Heart Failure and Risk Assessment in Systemic Autoimmune Disease: Do Inflammation, Autoantibodies and Sex Matter?

Heart failure (HF) is increasingly recognized as an important cardiovascular complication of systemic autoimmune rheumatic diseases (SARDs), which include rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjögren’s syndrome, and idiopathic inflammatory myopathies. Excess HF risk is only partly explained by conventional cardiovascular risk factors and ischemic heart disease. Chronic inflammation, endothelial and coronary microvascular dysfunction, immune-mediated myocardial injury, oxidative stress, fibrosis, and selected autoantibody-associated pathways may contribute to progressive myocardial dysfunction. Biological sex is also relevant because most SARDs predominantly affect women and sex influences immune regulation, vascular biology, myocardial remodeling, and HF phenotype. Current cardiovascular risk scores are primarily designed for atherosclerotic events and incompletely capture autoimmune disease-specific determinants of myocardial injury. This review summarizes HF across major SARDs and examines three interconnected modifiers of myocardial vulnerability—chronic inflammation, autoantibodies, and biological sex. We further discuss how disease activity and duration, biomarkers, global longitudinal strain, cardiovascular magnetic resonance, and conventional risk factors might be integrated into future risk assessment. A biology-centered approach may enable earlier recognition of subclinical myocardial involvement and individualized cardiovascular surveillance, but prospective validation is required before disease-specific HF-screening strategies can be recommended.