Causal Association between Periodontal Diseases and Cardiovascular Diseases.
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ABSTRACT:
SUBMITTER: Zhou M
PROVIDER: S-EPMC8775300 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background Cardiovascular diseases (CVD), including coronary heart disease (CHD), heart failure, ischemic heart disease (IHD), and atrial fibrillation, are prevalent in the aged. However, the influence of CVD on ED is less investigated. This study was performed to clarify the causal association between CVD and ED. Materials and methods Genome-wide association studies (GWAS) datasets targeting CHD, heart failure, IHD, and atrial fibrillation were downloaded to retrieve single nucleotide polymorphisms (SNPs). Further, single-variable Mendelian randomization and multivariable Mendelian randomization (MVMR) were adopted to explore the causal association between CVD and ED. Results Genetically predicted CHD and heart failure were found to increase the risks of ED (OR = 1.09, P < 0.05 and OR = 1.36, P < 0.05, respectively). However, no causal association was disclosed among IHD, atrial fibrillation and ED (all P > 0.05). These findings remained consistent in sensitivity analyses. After controlling for body mass index, alcohol, low density lipoprotein, smoking and total cholesterol levels, the results of MVMR support the causal role of CHD on ED (P < 0.05). Similarly, the direct causal effect estimates of heart failure on ED were significant in MVMR analyses (P < 0.05). Conclusion Using genetic data, this study revealed that genetically predicted CHD and heart failure may predict better ED compared with atrial fibrillation and IHD. The results should be interpreted with caution and the insignificant causal inference of IHD still needs further verification in future studies.
| S-EPMC9947236 | biostudies-literature
Project description:BackgroundExcessive daytime sleepiness (EDS), experienced in 10% to 20% of the population, has been associated with cardiovascular disease and death. However, the condition is heterogeneous and is prevalent in individuals having short and long sleep duration. We sought to clarify the relationship between sleep duration subtypes of EDS with cardiovascular outcomes, accounting for these subtypes.Methods and resultsWe defined 3 sleep duration subtypes of excessive daytime sleepiness: normal (6-9 hours), short (<6 hours), and long (>9 hours), and compared these with a nonsleepy, normal-sleep-duration reference group. We analyzed their associations with incident myocardial infarction (MI) and stroke using medical records of 355 901 UK Biobank participants and performed 2-sample Mendelian randomization for each outcome. Compared with healthy sleep, long-sleep EDS was associated with an 83% increased rate of MI (hazard ratio, 1.83 [95% CI, 1.21-2.77]) during 8.2-year median follow-up, adjusting for multiple health and sociodemographic factors. Mendelian randomization analysis provided supporting evidence of a causal role for a genetic long-sleep EDS subtype in MI (inverse-variance weighted β=1.995, P=0.001). In contrast, we did not find evidence that other subtypes of EDS were associated with incident MI or any associations with stroke (P>0.05).ConclusionsOur study suggests the previous evidence linking EDS with increased cardiovascular disease risk may be primarily driven by the effect of its long-sleep subtype on higher risk of MI. Underlying mechanisms remain to be investigated but may involve sleep irregularity and circadian disruption, suggesting a need for novel interventions in this population.
| S-EPMC10863774 | biostudies-literature
Project description:Positive association between cardiovascular diseases and osteoporosis is important because it concerns two major public health problems. Men and women with cardiovascular diseases (including severe abdominal aortic calcification (AAC) and peripheral arterial disease) tend to have lower areal and volumetric bone mineral density (BMD) as well as faster bone loss, although findings vary according to skeletal site. On one hand, severe forms of cardiovascular diseases (heart failure, myocardial infarction, hypertension, severe AAC) are associated with higher risk of osteoporotic fracture, especially hip fracture. This link was found in the studies based on healthcare databases and the cohort studies. On the other hand, low BMD, history of fragility fracture, vitamin D deficit and increased bone resorption are associated with higher risk of major cardiovascular events (myocardial infraction, stroke, cardiovascular mortality). Moreover, osteocalcin secreted by osteoblasts may be involved in the regulation of energetic and cardiovascular metabolism. The association between both pathologies depends partially on the shared risk factors, and also on the mechanisms that are involved in the regulation of bone and cardiovascular metabolism. Interpretation of the data should take into account methodological limitations: representativeness of the cohorts, quality of the registers and the information obtained from questionnaires, severity of diseases, number of events (statistical power) and their temporal closeness, availability of the information on potential confounders. It seems that patients with severe form of osteoporosis would benefit from assessment of the cardiovascular status and vice versa. However, official guidelines for the clinical practice are still lacking.
| S-EPMC3727856 | biostudies-other
Project description:Background We aimed to determine whether the plasma cystatin C is a causal risk factor for cardiovascular events, stroke, myocardial infarction (MI), and cardiovascular disease (CVD) mortality by conducting Mendelian randomization (MR) designs. Methods Our study included 277,057 individuals free of CVDs or cancer at baseline in the UK Biobank. The genetic scores of plasma cystatin C comprising 67 single-nucleotide polymorphisms were calculated on the basis of data from a large genome-wide association study. By stratifying the genetic score, we conducted cox regression to assess the relationship between plasma cystatin C and CVDs. In this study, linear MR analysis was used to estimate the causal association between plasma cystatin C and CVDs. Results Observational analyses showed that plasma cystatin C concentrations were associated with the risk of CVDs [hazard ratios (HR) per standard deviation (SD) 1.09, 95% confidence interval (CI); 1.07–1.10] and CVD mortality (1.14, 1.11–1.17). Among CVDs, plasma cystatin C were associated with stroke (1.10, 1.08–1.11) and MI (1.08, 1.07–1.10). Linear MR analysis did not provide evidence of a causal association between plasma cystatin C and the risk of CVDs [odds ratio (OR) per SD 0.96, 95% CI;0.90–1.03], stroke (0.96, 0.93–1.01), MI (0.97, 0.91–1.03), and CVD mortality (0.98, 0.96–1.01), with consistent estimates from sensitivity analyses. Conclusion Observational findings indicated that higher plasma cystatin C is associated with a higher risk of CVDs; According to MR studies, there is no causal association between plasma cystatin C and the risk of CVDs and CVD mortality.
| S-EPMC10472449 | biostudies-literature
Project description:BackgroundObservational studies have suggested that paternal longevity is associated with reduced risks of cardiovascular diseases, yet the causal association remains to be determined.ObjectivesTo investigate whether Mendelian randomization (MR) results support a causal role of paternal longevity for risks of cardiovascular diseases.MethodsGenetic variants associated with paternal longevity and cardiovascular diseases were obtained from public genome-wide association study data. We used inverse variance weighted MR under a random-effects model to provide causal estimates between paternal longevity and cardiovascular diseases.ResultsPaternal longevity was associated with decreased risks of coronary heart disease (odds ratio (OR): 0.08; 95% confidence interval (CI): 0.02-0.37; p = 0.001) and peripheral artery disease (OR: 0.15; 95% CI: 0.03-0.65; p = 0.011). No significant differences were observed in hypertension, atrial fibrillation, heart failure, transient ischemic attack, ischemic stroke, or cardiac death. The weighted median method revealed consistent results between genetically instrumented paternal longevity and decreased risk of coronary heart disease and peripheral artery disease. No significant differences were observed in the MR-Egger results. Multivariable MR consistently indicated causal associations between paternal longevity and decreased cardiovascular diseases. The leave-one-out analysis suggested that the causal associations were not affected by individual single-nucleotide polymorphisms. The intercept of the MR-Egger estimator and funnel plot revealed no indication of horizontal pleiotropic effects.ConclusionsOur MR analyses supported a causal role of paternal longevity for decreased risks of coronary heart disease and peripheral artery disease, which highlighted the need for better monitoring and intervention of cardiovascular diseases in populations with premature paternal death.
| S-EPMC9332106 | biostudies-literature
Project description:ObjectivesTo assess the relationship between the presence of periodontal disease and halitosis.MethodsA total of 120 patients were enrolled and divided into 2 groups, 60 patients with probing depth (PD) > 3.0 mm (group 1) and 60 patients with PD ≤ 3.0 mm (group 2). Clinical parameters including, plaque index (PI), bleeding index (BI), and PD were obtained. Breath samples were collected and analyzed using a portable gas chromatograph to measure the concentration of volatile sulfur compounds (VSC).ResultsHalitosis was found to affect 58.3% of the total patients. The means of PI, BI, and VSC were significantly higher in group 1 (PD > 3.0 mm) than in group 2 (PD ≤ 3 mm).ConclusionsThe percentage of patients suffering from halitosis in the Saudi population are comparatively high. In addition, there was a positive association between periodontal disease and halitosis.
| S-EPMC7801244 | biostudies-literature
Project description:Disorders of lipoprotein metabolism have been linked with an increased risk of cardiovascular diseases (CVDs) but the causal association is unclear. In this study, we investigated the causal association between disorders of lipoprotein metabolism and CVDs using two-sample Mendelian randomization (MR). The exposure was obtained from Finn genome-wide association studies (14,010 cases, 197,259 controls), and the corresponding CVDs were extracted from the largest published genome-wide association studies. A random-effects inverse-variance weighted method was used for the main analyses with a complementary analysis using the weighted median and MR-Egger approaches. Multiple sensitivity analyses were performed to assess horizontal pleiotropy. The MR analysis indicated positive associations of disorders of lipoprotein metabolism with coronary artery disease (odds ratio [OR] 1.670, 95% confidence interval [CI] 1.373-2.031; p < 0.001), aortic aneurysm (OR 1.394, 95% CI 1.199-1.619; p < 0.001), heart failure (OR 1.20, 95% CI 1.115-1.294; p < 0.001), hypertension (OR 1.011, 95% CI 1.006-1.091; p < 0.001), old myocardial infarction (OR 1.004, 95% CI 1.002-1.007; p = 0.001), and stroke (OR 1.002, 95% CI 1.001-1.003; p = 0.002). There is a suggestive causal relationship between disorders of lipoprotein metabolism and atrial fibrillation (OR 1.047, 95% CI 1.006-1.091; p = 0.026) and acute myocardial infarction (OR 1.003, 95% CI 1.001-1.005; p = 0.012). There was limited evidence of a causal association between disorders of lipoprotein metabolism and peripheral vascular disease and venous thromboembolism. Our findings indicate a significant causal association between disorders of lipoprotein metabolism and many CVDs, including coronary artery disease, aortic aneurysm, heart failure, hypertension, old myocardial infarction, and stroke. These associations may be useful for development of treatment strategies that regulate lipoprotein metabolism in patients with CVD.
| S-EPMC9593056 | biostudies-literature
Project description:ImportanceIt is uncertain whether depressive symptoms are independently associated with subsequent risk of cardiovascular diseases (CVDs).ObjectiveTo characterize the association between depressive symptoms and CVD incidence across the spectrum of lower mood.Design, setting, and participantsA pooled analysis of individual-participant data from the Emerging Risk Factors Collaboration (ERFC; 162 036 participants; 21 cohorts; baseline surveys, 1960-2008; latest follow-up, March 2020) and the UK Biobank (401 219 participants; baseline surveys, 2006-2010; latest follow-up, March 2020). Eligible participants had information about self-reported depressive symptoms and no CVD history at baseline.ExposuresDepressive symptoms were recorded using validated instruments. ERFC scores were harmonized across studies to a scale representative of the Center for Epidemiological Studies Depression (CES-D) scale (range, 0-60; ≥16 indicates possible depressive disorder). The UK Biobank recorded the 2-item Patient Health Questionnaire 2 (PHQ-2; range, 0-6; ≥3 indicates possible depressive disorder).Main outcomes and measuresPrimary outcomes were incident fatal or nonfatal coronary heart disease (CHD), stroke, and CVD (composite of the 2). Hazard ratios (HRs) per 1-SD higher log CES-D or PHQ-2 adjusted for age, sex, smoking, and diabetes were reported.ResultsAmong 162 036 participants from the ERFC (73%, women; mean age at baseline, 63 years [SD, 9 years]), 5078 CHD and 3932 stroke events were recorded (median follow-up, 9.5 years). Associations with CHD, stroke, and CVD were log linear. The HR per 1-SD higher depression score for CHD was 1.07 (95% CI, 1.03-1.11); stroke, 1.05 (95% CI, 1.01-1.10); and CVD, 1.06 (95% CI, 1.04-1.08). The corresponding incidence rates per 10 000 person-years of follow-up in the highest vs the lowest quintile of CES-D score (geometric mean CES-D score, 19 vs 1) were 36.3 vs 29.0 for CHD events, 28.0 vs 24.7 for stroke events, and 62.8 vs 53.5 for CVD events. Among 401 219 participants from the UK Biobank (55% were women, mean age at baseline, 56 years [SD, 8 years]), 4607 CHD and 3253 stroke events were recorded (median follow-up, 8.1 years). The HR per 1-SD higher depression score for CHD was 1.11 (95% CI, 1.08-1.14); stroke, 1.10 (95% CI, 1.06-1.14); and CVD, 1.10 (95% CI, 1.08-1.13). The corresponding incidence rates per 10 000 person-years of follow-up among individuals with PHQ-2 scores of 4 or higher vs 0 were 20.9 vs 14.2 for CHD events, 15.3 vs 10.2 for stroke events, and 36.2 vs 24.5 for CVD events. The magnitude and statistical significance of the HRs were not materially changed after adjustment for additional risk factors.Conclusions and relevanceIn a pooled analysis of 563 255 participants in 22 cohorts, baseline depressive symptoms were associated with CVD incidence, including at symptom levels lower than the threshold indicative of a depressive disorder. However, the magnitude of associations was modest.
| S-EPMC7739139 | biostudies-literature
Project description:BackgroundSleep-disordered breathing (SDB) is a chronic sleep-related breathing disorder, considered associated with increased risk of cardiovascular disorders, metabolic disorders, cognitive dysfunction and behavior changes. Periodontal diseases are chronic infectious diseases that are also believed to be associated with cardiovascular diseases, metabolic syndrome and cognitive dysfunction. Several studies have indicated that SDB may be associated with periodontal diseases through certain mechanisms such as inflammation response, oxidative stress and oral dryness. The aim of this systematic review is to explore the association between SDB and periodontal diseases in an integrated approach.Materials and methodsThis systematic review will include cohort studies, cross-sectional studies and case-control studies that are identified by electronic and manual searches. Electronic searches will be conducted in the following databases: PubMed, Embase, Scopus and Web of Science. Our search will cover articles published from inception of databases to March 2022 without restrictions in language and settings. Pre-determined eligibility criteria include: participants (participants without a history of respiratory diseases, history of periodontal treatment within the past 6 months and history of medication that is known to influence SDB or periodontal diseases); exposure (participants who have been diagnosed with SDB or at high-risk for SDB); comparison (participants without SDB); and outcome (periodontal parameters, such as probing depth, clinical attachment level, bleeding on probing, radiographic bone loss). Two authors will perform study screening and data extraction independently and in duplicate. All discrepancies will be solved by discussion. The methodological quality of included studies will be assessed using the Newcastle-Ottawa Scale.DiscussionThis systematic review will summarize the existing evidence on the association between SDB and periodontal diseases, a topic of controversy and clinical significance. Its findings can provide evidence for the development of relevant prevention and treatment strategies. The results will be disseminated through peer-reviewed journals.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42022313024. Registered on March 28th 2022.
| S-EPMC9393785 | biostudies-literature
Project description:Major depressive disorder (MDD) is phenotypically associated with cardiovascular diseases (CVD). We aim to investigate mechanisms underlying relationships between MDD and CVD in the context of shared genetic variations. Polygenic overlap analysis was used to test genetic correlation and to analyze shared genetic variations between MDD and seven cardiovascular outcomes (coronary artery disease (CAD), heart failure, atrial fibrillation, stroke, systolic blood pressure, diastolic blood pressure, and pulse pressure measurement). Mendelian randomization analysis was used to uncover causal relationships between MDD and cardiovascular traits. By cross-trait meta-analysis, we identified a set of genomic loci shared between the traits of MDD and stroke. Putative causal genes for MDD and stroke were prioritized by fine-mapping of transcriptome-wide associations. Polygenic overlap analysis pointed toward substantial genetic variation overlap between MDD and CVD. Mendelian randomization analysis indicated that genetic liability to MDD has a causal effect on CAD and stroke. Comparison of genome-wide genes shared by MDD and CVD suggests 20q12 as a pleiotropic region conferring risk for both MDD and CVD. Cross-trait meta-analyses and fine-mapping of transcriptome-wide association signals identified novel risk genes for MDD and stroke, including RPL31P12, BORSC7, PNPT11, and PGF. Many genetic variations associated with MDD and CVD outcomes are shared, thus, pointing that genetic liability to MDD may also confer risk for stroke and CAD. Presented results shed light on mechanistic connections between MDD and CVD phenotypes.
| S-EPMC8631916 | biostudies-literature