Introduction: Cardiovascular disease has recently been recognized as a primary cause of morbidity and mortality in systemic lupus erythematosus (SLE). Di-lated cardiomyopathy is a rare baseline clinical manifestation of SLE. Diagnosis can be difficult if there are no classical signs of lupus. Valvular involvement is the most common cardiac manifestation and premature atherosclerosis is a major comorbid condition in SLE. We present the case of a young patient with signs of se-vere heart failure secondary to dilated cardiomyopathy as the first clinical manifestation of SLE.

Methods: We present the case of a 34-year-old patient with no cardiovascular history presenting with symptoms of heart failure manifested by dyspnoea and fa-tigability for several weeks. Laboratory tests reveal renal impairement, mild anemia, hepatocitolysis and inflammatory syndrome. Chest radiograph describes minimum pleural effusion. Echocardiography shows an increased left ventricular size, severe mitral regur-gitation secondary to mitral annulus enlargement, de-pressed systolic function and secondary pulmonary hypertension. Additional haematological investigati-ons reveal the presence of L.E cells, anti-double stran-ded DNA antibodies. At hospital discharge, the case is redirected to rheumatology for specific treatment Results: SLE is an autoimmune disease that primari-ly affects young women. The diagnosis of SLE requires four or more of the ARA criteria. In our patient, the diagnosis was based on the following criteria: serositis, haematological abnormalities, proteinuria, anti-DNA antibodies. The autoimmune etiology should always be suspected in the young patient without a history of car-diovascular disease and with recent heart failure signs. Although dilated cardiomyopathy may be idiopathic or associated with a variety of clinical conditions, in-cluding viral infections, alcoholism, muscle disease, pregnancy or postpartum, in our case, most of these possibilities have been excluded from clinical history. Although occult viral infections underlie the etiology of so-called cases of idiopathic dilated cardiomyopathy, the immunological image of this case was not show-ing these. Proteinuria, pleural effusion, positive double stranded DNA, supports an autoimmune disease for diagnosis, and in particular, SLE. This also suggested the possible link between dilatation cardiomyopathy and SLE.

Conclusions: According to the literature, the prevalen-ce of cardiovascular involvement in SLE patients was estimated to be greater than 50%. In patients with SLE, musculoskeletal and mucocutaneous expression dominate, even in patients with cardiovascular disease. In our case, there are symptoms of heart failure, with no typical musculoskeletal manifestations. Dilated car-diomyopathy is a rare, initial clinical manifestation of SLE. Diagnosis may be difficult if there are no classic clinical signs of SLE. However, the possibility of secon-dary SLE cardiomyopathy should always be conside-red in the differential diagnosis of cardiomyopathy of unknown etiology.