[Cardiac abnormalities in patients with systemic lupus erythematosus: the role of antiphospholipid antibodies].

BACKGROUND: Systemic lupus erythematosus (SLE) is a chronic inflammatory disease that has protean manifestations and follows a relapsing and remitting course. More than 90% of cases of SLE occur in women, frequently starting at childbearing age. It is characterized by the presence of autoantibodies potentially directed toward every organ or apparatus. Cardiac alterations are frequent in patients affected by SLE and the simultaneous presence of antiphospholipid antibodies (aPL), able to cause arterial thrombosis in any vascular district, is considered a possible risk factor for cardiac damage in SLE patients. The aim of this study is to correlate the main cardiac disorders, estimable through transthoracic echocardiography, in SLE patients as well as the typical autoantibody pattern of the disease.

METHODS: Our study included 76 patients: 38 SLE and 38 controls patients. Control patients have been properly selected to be comparable in gender, age and risks factors for cardiovascular disease. We performed autoantibody panel to assess the prevalence of various autoantibodies during SLE development (antinuclear antibody [ANA], double-stranded DNA [dsDNA], extractable nuclear antigen antibodies [ENA], aPL). In the study, the determination of the IgG and IgM isotypes for aPL (cardiolipin, phosphatidylinositol [aPI], phosphatidylserine, phosphatidic acid [aPA], and anti-β2-glycoprotein I antibodies) were checked. Echocardiography was performed in all patients.

RESULTS: In patients affected by SLE, 94.7% was positive to ANA (relative risk 20; 95% confidence interval 4.9-340; p<0.0001) whereas 60.5% was positive for aPL. In patients with SLE, valvular alterations were observed, with a statistically significant correlation between mitral and aortic insufficiency (p=0.01 and p=0.02, respectively). Among aPL-positive patients, 68% (17/25) exhibited at least one hemodynamically significant echocardiographic alteration, vss 3/13 (23%) of patients with negative aPL, with a statistically significant correlation (relative risk 2; 95% confidence interval 1.0-29.8; p=0.01). Among positive-aPL patients, a statistically significant correlation was also observed between mitral insufficiency and aPI-IgG positivity (p=0.01) and, regarding non-valvular alterations, between left atrial enlargement and aPI-IgG positivity (p=0.01) and between left ventricular hypertrophy and aPA-IgG positivity (p=0.03).

CONCLUSIONS: The present study confirms that SLE is an important risk factor for the presence of cardiac alterations, especially for valvular damage. Moreover, the presence of aPL antibodies in patients with SLE is significantly associated with an increased risk of heart disease, and some specific cardiac alterations are correlated with the positivity of some subclasses of aPL.