Autoimmune Diseases and Coronary Artery Disease: Inflammatory Pathways and Clinical Implications

Autoimmune diseases (ADs) accelerate atherosclerosis and increase coronary artery disease (CAD) risk through chronic inflammation, immune dysregulation, and treatment effects.

Mechanisms Linking ADs to CAD

• Systemic inflammation: Elevated CRP, IL-6, TNF-α → endothelial dysfunction, plaque initiation/progression, plaque vulnerability.
• Autoantibodies: Anti-phospholipid (APS) → thrombosis; anti-oxLDL, anti-HSP60, anti-endothelial → vascular injury.
• Immune complexes: Deposit in vessel walls → complement activation → vasculitis.
• Endothelial dysfunction: Reduced NO bioavailability, increased adhesion molecules (VCAM-1, ICAM-1).
• Accelerated atherosclerosis: Premature, diffuse, more calcified plaques.
• Vasculitis: Direct vascular inflammation (SLE, RA, GPA, Takayasu, Kawasaki).
• Prothrombotic state: Platelet activation, hypercoagulability (APS, SLE).
• Metabolic syndrome promotion: Chronic steroids → weight gain, insulin resistance, dyslipidemia.

Disease-Specific Risks

• SLE: 2–10× CAD risk; young women; antiphospholipid syndrome overlap.
• RA: 1.5–2× CAD risk; inflammation-driven; "lipid paradox" (low cholesterol but high CVD).
• Psoriasis/PsA: 1.5× risk; severity correlates.
• Scleroderma: Microvascular disease, pulmonary hypertension.
• Giant cell arteritis/Takayasu: Large vessel involvement.

Clinical Recommendations

• Aggressive traditional risk factor control (BP, lipids, glucose, smoking).
• Treat inflammation to target (treat-to-target in RA, SLE).
• Minimize glucocorticoid dose/duration.
• Consider CAD screening (CAC scoring, stress testing) earlier than general population.
• Multidisciplinary care: rheumatology + cardiology + primary care.