Ann Thorac Surg 1997;63:1794-1796
© 1997 The Society of Thoracic Surgeons
Case Report
Extracardiac Right Atrium-to-Right Ventricle Homograft for Uncorrectable Tricuspid Valve Disease
Zohair Al-Halees, FRCSC,
Fadel Al-Fadley, FRCPC
Department of Cardiovascular Diseases, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia
Accepted for publication February 3, 1997.
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Abstract
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Surgically uncorrectable tricuspid valve disease in children is rare. However, when it happens the surgical options are very limited. Tricuspid valve replacement using a mechanical valve or stented bioprosthesis is impractical. Use of homografts in the "anatomic position" has its limitations. We report here the use of an extracardiac homograft connection between the right atrium and right ventricle in a 16-month-old boy in whom severe tricuspid valve stenosis developed after surgical repair of a complex ventricular septal defect associated with dextrocardia and anomalous systemic venous drainage. The patient remains well receiving no cardiac medication 12 months after the procedure.
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Introduction
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A 16-month-old male infant was diagnosed to have a large endocardial cushion-type ventricular septal defect (VSD) associated with situs inversus dextrocardia, superior inferior ventricles, and anomalous systemic venous drainage. He was palliated as a neonate by pulmonary artery banding. He underwent pulmonary artery debanding and VSD patch closure using bovine pericardium. The repair was carried out through the left-sided morphologic right atrium (RA). The tricuspid valve (TV) was smallish (1.5 cm; Z value of -1.2 standard deviation for body surface area). Nevertheless, it was thought to be adequate to proceed with a biventricular repair, particularly because the right ventricular (RV) size appeared almost normal. The base of the septal leaflet of the TV anchored multiple pledgeted sutures to support the VSD patch. An anomalous persistent right superior vena cava draining to an unroofed coronary sinus was ligated. The unroofed coronary sinus was repaired by reseptation of the atrium with a bovine pericardial patch.
Postoperatively the patient continued to have congestive heart failure. He was managed medically and discharged, but was readmitted in 3 months' time with worsening right-sided heart failure, severe liver congestion, and ascites requiring ventilatory support. The clinical and echocardiographic evaluation showed a residual VSD and severe TV stenosis (mean Doppler gradient, 10 mm), small TV annulus (1.2 cm; Z value of <-3 standard deviations for body surface area) as compared with a mitral valve annulus of 2.3 cm.
At operation, the TV was severely stenotic with a small annulus. There was severe fibrotic reaction at the area of the septal leaflet where the pledgets had been placed at the first operation, contributing to the valve stenosis. The bovine pericardial patch, although it showed no shrinkage, was taken down and all the pledgets were removed and the valve was dilated. The VSD was reclosed with another patch that was sutured with continuous suture without pledgets. Despite this the valve remained stenotic. With manipulation and attempts at repair, the valve also became incompetent. All attempts at repairing the valve failed. The TV was then closed completely with a bovine pericardial patch. The RA was connected to the RV using an extracardiac fresh antibiotic-preserved size 22 aortic homograft, which was placed in an inverted position to be in the direction of the circulation (Fig 1
). The ventricular end of the homograft was sewn to the right atrium directly with 5-0 Prolene (Ethicon, Somerville, NJ) suture. Because it was an aortic homograft there was enough length and natural curvature to reach the RV with a proper gentle alignment. A longitudinal ventriculotomy was made in the RV outflow tract below the pulmonary valve annulus. The distal end of the homograft was cut obliquely and anastomosed directly to the RV with 5-0 Prolene suture.
The patient came off pump without difficulty. Hemodynamic data obtained from cardiac catheterization postoperatively demonstrated no diastolic gradient across the homograft functioning as a TV. The RA pressure was 10/15 mm Hg (mean, 10 mm Hg); RV, 41/3 mm Hg (mean, 9 mm Hg); and pulmonary artery, 39/14 mm Hg (mean, 24 mm Hg) (Fig 2). The patient was discharged well. At follow-up he remains asymptomatic receiving no cardiac medication 12 months postoperative. By echocardiography, the homograft is functioning normally with no stenosis or regurgitation, good biventricular function, and no residual VSD.
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Fig 2. . (A) Right anterior oblique angiogram of the homograft conduit. (B) Schematic representation of the angiogram showing (A) right atrium (not shown in Fig 2A ), (C) extracardiac homograft conduit, (D) right ventricle, and (E) main pulmonary artery.
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Comment
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The use of extracardiac connections is not a new concept. A direct RA-to-RV anastomosis as well as a valved conduit between the RA and RV were described in the setting of a modified Fontan procedure [1, 2]. Here we report the use of the extracardiac homograft in the clinical setting of TV stenosis after repair of VSD associated with dextrocardia and anomalous systemic venous drainage. In this age group using a prosthesis in the anatomic position of the TV, whether a mechanical prosthesis or a stented or nonstented bioprosthesis, is impractical because of the small annulus and the question of durability. Use of homografts implanted with the "top hat" technique as reported by us [3] and others is limited by the size of the right atrium and the size of the TV annulus as well. Converting to a Fontan-type circulation in our patient was not possible because of the high pulmonary artery pressure, whereas a 1
-ventricle correction was also not a good option because the TV had become incompetent. The use of a large extracardiac homograft seemed the logical choice in this patient who clearly demonstrated that he could not tolerate a suboptimal repair. Technically, this is not a difficult procedure and a large homograft can be accommodated.
The thrombotic obstruction of the extracardiac connection in the Fontan circulation [4] is not expected to happen here because the heart is structurally normal. These homografts should last for a long time because they are in a low-pressure system. At least they should behave like a bioprosthesis in TV replacement, which demonstrated a very satisfactory long-term durability without serious calcification [5].
The described technique serves as a salvage procedure from an otherwise difficult problem. It is not proposed for routine use because generally one is able to repair the TV.
In conclusion, uncorrectable TV disease in children is a rare occurrence and a surgical challenge. We propose here the use of an extracardiac valved homograft connection from the RA to the RV as a solution to those rare instances where a surgeon is faced with such a problem.
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Acknowledgments
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We thank Dr Hend Al Mansour, Department of Cardiovascular Diseases, King Faisal Specialist Hospital & Research Centre, for making the drawing.
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Footnotes
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Address reprint requests to Dr Al-Halees, Department of Cardiovascular Diseases, King Faisal Specialist Hospital & Research Centre, MBC 16, PO Box 3354, Riyadh 11211, Saudi Arabia.
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References
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- Björk VO, Olin CL, Bjorke BB, Thoren CA. Right atrial-right ventricular anastomosis for correction of tricuspid atresia. J Thorac Cardiovasc Surg 1979;77:452–8.[Abstract]
- Coles JG, Leung M, Kielmanowicz S, et al. Repair of tricuspid atresia: utility of the right ventricular incorporation. Ann Thorac Surg 1988;45:384–9.[Abstract]
- Kumar N, Gallo R, Al-Halees Z, Al-Fadley F, Duran CMG. Unstented semilunar homograft replacement of the tricuspid valve in Ebstein malformation. Ann Thorac Surg 1995;59:320–2.[Abstract/Free Full Text]
- Laks H, Williams WG, Hellenbrand WE, et al. Results of right atrial to right ventricle and right atrial to pulmonary artery conduits for complex congenital heart disease. Ann Surg 1980;192:382–9.[Medline]
- Glower D, White W, Smith R, et al. In hospital and long term outcome after porcine tricuspid valve replacement. J Thorac Cardiovasc Surg 1995;109:877–84.[Abstract]
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Abstract
Introduction
