Ann Thorac Surg 2009;87:1954-1956. doi:10.1016/j.athoracsur.2008.10.048
© 2009 The Society of Thoracic Surgeons
Case Reports
Two Cases of Pulmonary Homograft Replacement for Isolated Pulmonary Valve Endocarditis
Victor Dayan, MDa,*,
Fabio Gutierrez, MDa,
Leandro Cura, MDa,
Gerardo Soca, MDa,
Alvaro Lorenzo, MDa,b
a Cardiovascular Centre, Hospital de Clinicas, Montevideo, Uruguay
b National Institute of Cardiac Surgery, Montevideo, Uruguay
Accepted for publication October 14, 2008.
* Address correspondence to Dr Dayan, 26 de Marzo 3459/602, Montevideo, 11300, Uruguay (Email: vdayan{at}adinet.com.uy).
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Abstract
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Isolated pulmonary endocarditis is rare. Two cases that required surgical treatment are reported: a 35-year-old woman with predisposing factors for right-sided endocarditis who presented with complete heart block; and a healthy 65-year-old man with no predisposing factors who was admitted with septic shock. Both patients presented with septic shock and pulmonary septic emboli requiring urgent surgical treatment. Surgical correction using pulmonary homograft was done, with immediate postoperative recovery. The current literature of isolated pulmonary endocarditis is also reviewed.
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Introduction
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Right-sided endocarditis (RSE) is rare, comprising only 5% of infective endocarditis cases [1, 2]. This disease most commonly affects the tricuspid valve. Sporadic cases of isolated pulmonary endocarditis (IPE) have been reported. Isolated RSE has a benign prognosis, with low in-hospital mortality [1]. Initial management is medical, and surgery is required in very few cases. We describe two cases of IPE that required pulmonary replacement with a pulmonary homograft.
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Case Reports
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Patient 1
A 35-year-old woman who was an intravenous drug user positive for human immunodeficiency virus, presented with a 15-day history of malaise, cough, and fever. She was admitted with a diagnosis of acute pneumonia, and antibiotic treatment was initiated. On day 10, chest pain, respiratory failure, and hemodynamic collapse with complete atrioventricular block prompted her transfer to intensive care unit. Blood cultures were positive for methicillin-sensitive Staphylococcus aureus, and antibiotic treatment was changed from ceftriaxone and ciprofloxacin to cephradine and gentamicin. Transesophageal echocardiography revealed small pulmonary valve vegetations of 3 x 8 mm. Thoracic computed tomography showed images compatible with bilateral septic emboli. After 30 days, her hemodynamic and respiratory status improved but she remained febrile. Blood cultures were negative. New transesophageal echocardiography showed motile pulmonary vegetations of 12 x 12 mm, severe tricuspid regurgitation, pulmonary trunk of 28 mm, and ejection fraction of 35%. Surgical intervention was indicated at this point.
The patient's chest was entered through a median sternotomy incision, and the patient was placed on cardiopulmonary bypass support. The pulmonary trunk was opened longitudinally. All pulmonic valve leaflets had been destroyed by friable and yellowish vegetations (Fig 1). Debridement and excision were performed, and the valve was then replaced with a 28-mm pulmonary homograft. To avoid pulmonary mismatch, ventricular and pulmonary pressures were measured. De Vega annuloplasty was performed because of tricuspid annulus dilatation.
Microbiologic study showed leukocytes with no bacteria. The patient was transferred to the intensive care unit for 3 days and then to a regular unit for 27 days. The postoperative course was uneventful. Transthoracic echocardiogram at postoperative day 10 revealed normal ventricular dimensions, no significant pulmonary gradient, no tricuspid regurgitation, and ejection fraction of 65%. After 30 days of postoperative antibiotic treatment with linezolid, the patient remained afebrile and was discharged home. Follow-up at 6 months revealed an asymptomatic patient with a normal functioning pulmonary homograft.
Patient 2
A 65-year-old man with a history of smoking (two packs per day) presented with a 20-day history of malaise and fever after sustaining a finger injury with an ovine bone. He was admitted to the intensive care unit with multiple organ failure and hemodynamic deterioration. Blood cultures were positive for methicillin-sensitive S aureus. Cephradine and ciprofloxacin were initiated. There was no improvement with this treatment. New blood cultures were positive for unidentified gram-negative bacilli, sensitive to ceftazidime and vancomycin. Transesophageal echocardiography revealed a pulmonary valve vegetation of 15 mm and moderate pulmonary regurgitation. The patient remained febrile on antibiotic treatment, and he had coughing and chest pain. Thoracic computed tomgraphy demonstrated bilateral pulmonary septic emboli. New transesophageal echocardiography reported a very motile pulmonary vegetation of 25 x 17 mm on the right pulmonary valve and a 28-mm pulmonary artery. Surgical intervention was required.
Cardiopulmonary bypass was initiated through a median sternotomy. The pulmonary trunk was opened longitudinally. A 2-cm lobulated vegetation was found on one of the pulmonary valves (Fig 2). Resection of the pulmonary valve was done, and it was replaced with a 29-mm pulmonary homograft. Bovine pericardial patch was required as the homograft diameter was greater than the pulmonary ring. No significant gradient across the homograft was recorded. Microbiologic valve study revealed yeasts. The patient's postoperative course was uneventful. Transthoracic echocardiogram performed 3 weeks after surgery showed no vegetations. Ceftazidime therapy was continued for 30 days after surgery based on the last blood culture. During this period, the patient remained afebril; therefore, based on the clinical and echocardiographic evolution, the microbiology valve report was not taken into account. After 7 years of follow-up, the patient has a normal functioning pulmonary homograft.

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Fig 2. The pulmonary trunk has been opened. A large lobulated mass at the pulmonary valve is being removed.
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Comment
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Isolated pulmonary endocarditis is the least common of RSE. It is associated with predisposing factors such as intravenous drug use, right-sided catheters, and pacing wires infection [2]. Clinical manifestations commonly affect the respiratory system owing to pulmonary septic embolization. High-grade maintained fever and marked increase of serum markers of inflammation differentiate septic pulmonary embolism due to RSE from nonseptic pulmonary embolism [3]. Characteristic computed tomgraphy findings include discrete nodules with varying degrees of cavitation, and subpleural, wedge-shaped heterogeneous areas of increased attenuation with rimlike peripheral enhancement [4]. Complete atrioventricular heart block associated with endocarditis is present in 4% of the patients, and it is related to aortic or mitral valve involvement [5]. No previous case of complete atrioventricular block associated with IPE has been described.
Indications for surgery for RSE include more than 3 weeks of persistent fever in patients on a regimen of adequate antibiotic treatment, repetitive pulmonary emboli, and vegetations larger than 20 mm [6]. Little evidence exists regarding the optimal replacement strategy for IPE. The most commonly used strategy involves stentless xenografts and pulmonary homografts [1, 7]. The use of stented biologic valves or the bovine jugular vein (Contegra) is supported by some [8].
Our two clinical cases represent good examples regarding when and for which patients should RSE be considered. Case 1 had the typical predisposing factors for RSE. Case 2 had no predisposing factors. Clinical suspicion based on persistent fever and respiratory manifestations were critical for the diagnosis of RSE. In our research, this is the first report of complete heart block associated with IPE. Excellent outcomes were achieved for both patients after pulmonary homograft replacement and a 30-day postoperative antibiotic regimen.
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References
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- The Task Force on Infective Endocarditis of the European Society of Cardiology Guidelines on prevention, diagnosis and treatment of infective endocarditis Eur Heart J 2004;00:1-37.
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