Cardiovascular Comorbidity in Rheumatic Diseases

Wright, Kerry; Crowson, Cynthia S.; Gabriel, Sherine E.

doi:10.1016/j.hfc.2013.10.003

Cited by 57 publications

(32 citation statements)

References 122 publications

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“…Elevated C-reactive protein, interleukin 6, and tumor necrosis factor-α have been linked to development of HF and mortality after HF development. 311 The presence of persistently elevated erythrocyte sedimentation rate levels, RA vasculitis, or RA lung disease was independently associated with worse mortality in patients with RA and HF. 312 In the National Databank for Rheumatic Disease, patients with RA had a higher risk of HF development than osteoarthritis, occurring at a rate of 3.9% over 2 years 313 ; however, in the absence of traditional HF risk factors, the rate of HF development was rare at 0.4%.…”

Section: Epidemiology and Prognosismentioning

confidence: 90%

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Bozkurt¹,

Colvin²,

Cook³

et al. 2016

Circulation

624

663

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CLINICAL STATEMENTS AND GUIDELINEST he intent of this American Heart Association (AHA) scientific statement is to summarize our current understanding of dilated cardiomyopathies. There is special emphasis on recent developments in diagnostic approaches and therapies for specific cardiomyopathies. Recommendations in this document are based on published studies, published practice guidelines from the American College of Cardiology (ACC)/AHA 1 and other organizations, 2,3 and the multidisciplinary expertise of the writing group. Existing evidence in epidemiology, classification, diagnosis, and management of specific cardiomyopathies is usually derived from nonrandomized observational studies, registries, case reports, or expert opinion based on clinical experience, not large-scale randomized clinical trials or systematic reviews. Therefore, in this document, rather than using the standard ACC/AHA classification schema of recommendations and level of evidence, 4 we have included key management strategies at the end of each section and categorized our recommendations according to the level of consensus. Although the format of our recommendations might resemble the ACC/AHA classification of recommendations used in the ACC/AHA practice guidelines, because of the preponderance of expert opinion or level of evidence C evidence in our document, we elected to use different terminology to provide a distinction from the practice guidelines, in which stronger levels and quality of evidence with randomized clinical trials or meta-analyses are usually present. 4 The levels of evidence follow the AHA and ACC methods of classifying the level of certainty of the treatment effect. 4 DEfINITIoN of DILATED CArDIoMyopAThyThe term dilated cardiomyopathy (DCM) refers to a spectrum of heterogeneous myocardial disorders that are characterized by ventricular dilation and depressed myocardial performance in the absence of hypertension, valvular, congenital, or ischemic heart disease. 5 In clinical practice, the pathogenesis of heart failure (HF) has often been placed into 2 categories: ischemic and nonischemic cardiomyopathy. The term nonischemic cardiomyopathy has been interchangeably used with DCM. Although this approach might be practical, it fails to recognize that nonischemic cardiomyopathy can include cardiomyopathies caused by volume or pressure overload (such as hypertension or valvular heart disease) that are not conventionally accepted under the definition of DCM. 1,5 Again, in general practice and clinical research trials, the term ischemic cardiomyopathy is defined as cardiomyopathy caused by ischemic heart disease. Current use of ischemic cardiomyopathy terminology implies ventricular dilation and depressed myocardial contractility caused by ischemia or infarction. CLASSIfICATIoN of CArDIoMyopAThIESThe first classification on this topic categorized cardiomyopathies as heart muscle diseases with dilated (DCM), hypertrophic, restrictive, arrhythmogenic right ventricular (ARVC), or nonclassifiable cardiomyopathy in 1980. 5 Subse...

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Section: Epidemiology and Prognosismentioning

confidence: 90%

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Bozkurt¹,

Colvin²,

Cook³

et al. 2016

Circulation

624

663

View full text Add to dashboard Cite

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“…Heart failure is a common evolution of atherosclerosis, and several studies have shown the safety and the usefulness of anti-IL-1 treatment in this condition, a clinical setting in which anti-TNF treatment is contraindicated [78][79][80][81]. It is well known that the incidence of impaired cardiac function is increased strongly both in RA and T2D, leading to a poor prognosis [82,83]. In this context, our experimental data, showing a strong up-regulation of IL-1b MO derived from patients with both RA and T2D, may support the hypothesis that blocking IL-1b may be considered the best therapeutic strategy to treat these patients, due to the upregulation of this cytokine in these patients and to the safety shown during chronic heart failure.…”

Section: Discussionmentioning

confidence: 99%

Monocytes from patients with rheumatoid arthritis and type 2 diabetes mellitus display an increased production of interleukin (IL)-1β via the nucleotide-binding domain and leucine-rich repeat containing family pyrin 3(NLRP3)-inflammasome activation: a possible implication for therapeutic decision in these patients

Ruscitti

Cipriani

Benedetto

et al. 2015

Clinical and Experimental Immunology

117

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Summary A better understanding about the mechanisms involved in the pathogenesis of type 2 diabetes mellitus (T2D) showed that inflammatory cytokines such as tumour necrosis factor (TNF) and interleukin (IL)‐1β play a pivotal role, mirroring data largely reported in rheumatoid arthritis (RA). IL‐1β is produced mainly by monocytes (MO), and hyperglycaemia may be able to modulate, in the cytoplasm of these cells, the assembly of a nucleotide‐binding domain and leucine‐rich repeat containing family pyrin (NLRP3)‐inflammosome, a cytosolic multi‐protein platform where the inactive pro‐IL‐1β is cleaved into active form, via caspase‐1 activity. In this paper, we evaluated the production of IL‐1 β and TNF, in peripheral blood MO of patients affected by RA or T2D or both diseases, in order to understand if an alteration of the glucose metabolism may influence their proinflammatory status. Our data showed, after 24 h of incubation with different glucose concentrations, a significantly increased production of IL‐1β and TNF in all evaluated groups when compared with healthy controls. However, a significant increase of IL‐1β secretion by T2D/RA was observed when compared with other groups. The analysis of relative mRNA expression confirmed these data. After 24 h of incubation with different concentrations of glucose, our results showed a significant increase in NLRP3 expression. In this work, an increased production of IL‐1β by MO obtained from patients affected by both RA and T2D via NLRP3‐inflammasome activation may suggest a potential IL‐1β targeted therapy in these patients.

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“…However, we recently showed that the increased risk in RA cannot be entirely explained by traditional cardiovascular risk factors (Willers and Hahn 2012). It is more likely that the increased risk for CVD in RA is related to inflammation and immune-mediated processes (Crowson et al 2005;Willers and Hahn 2012;Wright et al 2014). In RA, ADMA is assumed to play a particular, yet not fully understood role (Dimitroulas et al 2012(Dimitroulas et al , 2013Surdacki et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Plasma homoarginine, arginine, asymmetric dimethylarginine and total homocysteine interrelationships in rheumatoid arthritis, coronary artery disease and peripheral artery occlusion disease

et al. 2015

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Elevated circulating concentrations of total L-homocysteine (thCys) and free asymmetric dimethylarginine (ADMA) are long-established cardiovascular risk factors. Low circulating L-homoarginine (hArg) concentrations were recently found to be associated with increased cardiovascular morbidity and mortality. The biochemical pathways of these amino acids overlap and share the same cofactor S-adenosylmethionine (SAM). In the present study, we investigated potential associations between hArg, L-arginine (Arg), ADMA and thCys in plasma of patients suffering from rheumatoid arthritis (RA), coronary artery disease (CAD) or peripheral artery occlusive disease (PAOD). In RA, we did not find any correlation between ADMA or hArg and thCys at baseline (n = 100) and after (n = 83) combined add-on supplementation of omega-3 fatty acids, vitamin E, vitamin A, copper, and selenium, or placebo (soy oil). ADMA correlated with Arg at baseline (r = 0.446, P < 0.001) and after treatment (r = 0.246, P = 0.03). hArg did not correlate with ADMA, but correlated with Arg before (r = 0.240, P = 0.02) and after treatment (r = 0.233, P = 0.03). These results suggest that hArg, ADMA and Arg are biochemically familiar with each other, but unrelated to hCys in RA. In PAOD and CAD, ADMA and thCys did not correlate.

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Cardiovascular Comorbidity in Rheumatic Diseases

Cited by 57 publications

References 122 publications

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Plasma homoarginine, arginine, asymmetric dimethylarginine and total homocysteine interrelationships in rheumatoid arthritis, coronary artery disease and peripheral artery occlusion disease

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