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Ann Thorac Surg 2004;78:1453-1455
© 2004 The Society of Thoracic Surgeons
a Department of Critical Care and Pulmonary Services, University of Athens, Athens, Greece
b Department of Cardiothoracic Surgery, Athens, Greece
c Department of Pathology, Evagelismos Hospital, Athens, Greece
d Department of Microbiology, Evagelismos Hospital, Athens, Greece
Accepted for publication July 10, 2003.
* Address reprint requests to Dr Kotanidou, Department of Critical Care and Pulmonary Services, University of Athens, Ipsilantou 45-47, Athens 10675, Greece
akotanid{at}med.uoa.gr
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Abstract |
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Introduction |
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We present a case of a native valve of A. fumigatus endocarditis, illustrating the difficulties in diagnosis and management.
A previously healthy 61-year-old woman was admitted into the intensive care unit because of fever, cough, and confusion. A computed tomographic scan of the head and abdomen was normal. The diagnosis of thrombotic thrombocytopenic purpura was established, and the patient was treated with 30 plasma exchange sessions and pulse doses of up to 100 mg per day of prednisolone and broad-spectrum antibiotics for 6 weeks. In addition she received ganciclovir for cytomegalovirus pneumonia. A lipid-based preparation of amphotericin B was administrated (30 g, total) after Candida albicans was detected in the urine and sputum specimens. Serological tests for Aspergillus were negative. Transthoracic echocardiogram and transesophageal echocardiography showed only mild to moderate diffuse hypokinesia of the left and right ventricles (ejection fraction 
45% to 50%). The troponin test was negative. On day 45 of hospitalization, the patient was transferred from the intensive care unit to the ward.
The patient remained hospitalized because of critical illness polyneuropathy, but in relatively good condition, and on hospital day 75 she complained of sudden dyspnea and fever [3, 5]. On physical examination the patient appeared dyspneic and a harsh precordial systolic murmur was found during auscultation of the heart. Transesophageal echocardiography disclosed severe mitral valve insufficiency with an eccentric jet due to rupture of the posterior papillary muscle. Multiple nodes were detected on the chordae tendinea of the subvalvular apparatus and on the posterior leaflet (Fig 1A, B). The patient underwent emergency replacement of the mitral valve with a 25-mm prosthetic mechanical mitral valve (SJM masters series [St Jude Medical, St Paul MN]). Gross examination of the surgical specimen revealed excessive fungal hyphae spreading on the posterior leaflet of a normal appearing mitral valve and a ruptured papillary head (Fig 1C). Microscopically, the nodule consisted of uniform, compact, parallel hyphae arranged concentrically around the chordae and showing degenerative changes of frank necrosis. There was no invasion of the chordal tissue in which only a mild inflammatory infiltrate composed of histiocytes and eosinophils was noted.
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The patient was treated with intravenous lipid-based preparation of amphotericin B (5 mg/kg/d) in combination with oral itraconazole (800 mg daily). The amphotericin B daily dose was gradually increased (to 8 mg/kg).
One week after the first operation, the patient had a computed tomographic scan that revealed multiple embolic infarctions to the central nervous system, spleen, and left kidney, whereas both lungs showed no involvement. Ophthalmologic examination was negative with no signs consistent with embolism. At the same time, serial postvalve replacement transesophageal echocardiography showed gradually increasing new vegetation in the prosthetic valve, reaching 17 mm in size in 2 weeks. An intraventricular septum abscess was also detected.
Splenectomy was performed on postoperative day 14 followed by reoperation on postoperative day 16 for mitral valve replacement with thorough debridement of ring vegetations. Smears from the removed valve showed hyphae and A. fumigatus grew again.
The patient was continued on antifungal therapy. The patient spent 45 days in the intensive care unit after the second cardiac operation, and despite all efforts the patient expired with septic shock from Pseudomonas aeroginosa and Aspergillus disseminated infection without any lung involvement.
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Comment |
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Heart surgery for valvular replacement and pacemaker implantation, neoplastic disease, long-term parenteral feeding, wide-spectrum antimicrobials, steroids, immunosuppressive therapy, diabetes mellitus, and central lines are the most frequent risk factors for mycotic endocarditis.
Lack of pulmonary involvement in the presence of generalized infection with A. fumigatus is unique, because all earlier cases reported to date included severe pulmonary disease [1]. None of the chest roentgenograms or computed tomographic scans revealed the presence of lung aspergilloma or invasive pulmonary aspergillosis.
The strongest risk factor for disseminated aspergillosis is prolonged granulocytopenia in the context of immunosuppressive drug therapies. Our patient presented with normal leukocyte and granulocyte counts.
The identification of only 270 case reports in the English literature over the past 30 years supports the notion that fungal endocarditis is a rare disease, with fungi responsible for less than 10% of infective endocarditis cases [7]. Aspergillus endocarditis on native valves is very uncommon and the experience in diagnosis and treatment is limited [1]. Because of the ubiquitous nature of the organism, establishing a definitive diagnosis of disease caused by Aspergillus is difficult. The use of antibodies against Aspergillus to diagnose invasive aspergillosis has produced conflicting results [5]. In most cases, serologic methods are not used to establish the diagnosis, as antibody testing is not predictive of the invasiveness of the infection [3]. In our patient, all serological tests for Aspergillus were negative and did not help in the diagnosis and follow-up.
The optimum therapy in patients with Aspergillus endocarditis remains unclear. In general, the largest databases for therapy in aspergillosis concern amphotericin B deoxycholate and various surgical modalities [5]. In our patient we used a combination of amphotericin B, itraconazole, voriconazole, and aggressive surgical treatment. Surgical debridement of the fungal vegetation was instrumental in our case, although sometimes its usefulness seems difficult to determine. Despite our increased awareness, early surgical and adequate medical management, severe disseminated fungemia reappeared unexpectedly early in our patient, with recurrent endocarditis on the prosthetic valve. We hypothesize that microscopic valvular seeding of Aspergillus on apparently healthy cardiac tissue was the cause of the early endocarditis recurrence.
Timing of surgery in fungal endocarditis is another debatable point. The initial operation was on an emergency basis because of severe hemodynamic instability of the patient caused by acute mitral insufficiency. The reoperation, although performed rather early after the discovery of the brain embolic infarcts, was indicated because of uncontrolled infection and its paravalvular extension.
The transesophageal echocardiography findings in our patient were fundamental both in diagnosis and in our decision to refer the patient to immediate surgery. The vegetation size and its mobility were all criteria that led to the decision for reoperation, despite her clinical condition [4].
Aspergillus endocarditis is very uncommon and there is limited experience in the diagnosis and treatment of it. We suggest that native valve Aspergillus infective endocarditis is uniformly fatal without immediate and extensive surgical intervention combined with prolonged antifungal therapy. [6]
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This article has been cited by other articles:
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  P. Badiee, A. Alborzi, E. Shakiba, M. Ziyaeyan, and B. Pourabbas Molecular diagnosis of Aspergillus endocarditis after cardiac surgery J. Med. Microbiol., February 1, 2009; 58(2): 192 - 195. [Abstract] [Full Text] [PDF]
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