Asian Cardiovasc Thorac Ann 2003;11:213-216
© 2003 Asia Publishing EXchange Ltd
Primary Surgical Repair of Ventricular Septal Defect
M Kemal Demirag, MD,
Hasan Tahsin Keçeligil, MD,
Fersat Kolbakir, MD
Department of Cardiovascular Surgery, Ondokuz Mayis University Medical School, Samsun, Turkey
For reprint information contact: Hasan Tahsin Keçeligil, MD Tel: 90 362 457 6000/3222 Fax: 90 362 457 6029 email: santa{at}omu.edu.tr Ondokuz Mayis University Medical School, Department of Cardiovascular Surgery, 55139, Samsun, Turkey.
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ABSTRACT
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Between January 1983 and December 2000, 78 patients underwent primary repair of a ventricular septal defect. There were 42 males (54%) and 36 females (46%) of whom 13 (17%) were under 1 year old, 50 (64%) were aged 1–10 years, 11 (14%) were aged 10–20 years, and 4 (5%) were over 20 years old. The ventricular septal defect was a perimembranous type in 60 patients (77%), subarterial (outlet) type in 10 (13%), and atrioventricular canal (inlet) type in 4 (5%). Operative repair was performed with a patch in all except 2 patients. Early postoperative complications included insignificant aortic regurgitation in 4 patients, persistent complete heart block in 1, and residual shunt in 4. There were 5 early deaths (6.4%) and 1 late death (1.8%) in 56 patients followed up. Early primary closure of ventricular septal defects, usually via a right atriotomy, can be performed with acceptable mortality and morbidity rates.
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INTRODUCTION
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Isolated ventricular septal defect (VSD) is the most common congenital cardiac malformation which is observed in 1 in 1,000 live births. Half of the cases requiring surgical treatment have associated major cardiovascular malformations.1 The most common associated anomaly is patent ductus arteriosus (PDA) in 6%.2 The first successful intracardiac repair of VSD under direct vision was performed using the cross-circulation method by Lillehei and colleagues3 in 1955. Kirklin and colleagues4 described VSD repair using extracorporeal circulation in 1957.
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PATIENTS AND METHODS
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Records of 78 patients with VSD who underwent open heart surgery in Ondokuz Mayis University Cardiovascular Surgery Clinic between January 1983 and December 2000, were analyzed retrospectively. Patients with complex congenital heart defects (including aortic coarctation) were excluded, but those with PDA, atrial septal defect (ASD), systemic venous return anomaly, or insufficiency of the atrioventricular or semilunar valves were included. There were 42 males (54%) and 36 females (46%). Their preoperative characteristics are shown in Table 1
. Signs and symptoms, telecardiography (cardiothoracic index), and electrocardiogram (ECG) were taken into consideration in preoperative evaluation. Diagnoses were obtained by echocardiography and angiocardiography. Right-left pressures, degree of shunting, and ejection fraction were calculated in all cases (Table 1). During preoperative evaluation, an ASD was found in 9 patients (12%), PDA in 11 (14%), persistent left superior vena cava in 3 (4%), mild tricuspid insufficiency in 2 (3%), mild mitral insufficiency in 3 (4%), and aortic insufficiency in 9 (12%). Preoperative echocardiography and angiocardiography indicated the type of VSD, which was confirmed intraoperatively (Table 2).
Generally, surgery was indicated in a patient whose shunt ratio was 1.5 or more. In addition, those with congestive heart failure resistant to medical therapy, recurrent pulmonary infections, or deteriorating aortic valve function as shown by serial echocardiograms were operated without delay. Under general anesthesia and via a midline sternotomy, standard bicaval venous and ascending aortic cannulation was performed, and extracorporeal circulation was established. Just before starting bypass in 11 patients with PDA, the ductus was located intrapericardially and ligated. Systemic hypothermia was maintained at 30°C. In the first 48 patients, antegrade cold (4°C) crystalloid potassium cardioplegia was used before aortic clamping, and in the next 30 patients, antegrade cold (4°C) blood cardioplegia and topical cooling were employed. A right atriotomy was performed and the left ventricle and atrium were vented through the ASD or fossa ovalis. The right ventricle was explored through the tricuspid valve. The VSD could not be approached in 4 patients; they had a right ventriculotomy, with an aortotomy in 2 of them. The VSD was repaired with a Dacron patch in 72 cases (92%) and with a pericardial patch in 4 (5%), using pledgeted 4/0 polypropylene sutures. Primary suture repair was undertaken with 4/0 nonabsorbable multifilament suture in 2 cases (3%). In 2 patients with a wide ASD, the defects were repaired with Dacron patches secured by continuous sutures; primary suture repair was used in the other 7 cases of ASD. One patient with aortic insufficiency underwent concomitant aortic valve replacement. After closing the atrial septum and right atriotomy, de-airing was performed, the aortic crossclamp was removed, and the patient was rewarmed. Extracorporeal circulation was discontinued when the hemodynamic status was satisfactory. The mean crossclamp time was 45.5 ± 9.5 min, and cardiopulmonary bypass time was 60.2 ± 14.8 min. After hemorrhage control, the sternum was closed with an absorbable monofilament continuous suture in patients with body weight less than 40 kg. In heavier patients, stainless steel wires were used.
In the postoperative period, blood volume was carefully evaluated. In the first 48 hours, systemic arterial pressure, central venous pressure, hourly urinary flow, and continuous ECG monitoring were performed. Left atrial pressure and cardiac output were not monitored routinely. In the intensive care unit, 36 patients were extubated in the first 8 hours (46%), 32 were extubated within 16 hours (41%), and 10 were extubated after more than 16 hours (13%).
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RESULTS
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Five patients died in the early postoperative period; hospital mortality was 6.4%. Details of these patients are given in Table 3. The most common nonfatal postoperative complication was low cardiac output syndrome in 12 patients (15%). Respiratory insufficiency (ventilatory support > 48 hours) was noted in 6 cases (8%). Temporary atrioventricular dissociation was seen in 2 patients (3%) who normalized in the first postoperative day. One patient had complete heart block (1%). Two patients required reoperation within 8 hours because of excessive bleeding (3%). A central nervous system complication (hemiparesthesia) occurred in 1 patient, and resolved by the 8th postoperative day.
Of the 73 hospital survivors, 56 (77%) were followed up for 6.5 ± 4.2 years (range, 2–19 years) by physical examination, ECG, telecardiography and echocardiography. Their symptoms regressed to a large extent, especially in those who had congestive heart failure preoperatively. All of the children gained weight and developed in accordance with their age group. The ECG showed normal sinus rhythm in 35 (63%) patients, complete right bundle branch block in 18 (32%), left anterior hemiblock in 2 (4%), and one had a pacemaker implanted due to complete heart block. This patient died in the 5th month postoperatively because of endocarditis and septicemia (late mortality, 1.8%). Echocardiography showed a residual shunt in 4 patients (7%), which was hemodynamically important in 3 of them; angiocardiography was performed again in this group. The 3 patients with significant residual shunts underwent successful reoperation after 2–7 months; 2 of these patients had undergone initial VSD repair by primary suture but the sutures had torn away from the tissue, the other had an intact patch repair but there was a second VSD in another location. Two of the 9 patients with aortic insufficiency (7 first-degree, 1 second-degree, 1 third-degree) had a perimembranous VSD and 7 had a subarterial type. The patient with third-degree aortic insufficiency required aortic valve replacement, the others did not need any intervention. In late follow-up echocardiography, 4 patients had mild aortic insufficiency and 4 had no signs of aortic insufficiency; none had deteriorating aortic insufficiency.
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DISCUSSION
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Ventricular septal defect is the most common congenital heart lesion; 30% of patients with congenital heart disease have a VSD.5 A quarter of infants with a large VSD develop congestive heart failure in their first year of life, and 20% have progressive pulmonary vascular disease.6,7 Because medical therapy alone has a high mortality in this critically ill group, surgery is indicated.5 The physiopathology of VSD is related to the size of the defect and the pulmonary vascular resistance. The relationship between these variables affects the pressure gradient between the ventricles and the shunt volume. If the diameter of the VSD is similar to that of the aortic valve, there will be little resistance to the flow (nonrestrictive), the right ventricular systolic pressure will equal the left ventricular pressure, and there will be a large increase in pulmonary blood volume.
Because VSD has a tendency for spontaneous closure, its incidence is lower in the adult population. The perimembranous type of VSD closes more often than atrioventricular canal and subarterial types, and the probability of spontaneous closure is inversely related to age.1,2 The surgical indications are severity of symptoms, degree of pulmonary vascular resistance, type and diameter of the defect, and associated malformations.1,2 In infants with severe congestive heart failure despite optimal medical therapy, early surgery is indicated.1 Yacoub and colleagues8 advocated repair in the first year of life for a large VSD causing severe intractable heart failure or pulmonary hypertension. Yeage and colleagues9 recommended primary surgical treatment in patients deteriorating physically, those with congestive heart failure, and infants under 1 year of age with pulmonary arterial hypertension, which is the approach preferred in our clinic. Although there is a consensus on surgical repair of large defects, the approach in cases of restrictive VSD with a shunt ratio < 2.0 is still debated. According to Backer and colleagues,10 the indications for VSD repair should be extended because operative mortality and the incidence of residual VSD are currently very low. Good results of VSD operations in infancy have been reported by several groups.11–13
Aortic insufficiency in VSD patients is usually the result of prolapse of the right aortic cusp towards the VSD, and although it is common in conal defects, it is also seen in perimembranous VSD.10,14 Corone and colleagues15 found that 6.3% of VSD patients developed aortic insufficiency. Otterstad and colleagues16 reported that 12 (11%) of 109 patients older than 15 years of age developed aortic insufficiency. Aortic insufficiency was found in 9 (12%) cases in our series. Among these patients, 8 did not have surgical treatment because their aortic insufficiency was not more than second-degree; postoperatively, 4 had insignificant aortic insufficiency and 4 had no insufficiency. Generally, we prefer to avoid aortic valve replacement, and we recommend that VSD patients be operated on before serious damage to the aortic valve occurs.
Bacterial endocarditis arises as a consequence of turbulent flow due to VSD, and mainly affects the tricuspid valve. Corone and colleagues15 claimed that the risk of bacterial endocarditis in isolated VSD cases is 3.7%. Otterstad and colleagues16 studied 1,091 cases of isolated VSD and found the risk of bacterial endocarditis was 15%. The risk of bacterial endocarditis is not completely eliminated by surgical repair of VSD, but it is substantially decreased.10 In the Second Natural History Study, VSD repair was not found to reduce the incidence of bacterial endocarditis.17 Waldman and colleagues18 advocate considering a nonsurgical approach in children with a small VSD in view of the operative risks, cosmetic implications, and cost-effectiveness. Nygren and colleagues19 claim that surgical indications are becoming more liberal in cases of a small (restrictive) asymptomatic VSD when the shunt ratio is 1.5 to 1.99. We agree with this and consider that in addition to the conventional indications, defects with a shunt ratio of 1.5–1.99 and subarterial and perimembranous types with aortic valve insufficiency should be included. Because aortic insufficiency due to VSD is progressive, surgery should be performed before serious aortic damage occurs.
Significant residual shunt was observed in 2 patients who had primary suture repair of their VSD. We recommend patch repair using pledgeted sutures in all cases. Only one patient had persistent complete heart block. The incidence of complete heart block ranged from 0%–2.3% in various studies.9,10,14 Ventricular arrhythmias were common after VSD repair in our study, in agreement with other reports. Houyel and colleagues20 noted that right bundle branch block was more common after a right ventriculotomy, a right atriotomy did not prevent development of late atrioventricular block. Whichever surgical route is used, ventricular arrhythmias are observed frequently in the late period, similar to their prevalence after surgery for tetralogy of Fallot.20 We concluded that a right atriotomy should be the preferred approach, and the recommendations based on our experience should ensure better early and late results.
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REFERENCES
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- Tchervenkov CI, Shum-Tim D. Ventricular septal defect. In: Baue A, Geha AS, Hammond GL, Laks H, Naunheim KS, editors. Glenn’s thoracic and cardiovascular surgery. Vol II. Stanford, CT: Appleton & Lange, 1996:1127–36.
- Pillai R. Atrial, ventricular and atrioventricular septal defects. In: Morris PJ, Malt RA, editors. Oxford textbook of surgery. Vol II. Oxford: Oxford University Press, 1994:1696–700.
- Lillehei CW, Cohen M, Warden HE. The results of direct vision closure of ventricular septal defects in eight patients by means of controlled cross circulation. Surg Gynecol Obstet 1955;101:446–51.
- Kirklin JW, Harshbarger HG, Donald DE, Edwards JE. Surgical correction of ventricular septal defect: anatomic and technical considerations. J Thorac Cardiovasc Surg 1957;33:45–9.
- Arciniegas A, Farooki ZQ, Hakimi M, Perry BL, Green EW. Surgical closure of ventricular septal defect during the first twelve months of life. J Thorac Cardiovasc Surg 1980;80:921–8.[Medline]
- Ritter DG, Felth RH, Weidman WH, Du Shane JW. Ventricular septal defect. Circulation 1965;32(Suppl III):42–52.
- Collins G, Calder L, Rose V, Kidd L, Keith J. Ventricular septal defect. Clinical and hemodynamic changes in the first five years of life. Am Heart J 1972;84:695–705.[Medline]
- Yacoub MH, Radley-Smith R, De Gasperis C. Primary repair of large ventricular septal in the first year of life. G Ital Cardiol 1978;8:827–31.[Medline]
- Yeager SB, Freed MD, Keane JF, Norwood WI, Castaneda AR. Primary surgical closure of ventricular septal defect in the first year of life: results of 128 infants. J Am Coll Cardiol 1984;3:1269–76.[Abstract]
- Backer CL, Winters RC, Zales VR, Takami H, Muster AJ, Benson DW Jr, et al. Restrictive ventricular septal defect: how small is too small to close? Ann Thorac Surg 1993;56:1014–9.[Abstract]
- Hardin JT, Muskett AD, Canter CE, Martin TC, Spray TL. Primary surgical closure of large ventricular septal defects in small infants. Ann Thorac Surg 1992;53:397–401.[Abstract]
- McGrath LB. Methods for repair of simple isolated ventricular septal defect. J Card Surg 1991;6:13–23.[Medline]
- Haneda K, Ishizawa E, Yamaki S, Itoh T, Horiuchi T, Mohri H, et al. Surgical closure of ventricular septal defect in the first year of life: forty-three consecutive successful cases. Tohoku J Exp Med 1988;156:39–45.[Medline]
- Erdil N, Birinciog lu CL, •I
can HZ, Çetin L, Akin G, Akgül A, et al. Early and late results in surgical treatment of isolated ventricular septal defects [Turkish]. T Klin J Cardiol 2000;13:83–90.
- Corone P, Doyon F, Gaudeau S, Guerin F, Vernant P, Ducam H, et al. Natural history of ventricular septal defect. A study involving 790 cases. Circulation 1977;55:908–15.[Abstract/Free Full Text]
- Otterstad JE, Nitter-Hauge S, Myhre E. Isolated ventricular septal defect in adults. Clinical and haemodynamic findings. Br Heart J 1983;50:343–8.[Abstract/Free Full Text]
- Gersony WM, Hayes CJ, Driscoll DJ, Keane JF, Kidd L, O’Fallon WM, et al. Bacterial endocarditis in patients with aortic stenosis, pulmonary stenosis, or ventricular septal defect. Circulation 1993;87(Suppl I):I121–6.
- Waldman JD. Why not close a small ventricular septal defect? Ann Thorac Surg 1993;56:1011–2.[Medline]
- Nygren A, Sunnegardh J, Berggren H. Preoperative evaluation and surgery in isolated ventricular septal defects: a 21-year perspective. Heart 2000;83:198–204.[Abstract/Free Full Text]
- Houyel L, Vaksmann G, Fournier A, Davignon A. Ventricular arrhythmias after correction of ventricular septal defects: importance of surgical approach. J Am Coll Cardiol 1990;16:1224–8.[Abstract]
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ABSTRACT
Introduction
