Lupus anticoagulant antibodies may be linked to rheumatic heart disease via cross-reactivity, causing valvular damage even without a clinical history of rheumatic fever.
Although known cross-reactivity between molecules of β2GPI and m-protein may promote cardiac damage, the correlation between lupus anticoagulant antibodies and rheumatic heart disease is not well understood. 37 year-old-female with positive lupus anticoagulant antibodies without a history of rheumatic fever presented to the clinic for a cardiovascular workup of a new murmur. Transesophageal echocardiogram revealed diffuse thickening of the mitral valve consistent with rheumatic disease. Due to the severity of her disease, she underwent valve replacement surgery. The surgical and gross pathology reports documented her native valve to have typical rheumatic features including foreshortening of the subvalvular apparatus, fusion of the commissures and fibrinous exudate on the posterior leaflet. The cardiac involvement of rheumatic fever can be explained by cross-reactivity of anti-m protein with myosin, tropomyosin and protein valvular endocarditis. There is an overlap between anti- β2GPI activity and anti m-protein/N-acetylglucosamine, suggesting a common mechanism that links the lupus anticoagulant antibody to rheumatic fever.
Morrison et al. (Mon,) studied this question.