Association of heart structure and function abnormalities with laboratory findings in patients with systemic lupus erythematosus.

Conventional risk factors of coronary artery disease fail to explain the increased frequency of cardiovascular morbidity in patients with systemic lupus erythematosus (SLE). The study was conducted to determine possible association between the heart structure and function abnormalities with established prognostic value assessed by non-invasive imaging techniques and markers of autoimmune and inflammatory phenomena typical for SLE. Echocardiography and single photon emission computerized tomography (SPECT; Tc-99m-MIBI) at rest were performed in 60 SLE patients in a stable clinical condition of their disease. Laboratory evaluation included serum levels of C-reactive protein (CRP), complement C3c and C4 components and antiphospholipid antibodies (aPL). The latter included serum anticardiolipin (aCL) and anti-β2-glycoprotein I (antiβ2GPI) antibodies, both of IgG and IgM class, and lupus anticoagulant (LA) in plasma. Echocardiography revealed pathologic thickening of valvular leaflets and/or pericardium in more than 60% of patients. Right ventricular systolic pressure (RVSP) was elevated (>30 mmHg) in 16.7%. Myocardial perfusion defects were present in 36.7% of patients, despite normal ECG recordings and a lack of clinical symptoms of myocardial ischaemia. There was a significant association between thickening of valvular leaflets and/or pericardium and high CRP and low C3c and C4 concentrations. On the other hand, increased RVSP and the presence of myocardial perfusion defects were associated with the presence of anticardiolipin and antiβ2GPI antibodies of the IgG class. Increased anticardiolipin IgG levels predicted perfusion defects in SPECT study with 100% sensitivity and 68% specificity, whereas elevated antiβ2GPI IgG levels predicted RVSP elevation (>30 mmHg) with 100% sensitivity and 78% specificity. In stable SLE patients pericardial and valve abnormalities may be associated with markers of an ongoing inflammation. Also, pulmonary systolic pressure elevation and myocardial perfusion defects are combined with elevated levels of anticardiolipin and antiβ2GPI antibodies of the IgG class. These results indicate that even clinically silent pulmonary hypertension and myocardial perfusion defects in SLE patients could be causally related to the presence of antiphospholipid antibodies.