Cardiovascular disease in patients with rheumatoid arthritis.
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ABSTRACT:
SUBMITTER: Liao KP
PROVIDER: S-EPMC5253086 | biostudies-other | 2017 Feb
REPOSITORIES: biostudies-other
Publications
Cardiovascular disease in patients with rheumatoid arthritis.
Trends in cardiovascular medicine 20160803 2
The risk of cardiovascular disease (CVD) in patients with rheumatoid arthritis (RA) is 1.5-2-fold higher than age- and sex-matched individuals from the general population. This excess risk is attributed to the systemic chronic inflammation which is a hallmark of RA. Challenges to optimizing CV risk management in RA include the need for improved methods to predict CV risk, and defining the target risk factor(s) to reduce CV risk. Lessons learned from RA studies can also inform CV risk prevention ...[more]
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Project description:BackgroundRheumatic disease and heart disease share common underpinnings involving inflammation. The high levels of inflammation that characterize rheumatic diseases provide a "natural experiment" to help elucidate the mechanisms by which inflammation accelerates heart disease. Rheumatoid arthritis (RA) is the most common of the rheumatic diseases and has the best studied relationships with heart disease.MethodsA review of current literature on heart disease and RA was conducted.ResultsPatients with RA have an increased risk of developing heart disease that is not fully explained by traditional cardiovascular risk factors. Therapies used to treat RA may also affect the development of heart disease; by suppressing inflammation, they may also reduce the risk of heart disease. However, their other effects, as in the case of steroids, may increase heart disease risk.ConclusionsInvestigations of the innate and adaptive immune responses occurring in RA may delineate novel mechanisms in the pathogenesis of heart disease and help identify novel therapeutic targets for the prevention and treatment of heart disease.
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Project description:ObjectivesPatients with rheumatoid arthritis (RA) have an increased mortality and morbidity due to cardiovascular disease (CVD). In this prospective 5-year follow up of patients with RA, we analysed several biomarkers, known to be associated with atherosclerosis and/or inflammation in the general population. The aim of this study was to find out whether the RA-disease per se affect these biomarkers and if those could be associated with the progression of atherosclerosis, as measured by intima media thickness (IMT) among patients with early RA.MethodsPatients from northern Sweden diagnosed with early RA, are consecutively recruited into an ongoing prospective study on CVD comorbidity. A subgroup of patients, aged ≤60 years (n = 71) was included for ultrasound measurements of IMT at inclusion (T0) and after 5 years (T5) together with age-sex-matched controls (n = 40). The patients were clinically assessed. Blood was analysed for lipids, ESR and CRP and several biomarkers known to be associated with atherosclerosis in the general population.ResultsAt T0, the patients with RA had significantly lower levels of MIF and significantly higher levels of interleukin (IL)-18 and MIC-1 compared with controls. At T5, the patients with RA had significantly higher levels of pentraxin3, MIC-1, TNF-R2, ICAM-1, VCAM-1 and endostatin compared with controls. At T0 the levels of MPO correlated with DAS28, sCD40L with CRP and IL-18 with systolic blood pressure and Reynolds risk score. Using PLSR on a CVD-panel analysed with multiplex immunoassay, the patients with RA could be correctly classified into those who had a worsening in their IMT over the five years or not. Here, MMP3 was identified as influential.ConclusionsThis study indicates that the RA disease itself could affect several of the biomarkers in this study, and possibly also the processes involved in the development of atherosclerosis.
| S-EPMC6681963 | biostudies-literature
Project description:Patients with rheumatoid arthritis (RA) suffer significantly increased cardiovascular (CV) morbidity and mortality, when compared with the general population. Both traditional CV risk factors and high levels of systemic inflammation have been linked to the increased CV risk in RA patients, but significant uncertainty remains regarding the mechanisms through which these factors contribute to CV disease (CVD). In addition, ongoing questions remain regarding how best to identify RA patients at high risk for CVD and what primary and secondary prevention strategies are effective at influencing CV outcome. The present review summarizes recent research in this field.
| S-EPMC3436948 | biostudies-literature
Project description:Patients with rheumatoid arthritis are at increased risk for cardiovascular disease. The prerequisites for reducing the risk of cardiovascular disease are adequate levels of knowledge and being aware of the risk. In this study, the levels of knowledge about cardiovascular disease among patients with rheumatoid arthritis and the perception were evaluated in relation to their actual 10-year risk of cardiovascular disease. This cross-sectional study of 200 patients with rheumatoid arthritis was conducted in a university-affiliated hospital in South Korea. The patients' actual risk of cardiovascular disease was estimated using the Framingham Risk Score. The most common risk factor was physical inactivity, with 77% of the patients not engaging in regular exercise. The patients lacked knowledge about the effects of physical inactivity and anti-inflammatory medication on the development of cardiovascular disease. Misperceptions about the risk of cardiovascular disease were common, i.e., 19.5% of the patients underestimated their risk and 41% overestimated. Hypertension, diabetes, obesity, and smoking were the most prevalent among the patients who underestimated their risk, and these same patients had the lowest level of knowledge about cardiovascular disease. This study demonstrated the rheumatoid arthritis patients' lack of knowledge about the effects of physical inactivity and anti-inflammatory medications on the development of cardiovascular disease, and their misperception of cardiovascular risk was common. As a preventive measure, educational programs about cardiovascular disease should be tailored specifically for patients with rheumatoid arthritis, and behavioral interventions, including routine exercise, should be made available at the time of diagnosis.
| S-EPMC5402932 | biostudies-literature
Project description:Cardiovascular (CV) disease is the most common cause of premature mortality in patients with rheumatoid arthritis (RA). It is the result of an accelerated atherosclerotic process. Both RA and atherosclerosis are complex polygenic diseases. Besides traditional CV risk factors and chronic inflammation, a number of studies have confirmed the role of genetic factors in the development of the atherogenesis observed in RA. In this regard, besides a strong association between the HLA-DRB1∗04 shared epitope alleles and both endothelial dysfunction, an early step in the atherosclerotic process, and clinically evident CV disease, other polymorphisms belonging to genes implicated in inflammatory and metabolic pathways, located inside and outside the HLA region, such as the 308 variant (G > A, rs1800629) of the TNFA locus, the rs1801131 polymorphism (A > C; position + 1298) of the MTHFR locus, or a deletion of 32 base pairs on the CCR5 gene, seem to be associated with the risk of CV disease in patients with RA. Despite considerable effort to decipher the genetic basis of CV disease in RA, further studies are required to better establish the genetic influence in the increased risk of CV events observed in patients with RA.
| S-EPMC3419432 | biostudies-literature
Project description:Objectives: Periodontal disease (PD) and rheumatoid arthritis (RA) are known chronic conditions with sustained inflammation leading to osteolysis. Cardiovascular diseases (CVD) are frequent comorbidities that may arise from sustained inflammation associated with both PD and RA. In order to determine CVD risk, alterations at the molecular level need to be identified. The objective of this study, therefore, was to assess the relationship of CVD associated biomarkers in RA patients and how it is influenced by PD. Methods: The study consisted of patient (26 RA with PD, 21 RA without PD, 51 patients with PD only) and systemically and periodontally healthy control (n = 20) groups. Periodontal parameters bleeding on probing, probing pocket depth, and marginal bone loss were determined to characterize the patient groups. Proteomic analysis of 92 CVD-related protein biomarkers was performed using a multiplex proximity extension assay. Biomarkers were clustered using the search tool for retrieval of interacting genes (STRING) to determine protein−protein interaction (PPI) networks. Results: RA patients with PD had higher detection levels for 47% of the measured markers (ANGPT1, BOC, CCL17, CCL3, CD4, CD84, CTRC, FGF-21, FGF-23, GLO1, HAOX1, HB-EGF, hOSCAR, HSP 27, IL16, IL-17D, IL18, IL-27, IL6, LEP, LPL, MERTK, MMP12, MMP7, NEMO, PAPPA, PAR-1, PARP-1, PD-L2, PGF, PIgR, PRELP, RAGE, SCF, SLAMF7, SRC, THBS2, THPO, TNFRSF13B, TRAIL-R2, VEGFD, VSIG2, and XCL1) as compared to RA without PD. Furthermore, a strong biological network was identified amongst these proteins (clustering coefficient = 0.52, PPI enrichment p-value < 0.0001). Coefficients for protein clusters involved in CVD (0.59), metabolic (0.53), and skeletal (0.51) diseases were strongest in the PD group. Conclusion: Periodontal disease augments CVD-related biomarkers in RA through shared pathological clusters, concurrently enhancing metabolic and skeletal disease protein interactions, independent of autoimmune status.
| S-EPMC8945365 | biostudies-literature
Project description:IntroductionThe aim of our study was to analyze the influence of the CCR5Δ32 polymorphism in the risk of cardiovascular (CV) events and subclinical atherosclerosis among patients with rheumatoid arthritis (RA).MethodsA total of 645 patients fulfilling the American Rheumatism Association 1987 revised classification criteria for RA were studied. Patients were genotyped for the CCR5 rs333 polymorphism using predesigned TaqMan assays. Also, HLA DRB1 genotyping was performed using molecular-based methods. Carotid intima-media thickness, flow-mediated endothelium-dependent dilatation (FMD) and endothelium-independent vasodilatation, which were used as surrogate markers of subclinical atherosclerosis, were measured in a subgroup of patients with no clinical CV disease.ResultsA lower frequency of carriers of the CCR5Δ32 allele among patients with CV events (3.4% versus 11.3%, P = 0.025, odds ratio 0.28, 95% confidence interval (95% CI) 0.06 to 0.89) was observed. However, after adjusting for gender, age at time of RA diagnosis, and the presence of shared epitope, rheumatoid factor and classic CV risk factors in the Cox regression analysis, this reduction of CV events in CCR5Δ32 allele carriers was slightly outside the range of significance (P = 0.097; hazard ratio 0.37 (95% CI 0.12 to 1.19)). Carriers of the CCR5Δ32 deletion also showed higher FMD values than the remaining patients (CCR5/CCR5Δ32 patients: 7.03% ± 6.61% versus CCR5/CCR5 patients: 5.51% ± 4.66%). This difference was statistically significant when analysis of covariance was performed (P = 0.024).ConclusionsOur results show a potential influence of the CCR5Δ32 deletion on the risk of CV disease among patients with RA. This may be due to a protective effect of this allelic variant against the development of vascular endothelial dysfunction.
| S-EPMC3239375 | biostudies-literature
Project description:Objective. To evaluate whether hyperuricemia is a risk factor for cardiovascular disease (CVD) in patients with rheumatoid arthritis (RA). Methods. A population-based inception cohort of patients diagnosed between 1980 and 2007 with adult-onset RA was assembled. A comparison cohort of age- and sex-matched subjects without RA (non-RA) was also assembled. All clinically obtained uric acid values were collected. CVD and noncardiac vascular events were recorded for each patient. Cox proportional hazards models were used to assess the impact of hyperuricemia on development of CVD, mortality, and noncardiac vascular disease. Results. In patients without RA, hyperuricemia was associated with heart failure (HR: 1.95; 95% CI: 1.13-3.39) and CVD (HR: 1.59; 95% CI: 0.99-2.55). In patients with RA, hyperuricemia was not significantly associated with CVD but was significantly associated with peripheral arterial events (HR: 2.52; 95% CI: 1.17-5.42). Hyperuricemia appeared to be more strongly associated with mortality among RA patients (HR: 1.96; 95% CI: 1.45-2.65) than among the non-RA subjects (HR: 1.57; 95% CI: 1.09-2.24). Conclusion. In patients with RA, hyperuricemia was a significant predictor of peripheral arterial events and mortality but not of CVD.
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Project description:IntroductionCardiovascular disease (CVD) is the leading cause of mortality in patients with rheumatoid arthritis (RA). Some studies have reported a decrease in CVD in patients with RA using hydroxychloroquine (HCQ). Most of these have had fewer participants and have analyzed only composite outcomes. We aimed to identify the association between the use of HCQ in patients with RA and the incidence of major adverse cardiac events (MACEs), cerebral infarction, and AMI.MethodsThis was a retrospective observational study using the TriNetX Diamond Network. Propensity score matching (PSM) was used to equilibrate the cohorts. The dependent variables in our study were MACE, cerebral infarction, and AMI.ResultsA total of 2,261,643 patients with RA were identified. Approximately 6% had been prescribed HCQ. Of those prescribed HCQ, 80% (112,743) were females, while of those not prescribed HCQ, 72.5% (1,536,937) were females. HCQ was associated with lower rates of MACE (HR 0.827, 95%CI 0.8,0.86), cerebral infarction (HR 0.824, 95% CI 0.78,0.87), and AMI (HR 0.9, 95% CI 0.85,0.96). These associations were not seen in patients taking biologics. HCQ was associated with lower MACE in all other subgroups.ConclusionIn conclusion, HCQ was slightly beneficial in decreasing MACE and cerebral infarction in patients with RA. These associations were significantly lower in patients taking methotrexate or biologics. Although there was a significant decrease in the risk of AMI in all patients with RA, these results were not replicated in subgroup analyses, and there was an apparent increased risk of AMI with the use of HCQ in patients using biologics.
| S-EPMC9532807 | biostudies-literature
Project description:BackgroundRheumatoid arthritis (RA) is characterized by increased cardiovascular (CV) mortality. CV events are particularly high in patients with RA-specific autoimmunity, including rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA), raising the question whether RA-specific autoimmunity itself is associated with CV events.MethodsNew CV events (myocardial infarction, stroke or death by CV cause) were recorded in 20,625 subjects of the Electricité de France - Gaz de France (GAZEL) cohort. Self-reported RA cases in the GAZEL cohort were validated by phone interview on the basis of a specific questionnaire. In 1618 subjects, in whom plasma was available, RF and ACPA were measured. A piecewise exponential Poisson regression was used to analyze the association of CV events with presence of RA as well as RA-specific autoimmunity (without RA).ResultsCV events in GAZEL were associated with age, male sex, smoking, hypertension, hyperlipidemia, and diabetes mellitus (HR from 1.06 to 1.87, p < 0.05). Forty-two confirmed RA cases were identified. Confirmed RA was significantly associated with CV risk increase (HR of 3.03; 95% CI: 1.13-8.11, p = 0.03) independently of conventional CV risk factors. One hundred seventy-eight subjects showed RF or ACPA positivity without presence of RA. CV events were not associated with ACPA positivity (HR: 1.52, 95% CI: 0.47-4.84, p = 0.48) or RF positivity (HR: 1.15, 95% CI: 0.55-2.40, p = 0.70) in the absence of RA.ConclusionsRA, as a clinical chronic inflammatory disease, but not mere positivity for RF or ACPA in the absence of clinical disease is associated with increased CV risk.
| S-EPMC8867622 | biostudies-literature