From joints to vessels: How rheumatoid arthritis therapy alters the fate of the heart

Table 1 Pathogenetic similarities between rheumatoid arthritis and atherosclerosis

Pathogenic mechanism	Rheumatoid arthritis	Atherosclerosis	Common features
Chronic inflammation	Synovial membrane activation, TNF-α, IL-1β, IL-6 release	Vascular wall inflammation, same cytokines	Systemic inflammation, TNF-α/IL-6 role
Autoimmune component	Autoantibodies (RF, ACPA)	Autoantibodies to oxidized LDL	Immune complexes, Th1 response
Macrophage activation	Synovial infiltration → pannus formation	Oxidized LDL uptake → foam cells	Macrophages as key effectors
Oxidative stress	ROS-mediated cartilage & synovium damage	LDL oxidation → plaque formation	ROS-driven tissue destruction
Endothelial dysfunction	Microangiopathy, synovial neovascularization	Impaired vascular barrier function	VCAM-1/ICAM-1 upregulation
Neoangiogenesis	Angiogenesis in synovium → arthritis progression	Plaque instability due to new vessels	Pathological vessel growth
Fibrosis/tissue remodeling	Joint deformity (excess collagen)	Fibrous cap formation on plaques	Fibroblast activation
Biomarkers	CRP, ACPA, RF	CRP, oxidized LDL, IL-6	Shared markers (CRP, IL-6)

TNF-α: Tumor necrosis factor-α; IL-1β: Interleukin-1β; IL-6: Interleukin-6; VCAM-1: Vascular cell adhesion molecule-1; ICAM-1: Intercellular adhesion molecule-1; LDL: Low-density lipoprotein; CRP: C-reactive protein; ACPA: Anti-citrullinated protein antibodies; RF: Rheumatoid factor; Th1: T-helper 1 cells; ROS: Reactive oxygen species.