Valvular Involvement in SLE

Posted by e-Medical PPT Monday, March 12, 2012
Valvular disease in SLE
Leaflet thickening tends to be diffuse; it usually involved the mitral and aortic valves and is associated with valve regurgitation (~75%) or valve masses (50%).

Lupus valve disease is frequent (75%) regardless of the presence or absence of antiphospholipid antibodies.
Antiphospholipid antibodies may not be a primary pathogenetic factor.

An echocardiographic study of valvular heart disease associated with systemic lupus erythematosus
Neither the presence of nor changes in valvular disease were temporally related to disease activity, therapy, or the duration of SLE.

Appreciable incidence of serious complications in the patients with valvular disease.
After a mean follow-up of almost five years, the combined incidence of stroke, peripheral embolism, heart failure, infective endocarditis, and death was 22% (with valve disease) vs 15% (without valvular disease).

The incidence of stroke in patients with valvular disease was 13 percent.

Valvular disease in SLE—Clinical course
5 year follow-up—20% risk of valve related complications:
Symptomatic severe MR
Infective endocarditis
Ischemic stroke
Mortality 20% at 5yrs.
Due to refractory heart failure, IE, CVA, complicated post-op course

Verrucous endocarditis
Libman-Sacks (verrucous) endocarditis is a not uncommon complication of SLE
Higher frequency (43 percent) has been noted when more sensitive transesophageal echocardiography is performed
Most commonly involve the mitral valve (any valve can be involved)
Most commonly found in the valve recess between the ventricular wall and the posterior leaflet
Can involve the surface of the valves, valve ring, commissures.

Pathogenesis of Libman-Sacks endocarditis—proposed mechanisms
Fibrin and platelet thrombi on the impaired valves-- organization leads to fibrosis, distortion, and subsequent valvular dysfunction
Immunologic injury--initial insult to the valvular apparatus, triggering the sequence of pathogenetic events.

Deposits of immunoglobulins and complement were shown in the subendothelial layer of the valves in patients with antiphospholipid antibodies
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