PurposeSystemic autoimmune disease (SAD) frequently affects the pericardium, and pathology is characterized by both immunological and inflammatory processes. We hypothesized that these processes simultaneously influence mitral-valve (MV) deterioration and left-ventricular (LV) wall thickening in SAD subjects. Methods101 SAD subjects were selected (76 female; 53±17years; systemic-lupus-erythematosus, 26%; vasculitis, 20%; scleroderma, 14%; polymyositis/dermatomyositis complex, 10%; mixed connective tissue disease, 11% and rheumatoid-arthritis, 2%). MV anterior-mitral-leaflet (AML) length, AML thickness index, AML doming height and LV mass index (LVMI) were measured using transthoracic-echocardiography (TTE) and the presence of MV calcification, MV sub-valvular thickening and pericardial effusion (PE) were estimated. AML thickness index was calculated as the ratio of AML thickness to aortic posterior wall thickness. The correlation between LVMI and ECG V1S+V5R voltage was used to assess the etiology of LV wall thickening. Results19 subjects (19%) had significant PE. PE subjects had a significantly greater AML thickness index (1.55±0.48 vs. 1.14±0.32, P<0.001), AML doming height (1.26±1.54mm vs. 0.03±0.91mm, P<0.001), more frequent MV sub-valvular thickening (26% vs. 5%, P=0.003) and greater LVMI (104.7±34.6g/m2 vs. 80.6±21.0g/m2, P=0.002). Significant correlation was observed between LVMI and ECG V1S+V5R voltage in 79 subjects without PE (R=0.39, P<0.001). However, in 18 subjects with PE, no such correlation was observed (R=0.30, P=0.23). ConclusionsMV, MV sub-valvular deterioration and increased LVMI, unrelated to high voltage ECG criteria, were frequently detected in SAD subjects with PE. Immunological and inflammatory processes in SAD may not only cause pericardium inflammation, but may also cause MV deterioration and LV wall thickening.