Mitral valve disease in rheumatic heart disease, systemic lupus erythematosus, antiphospholipid syndrome, and rheumatoid Arthritis
- 1Department and Clinic of Cardiology, Poznan University of Medical Sciences, Poznań, Poland
- 2Department of Rheumatology, Rehabilitation and Internal Diseases, Poznan University of Medical Sciences, Poznań, 61- 545 Poland
- 3Clinical Rehabilitation Laboratory, Department of Rehabilitation and Physiotherapy, Poznan University of Medical Sciences, Poznań, 60-545 Poland
Abstract
Mitral valve disease occurs in rheumatic heart disease (RHD) and selected systemic autoimmune rheumatic diseases, but similar lesions may have different underlying mechanisms. This structured narrative review examines epidemiological, mechanistic, imaging, and management evidence, distinguishing established pathways from incompletely validated mechanisms and hypotheses. In RHD, post-streptococcal valvulitis leads to fibrotic remodeling, commissural fusion, and chordal shortening, producing mitral stenosis, regurgitation, or mixed disease. A meta-analysis of 215,552 children and adolescents in endemic settings reported echocardiographically detected RHD in 24 per 1000. In systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), typical findings include leaflet thickening, Libman–Sacks vegetations, and regurgitation; embolic complications may occur despite mild valve dysfunction. Among 508 clinically selected patients with SLE undergoing echocardiography, 27.4% had heart valve involvement and 11.2% had mitral involvement. Immunothrombotic mechanisms may contribute to these lesions, but direct validation in human valve tissue remains incomplete. In rheumatoid arthritis (RA), a prospective cohort found an association with incident mitral regurgitation (adjusted hazard ratio 1.54, 95% confidence interval 1.32–1.81), but not mitral stenosis. Myocardial imaging findings do not establish a causal link to regurgitation. These findings support anatomy- and severity-based assessment in RHD, combined valvular and thromboembolic evaluation in SLE/APS, and assessment of conventional regurgitation mechanisms in RA. The framework informs clinical interpretation within existing guidelines, while proposed disease-specific mechanisms require further validation.
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BibTeX
@article{lucki2026mitral,
title = {{Mitral valve disease in rheumatic heart disease, systemic lupus erythematosus, antiphospholipid syndrome, and rheumatoid Arthritis}},
author = {Mateusz Lucki and Bogna Grygiel-Górniak and Ewa Lucka and Maciej Lesiak},
journal = {Rheumatology International},
year = {2026},
month = nov,
doi = {10.1007/s00296-026-06345-4},
url = {https://doi.org/10.1007/s00296-026-06345-4},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Mitral valve disease in rheumatic heart disease, systemic lupus erythematosus, antiphospholipid syndrome, and rheumatoid Arthritis
AU - Mateusz Lucki
AU - Bogna Grygiel-Górniak
AU - Ewa Lucka
AU - Maciej Lesiak
PY - 2026
DA - 2026/11/05
JO - Rheumatology International
DO - 10.1007/s00296-026-06345-4
UR - https://doi.org/10.1007/s00296-026-06345-4
AB - Mitral valve disease occurs in rheumatic heart disease (RHD) and selected systemic autoimmune rheumatic diseases, but similar lesions may have different underlying mechanisms. This structured narrative review examines epidemiological, mechanistic, imaging, and management evidence, distinguishing established pathways from incompletely validated mechanisms and hypotheses. In RHD, post-streptococcal valvulitis leads to fibrotic remodeling, commissural fusion, and chordal shortening, producing mitral stenosis, regurgitation, or mixed disease. A meta-analysis of 215,552 children and adolescents in endemic settings reported echocardiographically detected RHD in 24 per 1000. In systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), typical findings include leaflet thickening, Libman–Sacks vegetations, and regurgitation; embolic complications may occur despite mild valve dysfunction. Among 508 clinically selected patients with SLE undergoing echocardiography, 27.4% had heart valve involvement and 11.2% had mitral involvement. Immunothrombotic mechanisms may contribute to these lesions, but direct validation in human valve tissue remains incomplete. In rheumatoid arthritis (RA), a prospective cohort found an association with incident mitral regurgitation (adjusted hazard ratio 1.54, 95% confidence interval 1.32–1.81), but not mitral stenosis. Myocardial imaging findings do not establish a causal link to regurgitation. These findings support anatomy- and severity-based assessment in RHD, combined valvular and thromboembolic evaluation in SLE/APS, and assessment of conventional regurgitation mechanisms in RA. The framework informs clinical interpretation within existing guidelines, while proposed disease-specific mechanisms require further validation.
SN - 0172-8172
SN - 1437-160X
ER -