Cardiovascular Risk in Rheumatoid Arthritis

Gkaliagkousi, Εugenia; Gavriilaki, Eleni; Doumas, Michael; Petidis, Konstantinos; Aslanidis, Spyros; Δούμα, Στέλλα

doi:10.1097/rhu.0b013e31827846b1

Cited by 55 publications

(23 citation statements)

References 81 publications

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“…4 Future studies should continue to address, in various murine and human systems, whether more targeted PAD inhibition might have therapeutic effects in reversing atherosclerosis rather than preventing it. Furthermore, given the well-recognized association between inflammatory disorders and atherosclerosis, 45-48 this preventive data could still have significant clinical implications for the subset of patients known to be prone to accelerated atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Peptidylarginine Deiminase Inhibition Reduces Vascular Damage and Modulates Innate Immune Responses in Murine Models of Atherosclerosis

Knight

Luo

O’Dell

et al. 2014

Circulation Research

361

322

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Rationale Neutrophil extracellular trap (NET) formation promotes vascular damage, thrombosis, and activation of interferon-α-producing plasmacytoid dendritic cells in diseased arteries. Peptidylarginine deiminase inhibition is a strategy that can decrease in vivo NET formation. Objective To test whether peptidylarginine deiminase inhibition, a novel approach to targeting arterial disease, can reduce vascular damage and inhibit innate immune responses in murine models of atherosclerosis. Methods and Results Apolipoprotein-E (Apoe)−/− mice demonstrated enhanced NET formation, developed autoantibodies to NETs, and expressed high levels of interferon-α in diseased arteries. Apoe−/− mice were treated for 11 weeks with daily injections of Cl-amidine, a peptidylarginine deiminase inhibitor. Peptidylarginine deiminase inhibition blocked NET formation, reduced atherosclerotic lesion area, and delayed time to carotid artery thrombosis in a photochemical injury model. Decreases in atherosclerosis burden were accompanied by reduced recruitment of netting neutrophils and macrophages to arteries, as well as by reduced arterial interferon-α expression. Conclusions Pharmacological interventions that block NET formation can reduce atherosclerosis burden and arterial thrombosis in murine systems. These results support a role for aberrant NET formation in the pathogenesis of atherosclerosis through modulation of innate immune responses.

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Section: Discussionmentioning

confidence: 99%

Peptidylarginine Deiminase Inhibition Reduces Vascular Damage and Modulates Innate Immune Responses in Murine Models of Atherosclerosis

Knight

Luo

O’Dell

et al. 2014

Circulation Research

361

322

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“…Subclinical atherosclerosis and vascular structure are measured through a noninvasive method of carotid intima-media thickness (CIMT) measurements in patients with RA10 ) . In addition to predicting the presence of local atheroma, the findings of CIMT can reveal possible damage to the arterial system11 ) .…”

Section: Introductionmentioning

confidence: 99%

Is There Any Relationship between Joint Destruction and Carotid Intima-media Thickness in Patients with Rheumatoid Arthritis?

Tutoğlu

Boyacı

et al. 2014

J Phys Ther Sci

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[Purpose] The purpose of this study was to investigate the possible relationship between joint destruction and carotid intima-media thickness in patients with rheumatoid arthritis. [Subjects and Methods] Thirty-four RA patients and 31 healthy controls were enrolled in this study. The disease activity for 28 joints was recorded for each patient using the erythrocyte sedimentation rate (DAS28ESR), a visual analog scale (VAS0–10 cm), and a disability index, the health assessment questionnaire (HAQ). X-ray imagesof the patients were scored according to the modified Sharp/van der Heijde method, and the common carotid intimal medial thickness (CIMT) was automatically measured with software using high-resolution Doppler ultrasound. [Results] Contrary to our hypothesis, the modified total Sharp score (mTSS) and CIMT were not significantly associated. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels of the RA patients and the right CIMT, left CIMT, and mean CIMT scores were significantly elevated. Positive correlation was detected between the mean CIMT score and age, CRP levels, LDL concentration and triglycerides (TG) level. In the regression model, where the mean CIMT was the independent variable and age, CRP, LDL, and TG were dependent variables, age was found to be an independent predictor of CIMT. [Conclusions] Patients suffering from RA require close monitoring for cardiovascular risks, and the comorbidity of age-related cardiovascular disease should not be overlooked.

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“…Inflammation states, such as inflammatory bowel disease [121, 122], rheumatoid arthritis, and low-grade systemic inflammation with increased C-reactive protein [123], are associated with the arterial stiffening process. Several anti-inflammatory drugs tested were shown to reduce arterial stiffness [124].…”

Section: Influence Of Drugs On Arterial Stiffnessmentioning

confidence: 99%

Arterial Stiffness and Cardiovascular Therapy

Janić

Lunder

Šabovič

2014

BioMed Research International

120

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The world population is aging and the number of old people is continuously increasing. Arterial structure and function change with age, progressively leading to arterial stiffening. Arterial stiffness is best characterized by measurement of pulse wave velocity (PWV), which is its surrogate marker. It has been shown that PWV could improve cardiovascular event prediction in models that included standard risk factors. Consequently, it might therefore enable better identification of populations at high-risk of cardiovascular morbidity and mortality. The present review is focused on a survey of different pharmacological therapeutic options for decreasing arterial stiffness. The influence of several groups of drugs is described: antihypertensive drugs (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, beta-blockers, diuretics, and nitrates), statins, peroral antidiabetics, advanced glycation end-products (AGE) cross-link breakers, anti-inflammatory drugs, endothelin-A receptor antagonists, and vasopeptidase inhibitors. All of these have shown some effect in decreasing arterial stiffness. Nevertheless, further studies are needed which should address the influence of arterial stiffness diminishment on major adverse cardiovascular and cerebrovascular events (MACCE).

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Cardiovascular Risk in Rheumatoid Arthritis

Cited by 55 publications

References 81 publications

Peptidylarginine Deiminase Inhibition Reduces Vascular Damage and Modulates Innate Immune Responses in Murine Models of Atherosclerosis

Peptidylarginine Deiminase Inhibition Reduces Vascular Damage and Modulates Innate Immune Responses in Murine Models of Atherosclerosis

Is There Any Relationship between Joint Destruction and Carotid Intima-media Thickness in Patients with Rheumatoid Arthritis?

Arterial Stiffness and Cardiovascular Therapy

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