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Ann Thorac Surg 1998;66:1533-1538
© 1998 The Society of Thoracic Surgeons

Double patch closure of ventricular septal defect with increased pulmonary vascular resistance

^a Le Bonheur Children’s Medical Center, University of Tennessee, Memphis, Tennessee, USA
^b Kyyiv Institute of Cardiovascular Surgery, Kyyiv, Ukraine
^c Rebro University Hospital Zagreb, Zagreb, Croatia

Address reprint requests to Dr Novick, 777 Washington, Ste 215, Memphis, TN 38105
e-mail: (ichfno{at}aol.com)

Presented at the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.

	Abstract

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Background. Closure of a large ventricular septal defect (VSD) in children with elevated pulmonary vascular resistance is associated with significant morbidity and mortality. Pulmonary hypertensive episodes continue to be a major cause of postoperative morbidity and mortality. We designed a fenestrated flap valve double VSD patch in an effort to decrease the morbidity and mortality associated with the closure of a large VSD with elevated pulmonary vascular resistance.

Methods. Eighteen children (mean age, 5.7 years) with a large VSD and elevated pulmonary vascular resistance (mean, 11.4 Wood units) underwent double patch VSD closure using moderately hypothermic cardiopulmonary bypass and cardioplegic arrest. The routine VSD patch was fenestrated (4 to 6 mm) and on the left ventricular side of the patch, a second, smaller patch was attached to the fenestration along its superior margin before closure of the VSD.

Results. All children survived operation and were weaned from inotropic and ventilator support within 48 hours postoperatively. Postoperative pulmonary artery pressures were significantly lower than preoperative values. One child died 9 months postoperatively.

Conclusions. Closure of a large VSD in children with elevated pulmonary vascular resistance can be performed with low morbidity and mortality when a flap valve double VSD patch is used.

	Introduction

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Early closure of a large ventricular septal defect (VSD) before the onset of elevated pulmonary vascular resistance (PVR) is commonplace in most industrialized countries. The prognosis for children with surgical closure of a large VSD with severely elevated PVR is related to the patient’s age and PVR at closure [1]. Pulmonary hypertensive events continue to cause significant morbidity and mortality even when closure of a large VSD is performed in infancy [2]. In most industrialized countries, these pulmonary hypertensive episodes can be managed with sophisticated and expensive pharmacologic [3] and mechanical manipulations [4].

The diagnosis and surgical treatment of children with a large VSD is frequently delayed in many countries throughout the world [5]. This circumstance puts these children at increased risk for significant morbidity and mortality when closure of the VSD is performed. Since 1994, we have developed a program that provides cardiac surgery to children in developing countries. As a result of the older children with a large VSD and elevated PVR encountered, we developed a simple physiologic double patch modification for VSD closure. The purpose of this operative modification is to decrease the morbidity and mortality associated with the closure of a large VSD with elevated PVR. This report provides the early results of this surgical modification for closing a large VSD in children with elevated PVR.

	Patients and methods

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Eighteen patients with a large VSD and pulmonary hypertension (PHT) underwent operative closure of their VSD between May 1996 and November 1997. Ten patients were girls. The patients ranged in age from 1.5 to 15 years with a mean age of 5.7 ± 3.9 years. The cities in which operations were performed were Kyyiv, Ukraine (13); Memphis, Tennessee (3); Minsk, Belarus (1); and Zagreb, Croatia (1). Two of the children who received operations in Memphis were from Bosnia and 1 was from Ukraine.

Statistics
All data are presented as mean ± standard deviation. Comparison of preoperative and postoperative values was performed using the Student’s t test.

Preoperative evaluation
Predominant presenting signs or symptoms at the time of evaluation for surgical treatment were exertional dyspnea in 9 patients, cyanosis in 8, and feeding intolerance or failure to thrive in 1. Preoperative cardiac evaluation included an echocardiogram and a cardiac catheterization. In all instances, cardiac catheterization was performed in the child’s country of origin, and maneuvers to manipulate PVR were not used routinely. The VSD was isolated in 13 patients. Two patients had a VSD and patent ductus arteriosus, 1 had double-outlet right ventricle (DORV), 1 had a complete atrioventricular septal defect, and 1 had multiple VSDs. Previous pulmonary artery banding had been performed on 1 child with an isolated VSD and the child with DORV. Catheterization data for the child with DORV were incomplete owing to the absence of a pulmonary artery O₂ saturation.

Operative management
All surgical procedures were performed by two of the authors (W.M.N., V.V.L.). Moderately hypothermic cardiopulmonary bypass (CPB) with cold cardioplegic arrest was used in all patients. A flap valve fenestrated VSD patch was constructed from sauvage Dacron (C.R. Bard, Haverhill, MA) and Gore-Tex (W.L. Gore & Assoc, Flagstaff, AZ) cardiovascular patches (Figs 1, 2). The VSD patch was tailored to the appropriate size for primary closure of the VSD. A fenestration was then made in the central region of the VSD patch. The size of the fenestration was governed by the size of the child. Children weighing 15 kg or less received a 4-mm fenestration, children weighing between 15 and 20 kg received a 5-mm fenestration, and children weighing more than 20 kg received a 6-mm fenestration. A separate flap valve patch measuring at least 4 mm greater than the diameter of the fenestration was then constructed. The flap valve patch was sewn to the superior aspect of the fenestration on the left ventricular side. Interrupted sutures of 6-0 Prolene (Ethicon, Somerville, NJ) were placed along one third of the superior rim of the flap valve patch to anchor it to the VSD closure patch. A separate tethering suture was placed inferiorly and tied loosely to approximate the size of the fenestration. The VSD patch was then sewn into place using continuous 4-0 or 5-0 Prolene suture. No patient was left with an atrial level shunt. Before discontinuation of CPB, dopamine 5 to 15 µg · kg^-1 · min^-1, nitroprusside 1 to 6 µg · kg^-1 · min^-1 or the phosphodiesterase inhibitor milrinone (Sanofi-Winthrop Pharmaceuticals, New York, NY) 0.35 to 1.0 µg · kg^-1 · min^-1 were started. Transthoracic pulmonary artery catheters were placed before the discontinuation of CPB. Efforts to maintain moderate hypocarbia while in the operating room were used in all patients. Lung biopsies were not performed routinely.

View larger version (15K): [in this window] [in a new window]   Fig 1. Frontal view of flap valve ventricular septal defect (VSD) patch. (Ao Ann = aortic annulus; LV = left ventricle.)

View larger version (4K): [in this window] [in a new window]   Fig 2. Lateral view of flap valve ventricular septal defect (VSD) patch. (Ao Ann = aortic annulus; LV = left ventricle; RV = right ventricle.)

Follow-up evaluation
Follow-up with the parents or primary care physician of each patient was conducted by three of the authors (V.V.L., W.M.N., I.M.) during the interval between November 1, 1997, and December 15, 1997. No patient was lost to follow-up.

	Results

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Preoperative data
The mean preoperative room air arterial saturation obtained at cardiac catheterization was 89% ± 5%. The preoperative systolic pulmonary artery pressure was 105 ± 16 mm Hg. The mean PVR was 11.4 ± 4.1 Wood units. Pulmonary artery to systemic artery systolic pressure ratio was 0.93 ± 0.09. The calculated ratio of pulmonary to systemic blood flow was 1.4 ± 0.41:1. Preoperative values for all patients are displayed in Table 1.

Postoperative data
The pulmonary artery systolic pressure after repair was 42 ± 14 mm Hg (p < 0.001 versus preoperative value), with a corresponding systemic arterial systolic pressure of 95 ± 8 mm Hg for a ratio of 0.44 ± 0.12:1 (p < 0.001 versus preoperative ratio). Fluctuations in systemic saturations were observed when pulmonary artery pressures approached systemic pressures. Postoperative saturations on discharge from the hospital were 98% ± 2% (not significantly different from preoperative saturations), and saturations obtained at clinic follow-up were 96% ± 2%.

Follow-up data
All patients survived operation and were discharged from the hospital. One late death occurred 9 months postoperatively in the child with DORV. Echocardiographic analysis of this child revealed an estimated right ventricular systolic pressure of 75 mm Hg with a systemic arterial blood pressure of 90 mm Hg and room air saturation of 87%. Doppler examination of the pulmonary outflow tract estimated a supravalvar neopulmonary artery gradient of 40 mm Hg. Color flow mapping of the VSD patch imaged intermittent right-to-left shunting. Recommendations for repeat cardiac catheterization were made. Unfortunately, the child died 3 days before the scheduled date. Echocardiographic analysis was performed in all children within 2 weeks of the surgery. No other child demonstrated shunting across the VSD flap valve patch.

	Comment

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Pulmonary hypertension is a severe complication of a large VSD. Historically, surgical closure of a large VSD with PHT is associated with high mortality rates [6], and even in the recent surgical era, postoperative PHT remains a significant risk factor for morbidity and mortality [7]. However, the evolution of medical management of PHT after surgical correction of defects with preoperative PHT has resulted in a decrease in perioperative mortality [2, 7]. Moreover, the cost of these treatment modalities is considerable, and most patients must receive them while intubated in the intensive care unit [8, 9]. The creation of an intracardiac defect to prevent right ventricular failure has been used previously with variable success [10–12]. The modification we described allowed all patients to be extubated within 48 hours and there was no perioperative mortality. The double patch flap valve modification provides a means of maintaining systemic cardiac output during pulmonary hypertensive episodes and preventing acute right ventricular volume overload. We believe that this modification is analogous to the fenestration now commonly placed in lateral tunnel total cavopulmonary connections for patients to be considered high risk because of elevated PVR [13]. The possibility that reduced right ventricular forward flow leading to right ventricular dilation that compresses the left ventricle and causes a drop in systolic blood pressure during pulmonary hypertensive episodes [14] can be largely prevented with the modification we have described.

The results of closure of a large VSD in children with elevated PVR is well documented [15]. Current wisdom suggests that a PVR of at least 10 Wood units is to be considered a contraindication to surgical intervention [16]. The progression of pulmonary vascular disease after operative closure with the development of severe PHT and death is well known [17]. Ventricular septal defect closure in children with moderate to severe elevation in PVR preoperatively that decreases after closure of the defect has also been described [18]. Previous authors [19, 20] have reported that the immediate postrepair and 1-year follow-up PVR and pulmonary artery pressure after closure of high-resistance, high-pressure VSDs are related to the grade of Heath Edwards changes present at the time of repair. However, in 3 of the 6 patients in Freid and coworkers’ report [19], the immediate postrepair pulmonary artery pressure decreased. It remained unchanged in 1 and increased in only 2 patients. All 6 of these patients had at least grade 3 Heath Edwards changes on lung biopsy samples, and in 1 patient, who had a decrease in pulmonary artery pressure postoperatively, there were some grade 4 lesions noted on the biopsy sample.

The long-term survival of patients with severely elevated PVR and pulmonary artery pressure after closure of their defect is controversial. Hallidie-Smith and associates [21] reported 36 patients with VSD and PVR of at least 8 Wood units who underwent VSD closure. Twenty-eight of the 36 patients survived operation, and 25 of these underwent repeat cardiac catheterization 1 to 8 years postoperatively. Eighteen of the 25 patients had a normal to moderately elevated pulmonary artery pressure, and 9 of the patients had a PVR of 3 Wood units or less. Castañeda and colleagues [22] reviewed 55 patients with a high-pressure, high-resistance VSD who underwent closure and found that of the 22 patients who underwent repeat cardiac catheterization at 1 year, the PVR and pulmonary artery pressures fell, but remained above normal values. A major concern when surgically treating patients with increased pulmonary artery pressure and elevated PVR secondary to large left-to-right shunts is the possibility that patients with irreversible pulmonary vascular disease will undergo operation. Under such circumstances, the operation would unfavorably affect the natural history of Eisenminger’s syndrome [23] and lead to an earlier demise [17]. However, recent reports of patients with primary PHT who have improved hemodynamics and exercise capability after the use of intravenous [24] and high-dose oral calcium-channel blockers [25] or continuous intravenous prostacyclin infusion suggest that pulmonary vascular remodeling may take place [26], especially in children [27].

We have shown that a unidirectional flap valve VSD patch allows for a low-risk closure of a large VSD in the presence of PHT and elevated PVR. Long-term survival of these patients will depend on the degree of regression of the PVR. The possibility that calcium-channel blockers and prostacyclin could further help reduce PVR and pulmonary artery pressure in patients such as these deserves clinical investigation.

	Acknowledgments

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
We thank Melissa Patterson and Sandy McMahan for help preparing this manuscript, and Elizabeth Jameson, BSN, for help with the illustrations. A portion of the funds for this study was provided by the Variety Club of Memphis and the International Children’s Heart Foundation.

	References

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1. Blackstone E.H., Kirklin J.W., Bradley E.L., DuShane J.W., Appelbaum A. Optimal age and results in repair of large ventricular septal defects. J Thorac Cardiovasc Surg 1976;72:661-678.[Abstract]
2. Bando K., Turrentine M.W., Sharp T.G., et al. Pulmonary hypertension after operations for congenital heart disease: analysis of risk factors and management. J Thorac Cardiovasc Surg 1996;112:1600-1609.[Abstract/Free Full Text]
3. Goldman A.P., Delius R.E., Deanfield J.E., Macrae D.J. Nitric oxide is superior to prostacyclin for pulmonary hypertension after cardiac operations. Ann Thorac Surg 1995;60:300-306.[Abstract/Free Full Text]
4. Goldman A.P., Delius R.D., Deanfield J.E., et al. Nitric oxide might reduce the need for extracorporeal support in children with critical postoperative pulmonary hypertension. Ann Thorac Surg 1996;62:750-755.[Abstract/Free Full Text]
5. World Health Organization. Health manpower requirements for the achievement of health for all by the year 2000. WHO: Technical Report Series 717;1985.
6. Frontera-Izquierdo P., Cabezuelo-Huerta G. Natural and modified history of isolated ventricular septal defect: a 17-year study. Pediatr Cardiol 1992;13:193-197.[Medline]
7. Bando K., Turrentine M.W., Sun K., et al. Surgical management of complete atrioventricular septal defects. J Thorac Cardiovasc Surg 1995;110:1543-1554.[Abstract/Free Full Text]
8. Chang A.C., Zucker H.A., Hickey P.R., Wessel D.L. Pulmonary vascular resistance in infants after cardiac surgery: role of carbon dioxide and hydrogen ion. Crit Care Med 1995;23:568-574.[Medline]
9. Wessel D.L., Adatia I., Giglia T.M., Thompson J.E., Kulik T.J. Use of inhaled nitric oxide and acetylcholine in the evaluation of pulmonary hypertension and endothelial function after cardiopulmonary bypass. Circulation 1993;88:2128-2138.[Abstract/Free Full Text]
10. Lin S.F., Chiu I.S., Hsu R.B. Creation of a one-way interatrial communication in the treatment of critical pulmonary stenosis with intact ventricular septum: a case report. J Card Surg 1996;11:368-370.[Medline]
11. Karagoz H.Y., Tasdemir O., Yakut C., Bayazit K. Atrial septal defect for right ventricular failure. Ann Thorac Surg 1988;45:350-351.
12. Zhou Q., Lai Y., Wei H., Song R., Wu Y., Zhang H. Unidirectional valve patch for repair of cardiac septal defects with pulmonary hypertension. Ann Thorac Surg 1995;60:1245-1249.[Abstract/Free Full Text]
13. Kirklin J.W. Tricuspid atresia and the Fontan operation. In: Kirklin J.W., Barratt-Boyes B.G., eds. Cardiac surgery: morphology, diagnostic criteria, natural history, techniques, results, and indications. New York: Churchill Livingstone, 1993:1055-1104.
14. Del Nido P.J., Williams W.G., Villamater J., et al. Changes in pericardial surface pressure during pulmonary hypertensive crises after cardiac surgery. Circulation 1987;76(Suppl 3):III-93-III-96.[Medline]
15. Ikawa S., Shimazaki Y., Nakano S., et al. Pulmonary vascular resistance during exercise late after repair of large ventricular septal defects. J Thorac Cardiovasc Surg 1995;109:1218-1224.[Abstract/Free Full Text]
16. De Leval M. Ventricular septal defects. In: Stark J., de Leval M., eds. Surgery for congenital heart defects. Philadelphia: WB Saunders, 1994:355-372.
17. Momma K., Takao A., Ando M., Nakazawa M., Takamizawa K. Natural and postoperative history of pulmonary vascular obstruction associated with ventricular septal defect. Jpn Circ J 1981;45:230-237.[Medline]
18. Lillehei C.W., Anderson R.C., Eliot R.S., Wang Y., Ferlic R.M. Pre- and postoperative cardiac catheterization in 200 patients undergoing closure of ventricular septal defects. Surgery 1968;63:69-76.
19. Freid R., Falkovsky G., Newburger J., et al. Pulmonary arterial changes in patients with ventricular septal defects and severe pulmonary hypertension. Pediatr Cardiol 1986;7:147-154.[Medline]
20. Rabinovitch M., Keane J.F., Norwood W.I., Castañeda A.R., Reid L. Vascular structure in lung tissue obtained at biopsy correlated with pulmonary hemodynamic findings after repair of congenital heart defects. Circulation 1984;69:655-667.[Abstract/Free Full Text]
21. Hallidie-Smith K.A., Hollman A., Cleland W.P., Bentall H.H., Goodwin J.F. Effects of surgical closure of ventricular septal defects upon pulmonary vascular disease. Br Heart J 1969;31:249-260.
22. Castañeda A.R., Zamora R., Nicoloff D.M., et al. High-pressure, high-resistance ventricular septal defect. Ann Thorac Surg 1971;12:29-38.[Abstract/Free Full Text]
23. Kidd L., Driscoll D.F., Gersony W.M., et al. Second natural history study of congenital heart defects: results of treatment of patients with ventricular septal defects. Circulation 1993;87(Suppl 1):I-38-I-51.[Medline]
24. Mali I., Richter D. Verapamil in primary pulmonary hypertension. Br Heart J 1985;53:345-347.[Abstract/Free Full Text]
25. Rich S., Kaufmann E., Levy P.S. The effect of high doses of calcium-channel blockers on survival in primary pulmonary hypertension. N Engl J Med 1992;327:76-81.[Medline]
26. Barst R.J., Rubin L.J., Long W.A., et al. A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. N Engl J Med 1996;334:296-301.[Medline]
27. Barst R.J. Pharmacologically induced pulmonary vasodilation in children and young adults with primary pulmonary hypertension. Chest 1986;89:497-503.[Abstract/Free Full Text]

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