High-grade systemic inflammation acts as a key trigger of ischaemic and non-ischaemic heart diseases in rheumatoid arthritis, with anti-TNF-α therapies impacting disease development and progression.
This review outlines the pathogenesis of heart failure in rheumatoid arthritis, emphasizing the impact of systemic inflammation and antirheumatic therapies on cardiovascular outcomes.
Rheumatoid arthritis (RA) is characterised by a chronic inflammatory condition of the joints, but the comorbidities of RA predominantly contribute to the reduced lifespan associated with this disease. Clinical data indicate that cardiovascular disease is the major comorbidity associated with mortality in RA. In this review, we aimed to describe the pathogenesis of heart failure in RA. First, we emphasised the fundamental differences between ischaemic and non-ischaemic heart diseases and referred to their relevance in excessive cardiovascular-dependent mortality in RA. Second, we highlighted aspects of asymptomatic changes in cardiac tissue and in coronary blood vessels that are commonly found in patients with diagnosed RA. Third, we focused on high-grade systemic inflammation as a key trigger of ischaemic and non-ischaemic heart diseases in RA, and described the implication of conventional and biologic antirheumatic medications on the development and progression of heart disease. In particular, we discussed the roles of tumour necrosis factor-alpha (TNF-α) and anti-TNF-α therapies on the development and progression of ischaemic and non-ischaemic heart diseases in RA.
Błyszczuk et al. (Wed,) conducted a review in Rheumatoid arthritis. Anti-TNF-α therapies was evaluated. High-grade systemic inflammation acts as a key trigger of ischaemic and non-ischaemic heart diseases in rheumatoid arthritis, with anti-TNF-α therapies impacting disease development and progression.