Background In patients with SLE of long duration cardiovascular disease is the most important cause of increased mortality. Valvular lesions are common in SLE patients but it has not been studied how these abnormalities relate to arterial disease in general in SLE.
Objectives To study cardiac heart and valve function in SLE patients with and without arterial disease and to compare these groups to each other and to population controls.
Methods Twenty-six women and two men (mean age 53 ± 8 years) with SLE and arterial disease (objectively verified history of myocardial infarction, angina, cerebral infarction or intermittent claudication) (SLE cases) were compared to SLE patients with no signs of arterial disease (SLE controls) and to population controls. The three groups were matched for age and gender. Echocardiography was performed on all together with a thorough clinical and laboratory evaluation.
Results 15/28 SLE cases had cardiac valvular abnormalities. Three of these had undergone valve replacement, one had a significant aortic insufficiency, and the other eleven had thickening of valvular leaflets of no measurable haemodynamic importance. Only 1/28 SLE controls and 2/28 population controls had similar valvular thickening. Among SLE cases those with valvular abnormalities had significantly higher levels of plasma homocysteine (p < 0.0001), orosomucoid (p = 0.05), plasma triglycerides (p = 0.02) and the cholesterol fraction of very low-density lipoproteins (VLDL) (p = 0.01). There was no association with antiphospholipid antibodies (antibodies to cardiolipin IgG, cardiolipin IgM, b2 glykoprotien-1 or lupus anticoagulant).
Conclusion SLE patients with arterial disease have a high prevalence of valvular abnormalities 54%. The most common abnormality is diffuse valvular thickening. In SLE patients without clinical signs of arterial disease valve abnormalities are as uncommon as in age matched population controls. Hyperhomocysteinemia and dyslipidemia, both of which have been linked to endothelial dysfunction, correlated strongly with valvular abnormalities. It is thus possible that valvular thickening in SLE patients may be a manifestation of endothelial damage, which needs further attention and prospective clinical evaluation.
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