Pathogenesis of ischaemic and non-ischaemic heart diseases in rheumatoid arthritis

Błyszczuk, Przemysław; Szekanecz, Zoltán

doi:10.1136/rmdopen-2019-001032

Cited by 24 publications

(30 citation statements)

References 72 publications

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“…Unlike for HFrEF patients, a long-term anti-TNF-α therapy in patients with autoimmune inflammatory diseases is generally not harmful, and it may even protect from enhanced cardiovascular complications and cardiovascular death [ 53 , 54 ]. Although heart failure cases have been reported in patients treated with TNF-α inhibitors [ 55 ], the risk of new onset of heart failure in patients under age 50 receiving etanercept or infliximab is low [ 56 ].…”

Section: Anti-tnf-α Therapy and Cardiovascular Diseases In Humansmentioning

confidence: 99%

Complexity of TNF-α Signaling in Heart Disease

Rolski

Błyszczuk

2020

JCM

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Heart disease is a leading cause of death with unmet clinical needs for targeted treatment options. Tumor necrosis factor alpha (TNF-α) represents a master pro-inflammatory cytokine that plays an important role in many immunopathogenic processes. Anti-TNF-α therapy is widely used in treating autoimmune inflammatory disorders, but in case of patients with heart disease, this treatment was unsuccessful or even harmful. The underlying reasons remain elusive until today. This review summarizes the effects of anti-TNF-α treatment in patients with and without heart disease and describes the involvement of TNF-α signaling in a number of animal models of cardiovascular diseases. We specifically focused on the role of TNF-α in specific cardiovascular conditions and in defined cardiac cell types. Although some mechanisms, mainly in disease development, are quite well known, a comprehensive understanding of TNF-α signaling in the failing heart is still incomplete. Published data identify pathogenic and cardioprotective mechanisms of TNF-α in the affected heart and highlight the differential role of two TNF-α receptors pointing to the complexity of the TNF-α signaling. In the light of these findings, it seems that targeting the TNF-α pathway in heart disease may show therapeutic benefits, but this approach must be more specific and selectively block pathogenic mechanisms. To this aim, more research is needed to better understand the molecular mechanisms of TNF-α signaling in the failing heart.

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Section: Anti-tnf-α Therapy and Cardiovascular Diseases In Humansmentioning

confidence: 99%

Complexity of TNF-α Signaling in Heart Disease

Rolski

Błyszczuk

2020

JCM

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“…IHD, known as coronary heart disease (CHD), is a condition that produces an insufficient blood supply to the cardiac muscle. It is also named coronary artery disease (CAD) due to the role of coronary arteries in the process [ 5 ].…”

Section: Cardiac Involvement In Rheumatoid Arthritismentioning

confidence: 99%

“…Patients with RA present an increased risk for ischemic and non-ischemic heart disease due to subclinical pathological alterations in heart muscle and coronary arteries. It is known that systemic inflammation is a significant contributing factor for the increased cardiovascular (CV) risk in patients with this disease [ 2 , 3 ] and is connected with arterial stiffness, lipid-salvage processes, and destabilization of atherosclerotic plaques [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Ischemic Heart Disease and Rheumatoid Arthritis—Two Conditions, the Same Background

Rezuş

Macovei

Burlui

et al. 2021

Life

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Rheumatoid arthritis (RA) is one of the most frequent inflammatory rheumatic diseases, having a considerably increased prevalence of mortality and morbidity due to cardiovascular disease (CVD). RA patients have an augmented risk for ischemic and non-ischemic heart disease. Increased cardiovascular (CV) risk is related to disease activity and chronic inflammation. Traditional risk factors and RA-related characteristics participate in vascular involvement, inducing subclinical changes in coronary microcirculation. RA is considered an independent risk factor for coronary artery disease (CAD). Endothelial dysfunction is a precocious marker of atherosclerosis (ATS). Pro-inflammatory cytokines (such as TNFα, IL-1, and IL-6) play an important role in synovial inflammation and ATS progression. Therefore, targeting inflammation is essential to controlling RA and preventing CVD. Present guidelines emphasize the importance of disease control, but studies show that RA- treatment has a different influence on CV risk. Based on the excessive risk for CV events in RA, permanent evaluation of CVD in these patients is critical. CVD risk calculators, designed for the general population, do not use RA-related predictive determinants; also, new scores that take into account RA-derived factors have restricted validity, with none of them encompassing imaging modalities or specific biomarkers involved in RA activity.

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“…3 4 In addition, chronic inflammation in RA is regarded as an important contributor to accelerated atherosclerosis leading to increased cardiovascular disease (CVD) that eventually leads to increased rates of premature death in RA. [5][6][7][8][9][10][11] There are indications that improved medical treatment with new biological disease modifying antirheumatic drugs (DMARDs) and targeted synthetic DMARDs in addition to use of conventional DMARDs at higher doses and an earlier disease stage led to reduced inflammation, [12][13][14] which in turn has contributed to reduced mortality in patients with RA in short-term studies. 15 16…”

Section: Introductionmentioning

confidence: 99%

Reduced cardiorespiratory fitness is a mediator of excess all-cause mortality in rheumatoid arthritis: the Trøndelag Health Study

2021

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ObjectivesInvestigate if low cardiorespiratory fitness (CRF) was associated with and acted as a mediator of excess all-cause mortality rate in persons suffering from rheumatoid arthritis (RA) compared with the general population.MethodsAll-cause mortality was analysed using Cox regression modelling in patients with RA (n=348) and controls (n=60 938) who took part in the second (1995–1997) and third (2006–2008) waves of the longitudinal population-based Trøndelag Health Study in Norway. A mediation analysis was performed to investigate if excess relative risk of mortality in RA was mediated by low estimated CRF (eCRF).ResultsDuring the follow-up until 31 December 2018 (mean 19.3 years), the mortality rate among patients with RA (n=127, 36.5%) was higher than among controls (n=12 942, 21.2%) (p<0.001). Among controls and patients with RA, 51% and 26%, respectively, had eCRF above the median for their age and sex (p<0.001). The final Cox model included RA status and eCRF, adjusted for hypertension, body mass index, smoking, cholesterol, diabetes and creatinine. eCRF below median for sex and age category was associated with increased mortality (p<0.001). The total excess relative risk of mortality in patients with RA was 28% (95% CI 2% to 55%, p=0.035), in which RA itself contributed 5% and the direct and indirect contributions of low eCRF accounted for 23%.ConclusionsLow eCRF was an important mediator of the increased all-cause mortality rate found in RA. Our data indicate that patients with RA should be given advice to perform physical activity that increases CRF, along with optimised treatment with antirheumatic drugs, from the time of diagnosis.

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Pathogenesis of ischaemic and non-ischaemic heart diseases in rheumatoid arthritis

Cited by 24 publications

References 72 publications

Complexity of TNF-α Signaling in Heart Disease

Complexity of TNF-α Signaling in Heart Disease

Ischemic Heart Disease and Rheumatoid Arthritis—Two Conditions, the Same Background

Reduced cardiorespiratory fitness is a mediator of excess all-cause mortality in rheumatoid arthritis: the Trøndelag Health Study

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