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Superior Vena Cava Syndrome As the First Manifestation of a Primary Cardiac Leiomyosarcoma

perfusion scintigraphy or chest and abdominal CT scan, and Holter monitoring showed no arrhythmias. Coronary angiography/catheterization showed normal coronary arteries, left ventricle end-diastolic pressure 20 mm Hg, pulmonary capillary pressure 18 mm Hg, and pulmonary artery systolic pressure 30 mm Hg, with no constriction/restriction pattern. Conventional therapy for heart failure was started (ramipril, carvedilol, and digoxin at very low doses due to hypotensionrelated intolerance), with mild improvement of the analytical parameters and LVEF at 30% in echocardiographic followup after treatment, but the patient continued with symptoms. The analyses revealed an increase in inflammatory parameters, with rheumatoid factor 221 U/mL, positive ANA 9.7, IFI 640 with a granular pattern (positive anti-SS-A and anti-SS-B, 995 and 494 U/mL). Because the patient did not meet the criteria of other recognized autoimmune diseases causing autoimmune myocarditis (eg, lupus erythematosus, rheumatoid arthritis, mixed connective tissue disease, and Churg-Strauss syndrome), primary Sjögren’s syndrome was diagnosed. Corticoid therapy was initiated, with rapid clinical improvement. At follow-up after 1 1/2 months of treatment, the patient was asymptomatic, with no clinical symptoms of heart failure or new episodes of presyncope-syncope. C-reactive protein had dropped to 1.6 mg/dL, and followup echocardiography indicated LVEF of 49%. We concluded with a diagnosis of heart failure due to severe systolic malfunction in the context of myocarditis caused by primary Sjögren’s syndrome, with multisystem involvement and good response to corticoid therapy. Primary Sjögren’s syndrome is rarely associated with a heart condition: the usual echocardiographic findings of the disease have been described in a large series in Mexico, and valvular involvement is the most common, with few functional repercussions. The relationship of the disease and its antibodies (which activate M1 muscarinic acetylcholine receptors) with congenital atrioventricular block is widely recognized; adults appear to be less sensitive, although antiSSB antibodies have been related to some cases of atrioventricular block in adulthood. Autonomic dysfunction in the disease has been discussed more thoroughly in the scientific literature, which includes both favorable and unfavorable studies. Lastly, several cases of myocarditis have been described in this syndrome, either alone or in the context of multisystem involvement, as in our case, with little response to conventional treatment but good response to corticoid therapy. The etiologic mechanism of this myocarditis has been related to a possible leukocytoclastic vasculitis. We consider that, in cases of severe dysfunction of uncertain etiology, systemic inflammatory activity and a specific autoimmune etiology should always be considered, as the most appropriate treatment may be simple and effective.