Cardiac Impairment in Rheumatoid Arthritis and Influence of Anti-TNFα Treatment

Abstract

There is evidence that rheumatoid arthritis (RA) is associated with higher overall and cardiovascular (CV) morbidity and mortality as compared with general population. Increased prevalence of traditional risk factors and chronic inflammation, that has been recognized as independent CV risk factor, may play an important role in atherosclerosis and subsequently ischemic heart disease development. However, myocardial dysfunction as a result of chronic inflammation and secondarily myocardial fibrosis markedly participates on heart failure development. Proinflammatory cytokines, such as C-reactive protein, tumor necrosis factor alpha (TNFα), interleukins 1 and 6, that are markedly increased in RA, play a role in the acceleration of atherosclerosis as well as myocardial fibrosis development. Several studies documented that increased CV risk was associated with seropositivity, disease activity score, citrullination, and duration of RA. Early detection of heart dysfunction is based on echocardiographic detection of diastolic dysfunction resulting from myocardial inflammation and fibrosis. Some studies showed also higher prevalence of left ventricular systolic dysfunction and increased prevalence of cardiac arrhythmias as compared to non-RA population. There are still controversies on the impact of NT-proBNP in predicting cardiac impairment in RA patients. Some authors consider it to be a sensitive noninvasive predictor of subclinical CV disease in these patients and also a predictor of all-cause mortality independently on traditional CV risk factors. However, the correlation with parameters of cardiac function was confirmed only in a few studies. The impact of biological treatment on progression of atherosclerosis and heart failure is still controversial and seems to be not harmful in young patients with normal left ventricular function. The effect of biologics, especially anti-TNFα drugs, is probably related to the cardiac function before treatment. Larger prospective clinical, echocardiographic, and magnetic resonance studies are needed.

Selected clinical parameters and changes in cardiac morphology and function assessed by magnetic resonance imaging in patients with rheumatoid arthritis and ankylosing spondylitis without clinically apparent heart disease

“…In addition, the results of regression analysis are also confirmed by the existence of the above relationships between RA and AS and morphological and functional changes of the heart in CMR in study group. The more frequent occurrence and greater severity of adverse cardiovascular changes in patients with RA in our study compared to the control group matches the results of other studies conducted so far, although most of them were conducted using echocardiography [18]. There are far fewer CMR studies.…”

Rheumatoid cachexia: the underappreciated role of myoblast, macrophage and fibroblast interplay in the skeletal muscle niche

“…Similarly, research from our group has demonstrated a significant increase in collagen accumulation within the vastus lateralis, soleus and gastrocnemius muscles in CIA rodents compared to that of control rodents [38], as well as impaired molecular remodelling with fibrotic deposition and impaired cardiomyofibre contractile function [91]. In humans, the presence of subclinical myocardial fibrosis resulting from low grade chronic inflammation in a large number of RA patients, has been linked to heart failure in approximately 3.9% of patients [92]. Furthermore, pulmonary fibrosis is often associated with RA as a result of increased TGF-β and Smad signalling leading to an increase in collagen deposition within the lung tissue [93].…”

Comorbid TNF-mediated heart valve disease and chronic polyarthritis share common mesenchymal cell-mediated aetiopathogenesis

“… 44 Similarly, in the Tg197 model, valvular pathology contributes to the observed extensive LV dilation with some degree of LV hypertrophy as well as to the concomitant contractile dysfunction. However, additional mechanisms that have been proposed as contributing factors in the increased prevalence of global heart failure in patients with RA/SpA, such as myocardial fibrosis and oedema as well as arterial blood pressure, coronary heart disease and myocardial remodeling 45 remain to be studied for their contribution in the global heart impairment observed in Tg197 animals. We have also detected repeated arrhythmic episodes in Tg197 mice which could explain the premature sudden deaths observed in this model recapitulating the increased risk of sudden cardiac death experienced by patients with RA/SpA, due to atrial fibrillation and other types of tachyarrhythmias which suggest diffuse myocardial electrical instability.…”