Accelerated atherogenesis in autoimmune rheumatic diseases.

Area of Science:

• Rheumatology
• Cardiovascular Medicine
• Immunology

Background:

• Systemic inflammatory rheumatic diseases (SIRDs), such as rheumatoid arthritis (RA), are linked to increased cardiovascular disease (CVD) rates, often at younger ages.
• Inflammation's role in atherogenesis is gaining attention in the general population.
• This review focuses on accelerated atherogenesis in RA.

Purpose of the Study:

• To examine evidence for accelerated atherogenesis in RA.
• To update the hypothesis that vasculitis plays a significant role in RA-related CVD.
• To explore the mechanisms and consequences of endothelial dysfunction in rheumatic diseases.

Main Methods:

• Literature review of accumulating evidence.
• Analysis of studies on endothelial dysfunction (ECD) in vasculitis.
• Presentation of a model for vasculitis-induced ECD in rheumatic diseases.

Main Results:

• Endothelial dysfunction (ECD), an early sign of atherogenesis, is common in primary vasculitis and affects multiple vascular beds.
• ECD in vasculitis is diffuse and potentially reversible with immunosuppressive therapy, suggesting mechanisms beyond focal inflammation.
• Inflammatory mediators like CRP and TNF may contribute to ECD in rheumatic diseases.

Conclusions:

• Vasculitis-induced endothelial dysfunction is a proposed major contributor to accelerated atherogenesis in rheumatic diseases.
• Diffuse ECD has implications for both rheumatic disease progression and cardiovascular events.
• Understanding these mechanisms may offer insights into 'idiopathic' atherosclerosis in the general population.