Ann Thorac Surg 1999;68:1411-1413
© 1999 The Society of Thoracic Surgeons
Case Reports
Pathologic finding of restenosis in stent-implanted right ventricle–pulmonary artery extracardiac conduit
Shintaro Nemoto, MDa,
Akira Sakai, MDa,
Yutaka Miyoshi, MDa,
Kiyomitsu Yasuhara, MDa,
Masashi Seguchi, MDb
a Department of Cardiovascular Surgery, Seirei Hamamatsu General Hospital, Shizuoka, Japan
b Department of Pediatric Cardiology, Seirei Hamamatsu General Hospital, Shizuoka, Japan
Address reprint requests to Dr Nemoto, Laboratories of Cardiac Molecular and Cellular Physiology, Baylor College of Medicine, Department of Medicine—Cardiology, Veterans Affairs Medical Center, Room 243, Bldg 110, 2002 Holcombe Blvd, Houston, TX 77030
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Abstract
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We describe an excised specimen of a stent-implanted valved equine pericardial extracardiac conduit in the right heart. It appears from careful pathologic examination that the stent acted as a nidus for thrombus formation followed by thick neo-intimal development over the stent, which caused restenosis. Restenosis occurred despite anticoagulation.
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Introduction
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Although stent implantation has improved the outcome of the use of right ventricle–pulmonary artery conduits, a major problem with restenosis still exists. We present the case of a patient in whom a stent that had not fully expanded served as the nidus for severe restenosis.
A male baby was born with tetralogy of Fallot, pulmonary atresia, and aortopulmonary window. When he was 6 months old, total repair was performed using a handmade equine pericardial extracardiac conduit (14 mm in diameter) with a fabricated trileaflet valve. Three years after repair, the conduit was severely stenosed, and balloon dilation was attempted. The pressure gradient across the conduit was reduced from 90 mm Hg to 42 mm Hg. One year later, there was major restenosis (gradient, 72 mm Hg). A second balloon dilation was not successful. When the patient was 5 years of age, a balloon-expandable stent (Palmaz-Schatz, Johnson & Johnson Interventional Systems) was successfully implanted. The gradient decreased from 70 mm Hg to 30 mm Hg. Aspirin (2 mg · kg-1 · day-1) was administered after this operation.
One year after the implantation, the patient had a high fever and complete atrioventricular block. Methicillin-resistant Staphylococcus aureus was detected in blood cultures. An echocardiogram showed severe restenosis of the conduit. After signs of infection had disappeared with antibiotic therapy, conduit replacement was performed.
With the patient under cold cardioplegic arrest, the right ventricular outflow tract was reconstructed by the technique of Cerfolio and colleagues [1]. Briefly, both the side and posterior parts of the fibrous tissue surrounding the conduit were preserved. A handmade monocuspid polytetrafluoroethylene patch was anastomosed to the preserved fibrous tissue, distal pulmonary artery stump, and proximal right ventricular incision. The patient made a good recovery. A postoperative echocardiogram showed a substantial reduction in the right ventricular to left ventricular pressure ratio (0.45).
The pathologic findings were as follows: Grossly, a continuous fibrous peel was present on the surface of the stent and in the space between the stent and the conduit wall (Fig 1). This peel was the major cause of conduit stenosis. The stent had not been uniformly deployed throughout the conduit, and this resulted in the space in which the peel developed. The stent along with thick granular fibrin seemed to be floating in the right ventricular cavity at the proximal end of the conduit (Fig 2). Histologic examination of the fibrous peel revealed similar fibrous connective tissue proliferation with hyalinosis.
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Fig 1. Cross section of excised conduit at distal anastomosis level. A continuous fibrous peel was present on the surface of the stent and in the space between the stent and the conduit wall, and it constituted the major cause of conduit stenosis. (graduation = 1 mm.)
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Fig 2. Cross section of excised conduit at proximal anastomosis level. The stent had not been uniformly deployed, and this created the space between it and the conduit wall. The stent along with thick granular fibrin seemed to be floating in the right ventricular cavity.
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Comment
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The pathologic finding in this case of stenosis may differ from the findings reported by Almagor [2], Hosking [3], and their associates in stented conduits. One characteristic of the stenosis in those reports was progressive thickening of the fibrous peel because of organization of thrombus between the peel and the Dacron conduit [4]. However, even with full expansion of the stent, a fibrous peel developed in the Dacron conduit, which was excised [2]. Thus, even full stent deployment may not prevent this process.
In contrast, Ando and coworkers [5] reported that degenerated valve leaflets and external compression by the sternum were the main causes of stenosis in a valved equine pericardial conduit. Intimal peel formation was not prominent in the absence of a stent. It appears from our findings and those of others that the stent acts as a nidus for thrombus formation, which is followed by development of a thick neo-intima over the stent. This possible mechanism of stenosis is different from that reported by Powell and colleagues [6] in which recurrent obstruction of stent-implanted homografts in the right ventricle–pulmonary artery position was caused by external compression and progressive stenosis outside the stented region.
In conclusion, although the indications for stenting stenosed right ventricle–pulmonary artery conduits are still evolving, it should be emphasized that an incompletely deployed stent can serve as a nidus for thrombus formation and progressive obstruction, even when anticoagulants are used.
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Acknowledgments
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We thank Dr Hiroshi Kobayashi of Seirei Hamamatsu General Hospital and Dr Yasuko Tomizawa of Tokyo Women’s Medical College for histologic studies and discussion.
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References
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Cerfolio R.J., Danielson G.K., Puga F.J., et al. Results of an autologous tissue reconstruction for replacement of obstructed extracardiac conduits. J Thorac Cardiovasc Surg 1995;110:1359-1366.[Abstract/Free Full Text]
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Almagor Y., Prevosti L.G., Bartorelli A.L., et al. Balloon expandable stent implantation in stenotic right heart valved conduits. J Am Coll Cardiol 1990;16:1310-1314.[Abstract]
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Hosking M.C., Williams W.G., Freedom R.M., et al. Intravascular stent prosthesis for right ventricular outflow obstruction. J Am Coll Cardiol 1992;20:373-380.[Abstract]
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Agarwal K.C., Edwards W.D., Feldt R.H., Danielson G.K., Puga F.J., McGoon D.C. Clinicopathological correlates of obstructed right-sided porcine-valved extracardiac conduits. J Thorac Cardiovasc Surg 1981;81:591-601.[Abstract]
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Ando M., Imai Y., Takanashi Y., Hoshino S., Seo K., Terada M. Fate of trileaflet equine pericardial extracardiac conduit used for the correction of anomalies having pulmonic ventricle–pulmonary arterial discontinuity. Ann Thorac Surg 1997;64:154-158.[Abstract/Free Full Text]
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Powell A.J., Lock J.E., Keane J.F., Perry S.B. Prolongation of RV-PA conduit life span by percutaneous stent implantation. Intermediate-term results. Circulation 1995;92:3282-3288.[Abstract/Free Full Text]
Accepted for publication March 25, 1999.
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Abstract
Introduction
