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J Thorac Cardiovasc Surg 2006;131:1401-1402
© 2006 The American Association for Thoracic Surgery


Brief Communication

A fibrous membrane causing left ventricular outflow tract stenosis as the result of endocarditis

Anita Pritisanac, MD * , Andreas Hannekum, MD, Helmut Gulbins, MD

Department of Cardiothoracic Surgery, University of Ulm, Germany.

Received for publication November 3, 2005; accepted for publication November 16, 2005.

* Address for reprints: Anita Pritisanac, MD, Department of Cardiothoracic Surgery, University Hospital Ulm, Steinhövelstr 9, 89075 Ulm, Germany. (Email: anita.pritisanac{at}medizin.uni-ulm.de).

A 68-year-old man with a history of open heart surgery was admitted to our cardiothoracic surgery department because of fever, dyspnea, and reduced cardiac performance during the last 2 months. Six years ago, the patient underwent biologic aortic valve replacement because of aortic insufficiency, conduit implantation because of aortic aneurysm, and aortocoronary bypasses in our department.

Case Report

The patient had been admitted to the hospital 4 weeks before with suspected bacteremia. Four teeth were suspected as the focus of infection and were extracted. During that period he showed signs of infection. Along with elevated temperatures blood cultures were drawn and revealed Streptococcus oralis. Transthoracic echocardiography showed no pathologic findings. Cardiac auscultation was repeatedly without pathologic murmurs. Electrocardiography showed no new pathologic findings and no signs of myocardial ischemia. The maximum temperature was 37.9°C. Laboratory investigations showed leukocytosis (17.000 Giga/L). C-reactive protein was 27 mg/L at maximum and urine analysis turned out to be normal. The chest x-ray showed no pathology. Repeated transesophageal echocardiography showed no vegetations or abscess of the biologic aortic prosthesis, and no paravalvular leakage. The mitral valve was also normal. A slightly impaired motion of all 3 cusps and a peak-to-peak gradient of 60 mm Hg were findings of aortic valve stenosis, which had not been documented before. Ejection fraction was 50%, as in the former study. Heart catheterization showed no pathologic findings. Because the clinical condition of the patient worsened without response to medical treatment, a surgical intervention was scheduled.

The suspected leading preoperative pathologic condition was an impaired cusp motility of the aortic prosthesis caused by acute endocarditis of the valve or aortic conduit, probably explaining the new findings of aortic valve stenosis.

In contrast, the intraoperative appearance of the conduit and aortic valve showed no signs of infection. The prosthesis was free of vegetations or abscess; the leaflet anatomy and its function were unremarkable (Figure 1). A rigid circular fibrous membrane was found below the annulus of the aortic prosthesis with no signs of infection. This fibrous membrane seemed to have impaired the aortic valve cusp movement and caused the pressure gradient between the left ventricle and the aorta (Figure 2). The membrane was excised completely and a specimen was sent for histologic and microbiologic investigation. The patient received a new conduit and mechanical prosthesis. Postoperative transesophageal echocardiography showed normal function of the new mechanical valve with no signs of stenosis.


Figure 1
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Figure 1. Bioprosthesis showed no macroscopic signs of endocarditis with normal leaflet anatomy and no vegetations or abscess.

 

Figure 2
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Figure 2. Intraoperative view of the newly developed rigid circular fibrous membrane below the anulus of aortic valve prosthesis.

 
Pathologic Discussion

Gram stain showed gram-positive Staphylococcus oralis on the biologic prosthesis. Specimens of the conduit were sterile, and all parts of the membrane were sterile. Microscopic evaluation showed a fibrous tissue, as it is found in granulation tissue. The valve cusps were infiltrated with fibroblasts and showed widely infiltrated granulocytic areas. It is believed that the membrane led to signs of aortic stenosis. As a result of inflammation, fibrous tissue developed due to acute endocarditis, probably during the time that teeth were extracted. The histopathologic findings estimated the fibrotic tissue to be approximately 2 months old.

Discussion

The clinical importance of this presented case consists in the discrepancy of the preoperative condition of the patient and intraoperative pathology of a fibrous membrane causing stenosis of the left ventricular outflow tract below the aortic prosthesis. Preoperative echocardiography did not show any vegetations or abscess as clear signs of endocarditis. The examination of the subvalvular region was disturbed by artefacts caused by the prosthetic aortic valve. However, Doppler sonography showed significant aortic stenosis. These findings were confirmed intraoperatively. The subvalvular stenosis could have been caused by 2 mechanisms: Pannus formation resulting from an acute infection or subvalvular fibrosis. The latter is a rare condition, described only in single case reports in pediatric patients. In addition, the fact that no subvalvular stenosis was determined in the echocardiographic investigation 4 weeks before, reveals this pathomechanism to be unlikely. The patient's endocarditis some weeks previously led to the development of this subvalvular stenosis by the mechanism of pannus formation after aortic valve replacement. This case shows an unusual pathoanatomic sequela of an acute endocarditis after prosthetic heart valve replacement and once more underlines the variety of possible presentations of this disease. The patient received 36 days of intravenous antibiotics and recovered with no major complications from surgery. The function of the mechanical valve was excellent, heart function was stable, and blood cultures were sterile. 1–5 Go

References

  1. Andres E, Baudoux C, Noel E, Goichot B, Schlienger JL, Blickle JF. The value of the Von Reyn and the Duke diagnostic criteria for infective endocarditis in internal medicine practice. A study of 38 cases. Eur J Intern Med 2003;14:411-414.[Medline]
  2. Bayer A, Bolger A, Taubert K, Wilson W, Steckelberg J. Diagnosis and management of infective endocarditis and its complications. Circulation 1998;98:2936-2948.[Free Full Text]
  3. Gulbins H, Kilian E, Roth S, Uhlig A, Kreuzer E, Reichart B. Is there an advantage in using homografts in patients with acute infective endocarditis of the aortic valve?. J Heart Valve Dis 2002;11:492-497.[Medline]
  4. Shapira N, Merin O, Rosenmann E, Dzigivker I, Bitran D, Yinnon AM, et al. Latent infective endocarditis: epidemiology and clinical characteristics of patients with unsuspected endocarditis detected after elective valve replacement. Department of Cardiothoracic Surgery, Shaare Zedek Medical Center, Jerusalem, Israel. Ann Thorac Surg 2004;78:1623-1629.[Abstract/Free Full Text]
  5. Sexton DJ, Spelman D. Current best practices and guidelines. Assessment and management of complications in infective endocarditis. Cardiol Clin 2003;21:273-282vii-viii.[Medline]




This Article
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Andreas Hannekum
Helmut Gulbins
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Right arrow Valve disease


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