Different Type of Carotid Arterial Wall Remodeling in Rheumatoid Arthritis Compared with Healthy Subjects: A Case-Control Study

2012 ◽  
Vol 39 (12) ◽  
pp. 2261-2266 ◽  
Author(s):  
ALPER M. VAN SIJL ◽  
KATJA VAN DEN HURK ◽  
MIKE J.L. PETERS ◽  
VOKKO P. VAN HALM ◽  
GIEL NIJPELS ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Healthy Subjects ◽  
Arterial Wall ◽  
Alternative Pathway ◽  
Wall Stress ◽  
Arterial Remodeling ◽  
Plaque Instability ◽  
Increased Risk ◽  
Carotid Arterial

Objective.Rheumatoid arthritis (RA) is associated with an increased cardiovascular (CV) risk, but mechanisms behind this increased risk have not been fully elucidated. Carotid arterial remodeling is the change of structural properties in response to hemodynamic or metabolic factors aimed at keeping wall stress within certain limits. This process might become maladaptive when stress on the arterial wall increases beyond these limits. We investigated whether maladaptive carotid arterial remodeling is present in RA compared with control subjects.Methods.The 2 cohorts were 96 patients with RA and 274 healthy subjects, who were investigated cross-sectionally. Carotid intima-media thickness (cIMT) and interadventitial diameter (IAD) were assessed by B-mode carotid ultrasonography. Lumen diameter (LD), circumferential wall stress (CWS), and circumferential wall tension (CWT) were calculated. Linear regression analyses were used to investigate the association between presence of RA and carotid arterial remodeling.Results.Compared with healthy subjects, RA was associated with a 0.40 mm (9.3%) greater LD, 0.41 mm (7.8%) greater IAD, 10% higher CWS, and 8% higher CWT. The groups had comparable cIMT. Associations remained similar after exclusion of patients with prior CV disease and after adjustment for demographic factors and CV risk factors.Conclusion.RA is associated with maladaptive outward carotid arterial remodeling. These results are relevant because maladaptive outward remodeling is associated with plaque instability and rupture. These results indicate an alternative pathway, beyond the traditional CV risk factors, in RA that amplifies the CV risk.

THU0044 Different type of carotid arterial wall remodeling in rheumatoid arthritis as compared to healthy subjects

2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 168.1-168
Author(s):  
A.M. van Sijl ◽  
K. van den Hurk ◽  
M.J. Peters ◽  
V.P. van Halm ◽  
G. Nijpels ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Healthy Subjects ◽  
Arterial Wall ◽  
Carotid Arterial

Cardiovascular Risk in Rheumatoid Arthritis and Mechanistic Links: From Pathophysiology to Treatment

2020 ◽  
Vol 18 (5) ◽  
pp. 431-446 ◽  
Author(s):  
George E. Fragoulis ◽  
Ismini Panayotidis ◽  
Elena Nikiphorou
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Current Evidence ◽  
Pharmacological Intervention ◽  
Cvd Risk ◽  
The Past ◽  
Increased Risk ◽  
Cv Disease ◽  
Obesity Hypertension ◽  
Inflammatory Burden

Rheumatoid arthritis (RA) is an autoimmune inflammatory arthritis. Inflammation, however, can spread beyond the joints to involve other organs. During the past few years, it has been well recognized that RA associates with increased risk for cardiovascular (CV) disease (CVD) compared with the general population. This seems to be due not only to the increased occurrence in RA of classical CVD risk factors and comorbidities like smoking, obesity, hypertension, diabetes, metabolic syndrome, and others but also to the inflammatory burden that RA itself carries. This is not unexpected given the strong links between inflammation and atherosclerosis and CVD. It has been shown that inflammatory cytokines which are present in abundance in RA play a significant role in every step of plaque formation and rupture. Most of the therapeutic regimes used in RA treatment seem to offer significant benefits to that end. However, more studies are needed to clarify the effect of these drugs on various parameters, including the lipid profile. Of note, although pharmacological intervention significantly helps reduce the inflammatory burden and therefore the CVD risk, control of the so-called classical risk factors is equally important. Herein, we review the current evidence for the underlying pathogenic mechanisms linking inflammation with CVD in the context of RA and reflect on the possible impact of treatments used in RA.

scholarly journals Cardiovascular Disease in Rheumatoid Arthritis: Risk Factors, Autoantibodies, and the Effect of Antirheumatic Therapies

2021 ◽  
Vol 14 ◽  
pp. 117954412110287
Author(s):  
Mir Sohail Fazeli ◽  
Vadim Khaychuk ◽  
Keith Wittstock ◽  
Boris Breznen ◽  
Grace Crocket ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Literature Review ◽  
Rheumatoid Factor ◽  
Qualitative Evidence Synthesis ◽  
Cvd Risk ◽  
Rheumatoid Arthritis Risk ◽  
Published Evidence ◽  
Increased Risk

Objective: To scope the current published evidence on cardiovascular risk factors in rheumatoid arthritis (RA) focusing on the role of autoantibodies and the effect of antirheumatic agents. Methods: Two reviews were conducted in parallel: A targeted literature review (TLR) describing the risk factors associated with cardiovascular disease (CVD) in RA patients; and a systematic literature review (SLR) identifying and characterizing the association between autoantibody status and CVD risk in RA. A narrative synthesis of the evidence was carried out. Results: A total of 69 publications (49 in the TLR and 20 in the SLR) were included in the qualitative evidence synthesis. The most prevalent topic related to CVD risks in RA was inflammation as a shared mechanism behind both RA morbidity and atherosclerotic processes. Published evidence indicated that most of RA patients already had significant CV pathologies at the time of diagnosis, suggesting subclinical CVD may be developing before patients become symptomatic. Four types of autoantibodies (rheumatoid factor, anti-citrullinated peptide antibodies, anti-phospholipid autoantibodies, anti-lipoprotein autoantibodies) showed increased risk of specific cardiovascular events, such as higher risk of cardiovascular death in rheumatoid factor positive patients and higher risk of thrombosis in anti-phospholipid autoantibody positive patients. Conclusion: Autoantibodies appear to increase CVD risk; however, the magnitude of the increase and the types of CVD outcomes affected are still unclear. Prospective studies with larger populations are required to further understand and quantify the association, including the causal pathway, between specific risk factors and CVD outcomes in RA patients.

scholarly journals Rheumatoid arthritis: influence of inflammation and anti-inflammatory therapy on cardiovascular risk factors

2020 ◽  
pp. 32-44
Author(s):  
D. I. Trukhan ◽  
D. S. Ivanova ◽  
K. D. Belus
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Cardiovascular Risk Factors ◽  
Chronic Inflammation ◽  
Pharmacological Intervention ◽  
Increased Risk ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Rheumatoid arthritis is a frequent and one of the most severe immuno-inflammatory diseases in humans, which determines the great medical and socio-economic importance of this pathology. One of the priority problems of modern cardiac rheumatology is an increased risk of cardiovascular complications in rheumatoid arthritis. In patients with rheumatoid arthritis, traditional cardiovascular risk factors for cardiovascular diseases (metabolic syndrome, obesity, dyslipidemia, arterial hypertension, insulin resistance, diabetes mellitus, smoking and hypodynamia) and a genetic predisposition are expressed. Their specific features also have a certain effect: the “lipid paradox” and the “obesity paradox”. However, chronic inflammation as a key factor in the development of progression of atherosclerosis and endothelial dysfunction plays a leading role in morbidity and mortality from cardiovascular diseases in rheumatoid arthritis. This review discusses the effect of chronic inflammation and its mediators on traditional cardiovascular risk factors and its independent significance in the development of CVD. Drug therapy (non-steroidal anti-inflammatory drugs, glucocorticosteroids, basic anti-inflammatory drugs, genetically engineered biological drugs) of the underlying disease also has a definite effect on cardiovascular risk factors in patients with rheumatoid arthritis. A review of studies on this problem suggests a positive effect of pharmacological intervention in rheumatoid arthritis on cardiovascular risk factors, their reduction to a level comparable to the populations of patients not suffering from rheumatoid arthritis. The interaction of rheumatologists, cardiologists and first-contact doctors (therapist and general practitioner) in studying the mechanisms of the development of atherosclerosis in patients with rheumatoid arthritis will allow in real clinical practice to develop adequate methods for the timely diagnosis and prevention of cardiovascular diseases in patients with rheumatoid arthritis.

Abstract 5825: Association between Patterns of FDG Uptake and Arterial Wall Calcification on PET/CT and Atherogenic Risk Factors in Healthy Subjects

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hiroya Narumi ◽  
Katsuya Yoshida ◽  
Nobusada Funabashi ◽  
Naotake Hashimoto ◽  
Isao Umehara ◽  
...  
Keyword(s):  
Risk Factors ◽  
Vascular Calcification ◽  
Healthy Subjects ◽  
Arterial Wall ◽  
Calcium Score ◽  
The Other ◽  
Fdg Uptake ◽  
Other Hand ◽  
Pet Ct ◽  
Fdg Pet Ct

Background: Augmented metabolic activity of macrophages leads to enough F-18 Fluorodeoxyglucose (FDG) uptake to allow visualization by positron emission tomography (PET). A large body of data, based on computed tomography (CT), has also accumulated concerning the relevance of vascular calcification to the atherosclerotic process. FDG PET/CT can localize both inflammatory changes and vascular calcification. The purpose of this study was to investigate risk factors contributing to these changes in the aorta in healthy subjects. Materials and Methods: A total of 66 consecutive healthy subjects (44 men, 22 women; age range, 30–82 years, mean age, 55.8 years) participating in a health check protocol including FDG PET/CT were evaluated retrospectively. We placed regions of interest on the arterial wall to measure FDG uptake by PET images. To assess arterial calcification, the calcium score of the aorta was measured on CT images. Results: FDG uptake was observed most commonly in proximal, followed by descending, thoracic, and abdominal segments. On the other hand, the most common site of vascular calcification was the descending thoracic aorta, followed by abdominal and, proximal segment. Whole aortic calcification (total calcium score of the whole aorta) was significantly correlated with age (r= 0.353, P= 0.004). On the other hand, FDG uptake (total SUV max of the whole aorta) was significantly correlated with systolic blood pressure (SBP) (r= 0.303, P= 0.013), triglyceride (TG) (r= 0.281, P= 0.022), fasting plasma glucose (FPG) (r= 0.317, P= 0.010), HbA1c (r= 0.433, P< 0.001), visceral abdominal fat area (r= 0.319, P= 0.005), and was negatively correlated with high density lipoprotein (HDL) (r= −0.317, P= 0.010), and adiponectin (r= −0.273, P= 0.029). Conclusions: Aortic calcification was significantly correlated with age. On the other hand, FDG uptake was significantly correlated with the components of metabolic syndrome such as SBP, TG, FPG, HbA1c, visceral adipose fat area and negatively correlated with HDL and adiponectin, but not with age. Our results may suggest that the components of metabolic syndrome and aging affect the progression of atherosclerosis differently.

scholarly journals Risk of Obstructive Sleep Apnea and Its Association with Cardiovascular and Noncardiac Vascular Risk in Patients with Rheumatoid Arthritis: A Population-based Study

2017 ◽  
Vol 45 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Katelynn M. Wilton ◽  
Eric L. Matteson ◽  
Cynthia S. Crowson
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Medical Information ◽  
Statistical Significance ◽  
Vascular Events ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
Large Joint

Objective.To define the incidence of obstructive sleep apnea (OSA) in patients with rheumatoid arthritis (RA) and determine whether OSA diagnosis predicts future cardiovascular disease (CVD) and noncardiac vascular events.Methods.Medical information pertaining to RA, OSA, CVD, and vascular diagnoses was extracted from a comprehensive medical record system for a geographically defined population of 813 patients previously diagnosed with RA and 813 age- and sex-matched comparator subjects.Results.The risk for OSA in persons with RA versus comparators was elevated, although not reaching statistical significance (HR 1.32, 95% CI 0.98–1.77; p = 0.07). Patients with RA were more likely to be diagnosed with OSA if they had traditional risk factors for OSA, including male sex, current smoking status, hypertension, diabetes, dyslipidemia, and increased body mass index. Features of RA disease associated with OSA included large joint swelling and joint surgery. Patients with RA with decreased renal function were also at higher risk of OSA. The increased risk of overall CVD among patients with RA who have OSA was similar to the increased CVD risk associated with OSA in the comparator cohort (interaction p = 0.86). OSA diagnosis was associated with an increased risk of both CVD (HR 1.9, 95% CI 1.08–3.27), and cerebrovascular disease (HR 2.4, 95% CI 1.14–5.26) in patients with RA.Conclusion.Patients with RA may be at increased risk of OSA secondary to both traditional and RA-related risk factors. Diagnosis with OSA predicts future CVD in RA and may provide an opportunity for CVD intervention.

scholarly journals Risk of venous thromboembolism associated with Janus kinase inhibitors for rheumatoid arthritis: case presentation and literature review

2021 ◽  
Author(s):  
Shunsuke Mori ◽  
Fumihiko Ogata ◽  
Ryusuke Tsunoda
Keyword(s):  
Rheumatoid Arthritis ◽  
Diabetes Mellitus ◽  
Risk Factors ◽  
Pulmonary Embolism ◽  
Venous Thromboembolism ◽  
Disease Activity ◽  
Janus Kinase ◽  
Advanced Age ◽  
Jak Inhibitors ◽  
Increased Risk

AbstractJanus kinase (JAK) inhibitors have been developed as disease-modifying antirheumatic drugs. Despite the positive therapeutic impacts of JAK inhibitors, concerns have been raised regarding the risk of venous thromboembolism (VTE), such as deep vein thrombosis (DVT) and pulmonary embolism (PE). A recent post hoc safety analysis of placebo-controlled trials of JAK inhibitors in rheumatoid arthritis (RA) reported an imbalance in the incidence of VTE for a 4-mg daily dose of baricitinib versus placebo. In a recent postmarketing surveillance trial for RA, a significantly higher incidence of PE was reported in treatment with tofacitinib (10 mg twice daily) compared with tofacitinib 5 mg or tumor necrosis factor inhibitors. We also experienced a case of massive PE occurring 3 months after starting baricitinib (4 mg once daily) for multiple biologic-resistant RA. Nevertheless, the evidence to support the role of JAK inhibitors in VTE risk remains insufficient. There are a number of predisposing conditions and risk factors for VTE. In addition to the known risk factors that can provoke VTE, advanced age, obesity, diabetes mellitus, hypertension, hyperlipidemia, and smoking can also contribute to its development. Greater VTE risk is noted in patients with chronic inflammatory conditions, particularly RA patients with uncontrolled disease activity and any comorbidity. Prior to the initiation of JAK inhibitors, clinicians should consider both the number and strength of VTE risk factors for each patient. In addition, clinicians should advise patients to seek prompt medical help if they develop clinical signs and symptoms that suggest VTE/PE. Key Points• Patients with rheumatoid arthritis (RA) are at increased risk of venous thromboembolism (VTE), especially those with uncontrolled, high disease activity and those with comorbidities.• In addition to the well-known risk factors that provoke VTE events, advanced age and cardiovascular risk factors, such as obesity, diabetes mellitus, hypertension, hyperlipidemia, and smoking, should be considered risk factors for VTE.• Although a signal of VTE/pulmonary embolism (PE) risk with JAK inhibitors has been noted in RA patients who are already at high risk, the evidence is currently insufficient to support the increased risk of VTE during RA treatment with JAK inhibitors.• If there are no suitable alternatives, clinicians should prescribe JAK inhibitors with caution, considering both the strength of individual risk factors and the cumulative weight of all risk factors for each patient.

scholarly journals Carotid Arterial Stiffness and Cardiometabolic Profiles in Women with Fibromyalgia

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1786
Author(s):  
Yunkyung Kim ◽  
Geun-Tae Kim ◽  
Jihun Kang
Keyword(s):  
Risk Factors ◽  
Arterial Stiffness ◽  
Central Obesity ◽  
Cardiometabolic Risk ◽  
Statistical Significance ◽  
Cardiometabolic Risk Factors ◽  
Control Group ◽  
Increased Risk ◽  
Carotid Arterial ◽  
High Triglyceride

Background: The present study aimed to evaluate the association between FM and cardiometabolic risk factors and carotid arterial stiffness in FM patients. Methods: The cardiometabolic risk profile was defined based on the Adult Treatment Panel III panel. Carotid intimal media thickness (cIMT) and arterial stiffness were assessed using high-resolution ultrasonography. Multivariate logistic analysis was performed to estimate the association between FM and cardiometabolic risk factors. We used a general linear regression to compare the cIMT and carotid beta-index between the participants with and without FM. Pearson’s coefficient was calculated to evaluate the potential correlation between cardiometabolic risk profiles, cIMT, and arterial stiffening in FM. Results: FM participants showed a higher risk of central obesity (odds ratio [OR] = 3.21, 95% confidence interval [CI] 1.49, 6.91), high triglyceride (OR = 4.73, 95% CI 2.29, 9.79), and impaired fasting glucose (IFG) (OR = 4.27, 95% CI 2.07, 8.81) compared to the control group. The FM group exhibited higher beta-index values than the control group (p = 0.003). Although IFG and triglyceride glucose index showed a tendency to correlate with the beta-index, statistical significance was not observed. Conclusions: FM was associated with an increased risk of central obesity, high triglyceride levels, and IFG. Furthermore, advanced arterial stiffness of the carotid artery was observed in FM, which might be correlated with insulin resistance.

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