Cardiovascular Morbidity and Mortality in Women Diagnosed With Rheumatoid Arthritis

Solomon, Daniel H.; Karlson, Elizabeth W.; Rimm, Eric B.; Cannuscio, Carolyn C.; Mandl, Lisa A.; Manson, JoAnn E.; Stampfer, Meir J.; Curhan, Gary C.

doi:10.1161/01.cir.0000054612.26458.b2

Cited by 1,104 publications

(797 citation statements)

References 28 publications

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“…There is also an association between AS and RA [74]. In reality, cardiovascular disease, including coronary heart disease is a significant cause of death in RA [75] and AD patients [76]. P. gingivalis secreting PPAD is related to both RA [14] and AS [77].…”

Section: Discussionmentioning

confidence: 99%

Citrullination as a plausible link to periodontitis, rheumatoid arthritis, atherosclerosis and Alzheimer’s disease

Olsen

Singhrao

Potempa

2018

Journal of Oral Microbiology

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Periodontitis, rheumatoid arthritis (RA), atherosclerosis (AS), and Alzheimer’s disease (AD) are examples of complex human diseases with chronic inflammatory components in their etiologies. The initial trigger of inflammation that progresses to these diseases remains unresolved. Porphyromonas gingivalis is unique in its ability to secrete the P. gingivalis-derived peptidyl arginine deiminase (PPAD) and consequently offers a plausible and exclusive link to these diseases through enzymatic conversion of arginine to citrulline. Citrullination is a post-translational enzymatic modification of arginine residues in proteins formed as part of normal physiological processes. However, PPAD has the potential to modify self (bacterial) and host proteins by deimination of arginine amino acid residues, preferentially at the C-terminus. Migration of P. gingivalis and/or its secreted PPAD into the bloodstream opens up the possibility that this enzyme will citrullinate proteins at disparate body sites. Citrullination is associated with the pathogenesis of multifactorial diseases such as RA and AD, which have an elusive external perpetrator as they show epidemiological associations with periodontitis. Therefore, PPAD deserves some prominence as an external antigen, in at least, a subset of RA and AD cases, with as yet unidentified, immune/genetic vulnerabilities.

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Section: Discussionmentioning

confidence: 99%

Citrullination as a plausible link to periodontitis, rheumatoid arthritis, atherosclerosis and Alzheimer’s disease

Olsen

Singhrao

Potempa

2018

Journal of Oral Microbiology

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“…While IA patients are treated with disease modifying anti-rheumatic drugs (DMARDs) and biologic agents that reduce disease activity, multiple studies have demonstrated increased cardiovascular (CV) risk despite conventional anti-rheumatic therapy [4][5][6][7]. Several studies of rheumatoid arthritis (RA) patients with disease durations of less than 5 years demonstrated an increased CV risk, suggesting this excess risk is an early feature of RA [4,[8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

“…Several studies of rheumatoid arthritis (RA) patients with disease durations of less than 5 years demonstrated an increased CV risk, suggesting this excess risk is an early feature of RA [4,[8][9][10][11]. The risk appears to accumulate over time and persists after adjustment for other cardiovascular risk factors (relative risk of MI is greater than three after 10 years of having the disease) [6,12] suggesting that RA independently doubles the hazard for myocardial infarction and sudden cardiac death. The degree of increased risk of myocardial infarction in SLE patients varies, with risks as high as 50-fold in premenopausal women and decreasing to the risk of the general population in the elderly [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

“…The severity of inflammatory activity predicts CV events and mortality in RA patients [6,18,19]. Certain medications used to treat IA and SLE may also contribute to the increased risk of CVD, including nonsteroidal anti-inflammatory drugs (NSAIDs) [20], COX-2 inhibitors [5,20], steroids [21,22], and anti-folate medications such as methotrexate [23,24].…”

Section: Introductionmentioning

confidence: 99%

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Lack of cardiovascular risk assessment in inflammatory arthritis and systemic lupus erythematosus patients at a tertiary care center

2011

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The purpose of this study is to evaluate cardiovascular risk assessment at a Canadian rheumatology center and describe the cardiovascular risk of inflammatory arthritis (IA) and systemic lupus erythematosus (SLE) patients using the Framingham risk score. A retrospective chart review of 504 patients attending nine rheumatology practices at the University of Alberta Hospital was performed. A pre-specified case report form detailed patient demographics, cardiac risk factors, variables for the Framingham 2008 score, disease activity, and medication use. In this group of 504 patients, 64 (12.7%) had SLE (male (M) to female (F) ratio=60:4) and 440 (87.3%) had an IA (M to F ratio=117:323). Of the SLE patients, 31 (48.4%) met four or more American College of Rheumatology (ACR) criteria, 33 (51.6%) had less than four ACR criteria. Of the IA patients, 156 (35.5%) were CCP positive and 257 (58.4%) were RF positive. Utilizing the chart data, retrospective Framingham risk scores were calculable for one (1.6%) SLE patient and three (0.68%) IA patients. The most common cardiac risk factors not documented in the medical records of both the SLE and IA patients included: (1) positive family history of MI, (2) diabetes, and (3) lipid status. The blood pressure was more frequently documented in the SLE patients (93.8%) compared to the IA patients (56.1%). While traditional cardiac risk factors only partially contribute to the increased cardiovascular risk in these patients, cardiovascular risk assessment was suboptimally performed amongst a large group of rheumatologists. A dedicated cardiovascular risk reduction clinic for inflammatory rheumatic diseases has been established at this site to fulfill this need and evaluate treatment strategies.

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“…The epidemiology of stroke in RA is not as well studied as that of MI, with some studies demonstrating an increased risk of stroke 3, 4, 5, 6 and others finding no association between RA and stroke 7, 8, 9, 10. Strokes can be classified into 2 subtypes: ischemic and hemorrhagic.…”

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confidence: 99%

Association Between Ischemic Stroke and Tumor Necrosis Factor Inhibitor Therapy in Patients With Rheumatoid Arthritis

Low

Mercer

Watson

et al. 2016

Arthritis & Rheumatology

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ObjectivePatients with rheumatoid arthritis (RA) are at an increased risk of ischemic stroke. Tumor necrosis factor inhibitors (TNFi) may influence risk and mortality after ischemic stroke by reducing inflammation. This study was undertaken to examine the association of TNFi with the risk of incident ischemic stroke and with 30‐day and 1‐year mortality after ischemic stroke.MethodsPatients with RA starting therapy with TNFi and a biologics‐naive comparator group treated with synthetic disease‐modifying antirheumatic drugs (DMARDs) only were recruited to the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis from 2001 to 2009. Patients were followed up via clinical and patient questionnaires as well as the national death register. Incident strokes were classified as ischemic if brain imaging reports suggested ischemia or if ischemic stroke was reported as the underlying cause of death on a death certificate. Patients with a previous stroke were excluded. Risk of ischemic stroke was compared between patients receiving synthetic DMARDs only and those ever‐exposed to TNFi using a Cox proportional hazards regression model adjusted for potential confounders. Mortality after ischemic stroke was compared between synthetic DMARD–treated patients and TNFi‐treated patients using logistic regression, adjusted for age and sex.ResultsTo April 2010, 127 verified incident ischemic strokes (21 in 3,271 synthetic DMARD–treated patients and 106 in 11,642 TNFi‐treated patients) occurred during 11,973 and 61,226 person‐years of observation, respectively (incidence rate 175 versus 173 per 100,000 person‐years). After adjustment for confounders, there was no association between ever‐exposure to TNFi and ischemic stroke (hazard ratio 0.99 [95% confidence interval (95% CI) 0.54–1.81]). Mortality 30 days or 1 year after ischemic stroke was not associated with concurrent TNFi exposure (odds ratio 0.18 [95% CI 0.03–1.21] and 0.60 [95% CI 0.16–2.28], respectively).ConclusionExposure to TNFi does not appear to influence the occurrence of ischemic stroke in the medium term in patients with RA. The impact on mortality after ischemic stroke remains inconclusive.

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Cardiovascular Morbidity and Mortality in Women Diagnosed With Rheumatoid Arthritis

Cited by 1,104 publications

References 28 publications

Citrullination as a plausible link to periodontitis, rheumatoid arthritis, atherosclerosis and Alzheimer’s disease

Citrullination as a plausible link to periodontitis, rheumatoid arthritis, atherosclerosis and Alzheimer’s disease

Lack of cardiovascular risk assessment in inflammatory arthritis and systemic lupus erythematosus patients at a tertiary care center

Association Between Ischemic Stroke and Tumor Necrosis Factor Inhibitor Therapy in Patients With Rheumatoid Arthritis

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