity. The objective of this study was to determine whether LTA polymorphisms influence the presence of cancer. METHODS: LTA polymorphisms C804A (rs1041981, T60N) and T495C (rs2229094, C13R) were determined in 1,536 consecutive autopsy cases and were registered in the Japanese single-nucleotide polymorphisms (SNPs) for geriatric research (JG-SNP) Internet database. Tumors were systematically reviewed, pathologically confirmed, and assessed in relation to LTA genotype. RESULTS: The study population consisted of 827 males and 709 females, with a mean age of 80 years. Altogether, we studied 606 subjects without cancer and 930 subjects with cancer of the stomach (n = 183), lung (n = 164), colon or rectum (n = 143), or other sites. The presence of cancer was higher in males than in females. The C804A and T495C polymorphisms were associated with cancer in males (CA + AA: CC, adjusted OR = 0.72, 95% CI = 0.53 - 0.99; TC + CC: TT, adjusted OR = 1.45, 95% CI = 1.04 - 2.02; respectively) but not in females. In males, the C804A polymorphism was associated with lung cancer (CA + AA: CC, adjusted OR = 0.60, 95% CI = 0.37 - 0.97), whereas the T495C polymorphism was associated with gastric cancer (TC + CC: TT, adjusted OR = 1.68, 95% CI = 1.06 - 2.65). CONCLUSION: We found some evidence of an association between LTA polymorphisms and cancer risk in elderly Japanese men. Further studies in larger populations should examine this hypothesis.
| S-EPMC2527017 | biostudies-literature
Project description:ObjectivesTo evaluate the risk of myocardial infarction and death from coronary heart disease after discontinuation of low dose aspirin in primary care patients with a history of cardiovascular events.DesignNested case-control study.SettingThe Health Improvement Network (THIN) database in the United Kingdom.ParticipantsIndividuals aged 50-84 with a first prescription for aspirin (75-300 mg/day) for secondary prevention of cardiovascular outcomes in 2000-7 (n=39,513).Main outcome measuresIndividuals were followed up for a mean of 3.2 years to identify cases of non-fatal myocardial infarction or death from coronary heart disease. A nested case-control analysis assessed the risk of these events in those who had stopped taking low dose aspirin compared with those who had continued treatment.ResultsThere were 876 non-fatal myocardial infarctions and 346 deaths from coronary heart disease. Compared with current users, people who had recently stopped taking aspirin had a significantly increased risk of non-fatal myocardial infarction or death from coronary heart disease combined (rate ratio 1.43, 95% confidence interval 1.12 to 1.84) and non-fatal myocardial infarction alone (1.63, 1.23 to 2.14). There was no significant association between recently stopping low dose aspirin and the risk of death from coronary heart disease (1.07, 0.67 to 1.69). For every 1000 patients, over a period of one year there were about four more cases of non-fatal myocardial infarction among patients who discontinued treatment with low dose aspirin (recent discontinuers) compared with patients who continued treatment.ConclusionsIndividuals with a history of cardiovascular events who stop taking low dose aspirin are at increased risk of non-fatal myocardial infarction compared with those who continue treatment.
| S-EPMC3139911 | biostudies-literature