Abstract 13004: Spelunking for a Cause of Heart Failure: A Fungus Amongst Us

Two months prior to presenting to our facility, a 63-year-old man was diagnosed with acute pericarditis and treated with colchicine. His chest pain resolved, but he was readmitted a few weeks later with tamponade due to a large exudative pericardial effusion requiring percutaneous drainage. He was discharged on colchicine and furosemide; however, he presented to our institution two weeks later with persisting dyspnea and edema. His blood pressure was 114/84 mmHg without a pulsus paradoxus. Jugular venous pressure was 13 cm H 2 O with a prominent Kussmaul’s sign and 3+ bilateral leg edema. Further evaluation with a transthoracic echocardiogram, cardiac MRI and cardiac catheterization were all consistent with effusive-constrictive pericarditis (Fig A-F). 8-months prior to admission a mediastinal lymph node biopsy noted histoplasma. During admission, chronic histoplasmosis was suspected and a serum histoplasma antigen was reactive (1:256). He was initiated on 12 weeks of itraconazole; however, despite anti-inflammatory therapies, he had refractory congestion. Cardiothoracic surgery was consulted and he underwent pericardial stripping (Fig. G). Pericardial fungal cultures were negative and histopathology noted acute and chronic fibrinous pericarditis without fungal organisms (Fig. H-I). He had an uncomplicated recovery with symptom resolution. Histoplasma capsulatum is endemic to the United States and despite >80% of individuals in endemic areas demonstrating exposure, cases of pericarditis, tamponade or pericardial constriction are rare. Pericardial inflammation likely reflects an autoimmune reaction to H. capsulatum rather than direct pericardial infection and may respond to anti-inflammatories. In sum, we describe a rare diagnosis of effusive-constrictive pericarditis secondary to chronic histoplasmosis. Our case highlights the salient findings of pericardial constriction and the continued importance of a detailed clinical history.