Project description:BACKGROUND The relationship between coronary heart disease (CHD) and the paraoxonase 2 (PON2) Ser311Cys polymorphism has received much attention. We conducted a meta-analysis on the results from published case-control studies examining this relation. MATERIAL AND METHODS A literature search was performed using PubMed and ISI Web of Knowledge databases until October 2015. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using Stata version 11.0 software. Data were pooled using the random-effects model. RESULTS Nine studies were eligible for statistical analysis and included a total of 5278 participants. The results did not support an association between the Ser311Cys polymorphism and CHD in the overall populations (Asians, Caucasians, and a Hispanic mixed population) under dominant (OR 1.07; 95% CI 0.91-1.28; Pz=0.413), recessive (OR 1.19; 95% CI 0.72-1.95; Pz=0.500), homozygote (OR 1.20; 95% CI 0.71-2.03; Pz=0.489), and allelic comparison (OR 1.08; 95% CI 0.91-1.28; Pz=0.390) models. However, in subgroup analysis according to ethnicity, we found that the Ser311Cys polymorphism was associated with CHD risk in Caucasians under recessive (OR 2.08; 95% CI 1.30-3.34; Pz=0.002) and homozygote (OR 2.16; 95% CI 1.33-3.50; Pz=0.002) models. Subgroup analysis indicated no significant association of this polymorphism with CHD in either Asian or Hispanic populations. CONCLUSIONS The PON2 Ser311Cys polymorphism is associated with CHD risk in Caucasians, but there is no association between this polymorphism and CHD in Asians or Hispanic populations.
Project description:Coronary heart disease (CHD) is a complex polygenic disease in which gene-environment interactions play a critical role in disease onset and progression. The Intercellular adhesion molecule 1 (ICAM-1) gene E469K polymorphism is one of the most commonly studied polymorphisms in this gene because of its association with CHD risks, but results were conflicting. The PubMed, Embase, and China National Knowledge Infrastructure databases were searched for case-control studies published up to November 2018. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated to assess the association. Eleven eligible studies, comprising 3435 cases and 3199 controls, were included in the meta-analysis. The pooled result showed that the ICAM-1 gene E469K polymorphism was significantly associated with an increased risk of CHD (OR = 1.20, 95% CI = 1.11-1.29, for the allele K versus allele E; OR = 1.66, 95% CI = 1.43-1.92, for the K allele carriers versus EE). Subgroup analysis supported the results in the Chinese populations and in the Caucasian populations. This meta-analysis suggests that the ICAM-1 gene K469E polymorphism is associated with CHD risk and the K allele is a more significant risk factor for developing CHD amongst Chinese and Caucasians populations.
Project description:The clinical association between atrial fibrillation (AF), coronary microvascular disease (CMD) and heart failure with preserved ejection fraction (HFpEF) is highly prevalent, however the mechanism behind this association is not known. We hypothesized that plasma proteomic analysis can identify novel biomarkers and the mechanistic pathways in concomitant AF, CMD and HFpEF. To discover circulating biomarkers for the association between AF, CMD and HFpEF, an unbiased label-free quantitative proteomics approach was used in plasma derived from patients who underwent coronary physiology studies (n=18). Circulating proteins were analyzed by liquid chromatography-mass spectrometry and screened to determine candidate biomarkers of the concomitant AF, CMD and HFpEF. We identified 130 dysregulated proteins across the groups with the independent patient replicates. Among those, 35 proteins were candidate biomarkers of the association between AF, CMD and HFpEF. We found significantly elevated SAA1, LRG1 and APOC3 proteins in the coexistence of AF, CMD and HFpEF, whereas LCP1, PON1 and C1S were markedly downregulated in their associations. AF was associated with reduced LCP1, KLKB1 and C4A in these patients. Combined downregulation of PON1 and C1S was a marker of concurrent HFpEF and CMD. PON1 was associated with HFpEF while C1S was a marker of CMD. These proteins are related to inflammation, extra cellular remodeling, oxidative stress, and coagulation. In conclusion, plasma proteomic profile provides biomarkers and mechanistic insight into the association of AF, CMD and HFpEF. SAA1, LRG1, APOC3, LCP1, PON1 and C1S are candidate markers for the risk stratification of their associations and potential underlying mechanistic pathways.
Project description:ObjectiveWe aimed to investigate the role of polymorphisms in IL-16 genes on the susceptibility of Coronary Artery Disease (CAD).MethodsA total of 260 CAD cases and 281 health controls were collected between January 2008 and November 2011. Genotyping of IL-16 rs8034928, rs3848180, rs1131445, rs4778889 and rs11556218 was conducted by polymerase chain reaction (PCR) and matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry technologies.ResultsThe frequencies of rs8034928 C allele and rs3848180 G allele in the CAD cases in CAD group were significantly higher than in controls. Compared with rs8034928 T/T genotype, a significant higher risk of CAD was found in C/C genotype (OR=1.87, 95%CI=1.17-3.03), and variant of rs8034928 showed a significant increased risk of CAD in dominant (OR=1.48, 95%CI=1.04-2.10) and recessive model (OR=1.70, 95%CI=1.10-2.67). The rs3848180 G/G was found to be associated with risk of CAD(OR=1.79, 95%CI=1.16-2.75), and G allele carries had a significant risk of CAD (OR=1.47, 95%CI=1.02-2.13).ConclusionsOur study indicated that rs8034928 and rs11556218 polymorphisms are associated with CAD risk in a Chinese population, and IL-16 gene polymorphisms may be used as a predictor to the susceptibility of CAD.
Project description:BACKGROUND: Periodontal disease is common among adults in the US and is a potential source of chronic inflammation. Recent data have suggested an important role for chronic inflammation in the development of coronary heart disease (CHD). OBJECTIVE: To aid the United States Preventive Services Task Force (USPSTF) in evaluating whether periodontal disease is an independent novel risk factor for incident CHD. METHODS: Studies were identified by searching Medline (1966 through March 2008) and reviewing prior systematic reviews, reference lists, and consulting experts. Prospective cohort studies that assessed periodontal disease, Framingham risk factors, and coronary heart disease incidence in the general adult population without known CHD were reviewed and quality rated using criteria developed by the USPSTF. Meta-analysis of good and fair quality studies was conducted to determine summary estimates of the risk of CHD events associated with various categories of periodontal disease. RESULTS: We identified seven articles of good or fair quality from seven cohorts. Several studies found periodontal disease to be independently associated with increased risk of CHD. Summary relative risk estimates for different categories of periodontal disease (including periodontitis, tooth loss, gingivitis, and bone loss) ranged from 1.24 (95% CI 1.01-1.51) to 1.34 (95% CI 1.10-1.63). Risk estimates were similar in subgroup analyses by gender, outcome, study quality, and method of periodontal disease assessment. CONCLUSION: Periodontal disease is a risk factor or marker for CHD that is independent of traditional CHD risk factors, including socioeconomic status. Further research in this important area of public health is warranted.
Project description:Background: Traditional observational studies have demonstrated an association between heart failure and Alzheimer's disease. The strengths of observational studies lie in their speed of implementation, cost, and applicability to rare diseases. However, observational studies have several limitations, such as uncontrollable confounders. Therefore, we employed Mendelian randomization of genetic variants to evaluate the causal relationships existing between AD and HF, which can avoid these limitations. Materials and Methods: A two-sample bidirectional MR analysis was employed. All datasets were results from the UK's Medical Research Council Integrative Epidemiology Unit genome-wide association study database, and we conducted a series of control steps to select the most suitable single-nucleotide polymorphisms for MR analysis, for which five primary methods are offered. We reversed the functions of exposure and outcomes to explore the causal direction of HF and AD. Sensitivity analysis was used to conduct several tests to avoid heterogeneity and pleiotropic bias in the MR results. Results: Our MR studies did not support a meaningful causal relationship between AD on HF (MR-Egger, p = 0.634 > 0.05; weighted median (WM), p = 0.337 > 0.05; inverse variance weighted (IVW), p = 0.471 > 0.05; simple mode, p = 0.454 > 0.05; weighted mode, p = 0.401 > 0.05). At the same time, we did not find a significant causal relationship between HF and AD with four of the methods (MR-Egger, p = 0.195 > 0.05; IVW, p = 0.0879 > 0.05; simple mode, p = 0.170 > 0.05; weighted mode, p = 0.110 > 0.05), but the WM method indicated a significant effect of HF on AD (p = 0.025 < 0.05). Because the statistical powers of IVW and MR-Egger are more than that of WM, we think that there is no causal effect of HF on AD. Sensitivity analysis and horizontal pleiotropy were not detected in the MR analysis. Conclusion: Our results did not provide significant evidence indicating any causal relationships between HF and AD in the European population. Therefore, more large-scale datasets or datasets related to similar factors are expected for further MR analysis.
Project description:BackgroundSeveral studies have demonstrated that coronary heart disease (CHD) is a high risk factor for cognitive impairment, whereas other studies showed that there was no association between cognitive impairment and CHD. The relationship between CHD and cognitive impairment is still unclear based on these conflicting results. Thus, it is of importance to evaluate the association between CHD and cognitive impairment. The present study made a meta-analysis to explore the association between CHD and risk of cognitive impairment.MethodsArticles exploring the association between CHD and cognitive impairment and published before November 2020 were searched in the following databases: PubMed, Web of Science, Medline, EMBASE, and Google Scholar. We used STATA 12.0 software to compute the relative risks (RRs), odds ratios (ORs), or hazard ratios (HRs) and 95% confidence intervals (CIs).ResultsThe meta-analysis showed a positive association between CHD and risk of all-cause cognitive impairment with a random effects model (RR = 1.27, 95% CI 1.18 to 1.36, I2 = 82.8%, p < .001). Additionally, the study showed a positive association between myocardial infraction (MI) and risk of all-cause cognitive impairment with a random effects model (RR = 1.49, 95% CI 1.20 to 1.84, I2 = 76.0%, p < .001). However, no significant association was detected between angina pectoris (AP) and risk of all-cause cognitive impairment with a random effects model (RR = 1.23, 95% CI 0.95 to 1.58, I2 = 79.1%, p < .001). Subgroup studies also showed that CHD patients are at higher risk for vascular dementia (VD), but not Alzheimer's disease (AD) (VD: RR = 1.34, 95% CI: 1.28-1.39; AD: RR = 0.99, 95% CI: 0.92-1.07).ConclusionIn a word, CHD was significantly associated with an increased risk of developing cognitive impairment.
Project description:Heart failure (HF) is a terminal stage of cardiovascular diseases, classified based on ejection fraction. Serum uric acid (SUA) has been implicated in the pathogenesis and progression of coronary artery disease (CAD) with HF, yet its predictive value remains unclear. This study aimed to evaluate the predictive role of SUA in the progression of HF in CAD patients and its potential to differentiate HF types. A retrospective analysis was conducted on 342 CAD patients, including 29 with CAD alone and 313 with CAD complicated by varied HF types. Biochemical parameters and HF severity were assessed, and logistic regression analyses were performed to identify independent predictors of HF progression. Significant differences were observed in biochemical parameters, including glutamic-pyruvic transaminase (ALT), glutamic oxalacetic transaminase (AST), alkaline phosphatase (ALP), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), creatine kinase-MB (CK-MB), SUA, lactate dehydrogenase (LDH), myoglobin (MTO), between groups. SUA levels were significantly higher in CAD patients with HF, particularly in those with reduced ejection fraction. Univariate and multivariate logistic regression analyses identified history of hypertension, AST, and SUA as independent predictors of HF progression, with SUA showing the highest odds ratio. In addition, SUA levels were positively correlated with Gensini scores, indicating its association with CAD severity. SUA is a strong predictor of HF progression in CAD patients, especially for patients with HFrEF, which can serve as a diagnostic and prognostic marker for HF progression in CAD patients.
Project description:BackgroundThe relationship between Parkinson's disease (PD) and coronary artery disease (CAD) is unclear.ObjectiveThis study aims to investigate whether PD and CAD are associated through systematic review and meta-analysis of observational studies.MethodsElectronic database search of PubMed, EMBASE, and Web of Science for observational studies published from 1 January 2010 to 1 August 2021 was conducted using terms related to PD and CAD. Unadjusted risk ratios (RR) and odds ratios (OR) of included cohort and case-control studies respectively were used to ascertain the association between PD and CAD. Study heterogeneity was evaluated using the I2 test.ResultsForty-one full-text studies were initially retrieved for eligibility assessment. Five studies that satisfied the inclusion criteria, consisting of three cohort and two case-control studies, were eventually included in this meta-analysis. The five studies enrolled 35,237 PD patients and 650,866 non-PD patients. PD and CAD were found to be significantly associated in cohort studies (RR = 2.23, 95% CI = 1.08-4.59, p = 0.03; Fig. 2), which held after sensitivity analysis (RR = 1.45, 95% CI = 1.31-1.60, p < 0.001; Fig. 3). Case-control studies found a trend towards association of PD and CAD approaching significance (OR = 1.47, 95% CI = 0.84-2.56, p = 0.18; Fig. 2).ConclusionOverall, this meta-analysis suggests that PD is associated with CAD. The underlying mechanisms, as well as the role of ethnicity and other comorbidities on the relationship between PD and CAD should be further explored.
Project description:BackgroundThe role of glaucoma in predicting Alzheimer's disease (AD) factors is unknown. This current meta-analysis was aimed at evaluating the risk of AD events in individuals suffering from glaucoma based on a meta-analysis.Materials and methodsDatabases which included Cochrane Library, PubMed, and EMBASE were searched to detect the relevant articles, with language being restricted to English. The risk of AD events in patients with glaucoma was analyzed using the combined hazard ratios.ResultsThis study included 8 articles with 131,987 subjects published after 2012. We identified glaucoma as the risk factor for disease-free survival (hazard ratio = 1.29; 95% confidence interval = 1.05-1.59; P = .000; I2 = 95.1%) in AD patients. According to subgroup analyses, normal tension glaucoma group was the major risk factor for disease-free survival of AD patients.ConclusionsAlthough diverse approaches have been used for AD cases of various events, the current meta-analysis indicates that that glaucoma patients have a higher AD risk.