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Ann Thorac Surg 1999;68:1407-1409
© 1999 The Society of Thoracic Surgeons
a Divisions of Pulmonary and Critical Care Medicine, Stanford, California, USA
b Division of Cardiology, Stanford, California, USA
c Division of Cardiothoracic Surgery, Stanford, California, USA
d Department of Pathology, Stanford University Medical Center, Stanford, California, USA
Address reprint requests to Dr Berry, Department of Pathology, Stanford University Medical Center, Stanford, CA 94305-5407
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| Introduction |
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A 20-year-old man was referred with a 6-month history of dyspnea and chest tightness. He reported a 15-pound weight gain over 1 month, without a change in appetite. His past medical history was unremarkable and he did not abuse alcohol, illicit drugs, or tobacco. He was a college student who was active in sports until the onset of his illness. He denied orthopnea and pedal edema. His family history was negative for cardiac disease. On admission, the pulse was regular, 88 beats/min, blood pressure 100/80 mm Hg, without a pulsus paradoxus, and he was afebrile. The jugular venous pressure was raised at 14 cm with a positive Kussmauls sign. The heart sounds were normal without a third heart sound, or evidence of pericardial rub or knock. The lung bases were dull. There was no ascites and no pedal edema. A chest radiograph revealed a normal heart size and bilateral pleural effusions (left larger than right). Electrocardiography showed widespread symmetric T-wave inversion in the precordial leads. Echocardiography demonstrated normal right and left ventricular size, and thickness, but reduced left ventricular systolic function. The pericardium appeared thickened (Fig 1). Cardiac catheterization revealed elevated right atrial pressure (14 mm Hg), with prominent x and y descent patterns. The right ventricular pressure was 30/14 mm Hg, pulmonary artery pressure was 30/14 mm Hg, and the mean pulmonary capillary wedge pressure was 14 mm Hg. The estimated cardiac output was 2.9 L/min (cardiac index, 1.8 L/min per m2) and no oxygen saturation step-up was observed from the superior vena cava to the pulmonary artery. The aortic pressure was 110/70 mm Hg and the coronary arteries were normal. The left ventricular ejection fraction was 49%. Simultaneous measurements of left and right ventricular diastolic pressures were perfectly equivalent, without separation during the Valsalva maneuver or premature ventricular complex (PVC) induction. Right ventricular endocardial biopsies showed no histologic evidence of myocarditis, hemochromatosis, amyloidosis, or granulomatous inflammation. A diagnosis of constrictive pericarditis was made and the patient was referred for operation.
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Coccidiomycosis frequently involves all layers of the heart [2, 4]. Fibrogranulomatous pericarditis, miliary granulomas, and cardiac muscle abscesses can occur [5]. Autopsy studies suggest that 5% to 15% of patients with disseminated coccidiomycosis have lesions in the myocardium [2, 5] and rare cases of endocarditis attributable to coccidiomycosis have also been reported [6]. Pericarditis can result from rupture of a superficial granuloma located just beneath the pericardium or by direct extension from the lung, pleura, or mediastinal lymph nodes [4]. Although no evidence of coccidiomycosis was seen on right ventricular myocardial biopsy in this patient, the grossly abnormal electrocardiograph and reduced left ventricular systolic function (evident on echocardiography) were suggestive of myocardial involvement [7].
Currently, there are no data on the possible long-term effects of coccidioidal myocarditis and pericarditis. It is unknown whether therapy with antifungal agents, in addition to surgical pericardiectomy, can lead to a cure of pericardial coccidioidal infections but treatment with oral fluconazole and amphotericin on an empiric basis would seem worthwhile [8]. Schwartz and colleagues [5] have described coccidioidal constrictive pericarditis that resulted from a chronic (> 1 year) pericardial effusion. In that report pericardiocentesis and pericardial window proved ineffective at preventing the development of constrictive pericarditis. Our patient demonstrated an occult progression to constriction in the absence of clinically overt pericarditis, pericardial effusion, or cardiac tamponade.
Most cases of coccidioidal pericarditis have been reported before the availability of amphotericin B therapy. In this patient, the surgical resection of constrictive pericarditis due to coccidiomycosis proved an effective management strategy, although the long-term clinical outlook is unclear. Current therapeutic options for fungal pericarditis include local installation of antifungal chemotherapy, intravenous amphotericin B, and oral agents. Antiinflammatory therapies, including corticosteroids, are sometimes used in the management of idiopathic constrictive pericarditis [1]. The current case care underscores the need to evaluate the possibility of alternative diagnoses, such as tuberculous and fungal infections, before initiating potentially deleterious immunosuppressive therapy.
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