Recurrent Ventricular Septal Defect Research Articles

Methods for Repair of Simple Isolated Ventricular Septal Defect

One hundred fifteen consecutive patients underwent repair of a variety of "isolated" simple ventricular septal defects (VSD), from February 1985 through December 1989. In no patient was a ventriculotomy required to accomplish the ventricular septal defect closure. There were no instances of permanent complete atrioventricular dissociation, and there have been no reoperations for residual or recurrent VSD. Postoperative echocardiographic and Doppler studies were performed in each patient and revealed good surgical results. There was one hospital death. The technical strategies used to accomplish the repair are described. These include methods for transatrial, transaortic, and transpulmonary approach to VSD closure. Enabling methodologies described include detaching the septal leaflet of the tricuspid valve to enhance VSD exposure in patients wherein the defect is obstructed by the tricuspid valve with "aneurysm of the membranous septum." Also, splitting of the VSD patch in order to manage tricuspid valve chordal straddling is outlined.

Surgical intervention for drug-resistant ventricular tachycardia

EndocardiaL resection was required in 26 patients with sustained drug-resistant ventricular tachycardia. The early mortality rate (within 30 days after operation) was 12%. Two deaths were the result of low cardiac output, and the third death was related to recurrent ventricular septal defect after septal endocardial resection. The survivors of endocardial resection were followed up from 6 to 92 months (mean 43). There were no recurrences of ventricular arrhythmias, and patients did not require antiarrhythmic drug therapy. The late mortality rate after endocardial resection was 19%. There were two late cardiac-related deaths (unrelated to arrhythmias) and three late deaths from noncardiac causes.Complete endocardial resection successfully ablates drug-resistant ventricular tachycardia, but is associated with an increased perioperative mortality rate in those patients who have severely depressed left ventricular function without a well defined left ventricular aneurysm.

Survival, functional status, and reoperations after repair of tetralogy of Fallot with pulmonary atresia

Among 139 patients who underwent repair of tetralogy with pulmonary atresia, survival rates at 1 month and at 1, 5, 10, and 20 years were 85%, 82%, 76%, 69%, and 58%, respectively. The hazard function (instantaneous risk of dying) was greatest immediately after operation and declined thereafter, but a low constant hazard persisted for as long as the patients were followed up. Multivariately, the postrepair ratio between peak right ventricular and left ventricular pressures measured in the operating room provided the most information relative to the probability of death after repair, and cardiopulmonary bypass time the next. When morphologic abnormalities of the pulmonary circulation were considered in the multivariate analysis for risk factors for death, the size of the pulmonary arteries provided the most information, followed by the number of large aortopulmonary collateral arteries. The postrepair peak right ventricular/left ventricular pressure ratio was lower the day after operation than in the operating room in 65% of the patients in whom the measurements were made. Recurrent or residual ventricular septal defects necessitating rerepair occurred in four patients (3% of hospital survivors). Most surviving patients were in New York Heart Association class I at the time of follow-up. Early, intermediate, and long-term survival is less good after repair of tetralogy with pulmonary atresia than after repair of tetralogy with pulmonary stenosis. This is related primarily to the greater prevalence of high peak right ventricular/left ventricular pressure ratio measured in the operating room in the former group. Both the postrepair peak right ventricular/left ventricular pressure ratio in the operating room and the probability of death are inversely related to the size of the pulmonary arteries and directly to the number of large aortopulmonary collateral arteries. This and inferences from other risk factors may be helpful in achieving better results in the future.

Repair of ventricular septal defect in adults.

To evaluate the outcome of ventricular septal defect (VSD) with long duration of haemodynamic derangement, a retrospective study was made of 42 consecutive patients who underwent closure of VSD as adults (age range 15-48, mean 27 years). The mean systolic pulmonary arterial pressure was 53 mmHg, mean pulmonary vascular resistance 2.5 Wood units and mean pulmonary/systemic flow ratio 2.4. VSD was complicated by aortic regurgitation in 12 cases, mitral regurgitation in 4, and sinus of Valsalva fistula in 6 cases. There were 15 supracristal, 24 infracristal and 3 muscular VSDs. In addition to VSD closure, surgery included aortic valve replacement (7 cases), mitral valve replacement (2), valve repair by suture (7) and repair of Valsalva sinus fistula (6 cases). Two patients died in the early postoperative period and two during follow-up (1-10, mean 4.5 years). The early and the late mortality were related to large infracristal VSD, pulmonary hypertension and irreversible pulmonary vascular changes which could not be anticipated on the basis of high calculated shunt flow at preoperative catheterization. No patient with supracristal VSD died. Recurrent VSD was diagnosed in five patients, three of whom needed reoperation and recovered uneventfully. Reduction of heart size and improved exercise tolerance were the most pertinent follow-up findings. The results suggest that large supracristal VSD with aortic valve involvement can be successfully closed in adults, but that the prospect for large infracristal VSD is less favourable if correction is postponed until adulthood.

Encircling endocardial resection with complete removal of endocardial scar without intraoperative mapping for the ablation of drug-resistant ventricular tachycardia

Encircling endocardial resection, with complete removal of endocardial scar unguided by intraoperative mapping, was employed in 10 patients with drug-resistant sustained ventricular tachycardia. Reproducible sustained ventricular tachycardia was induced in all patients preoperatively with programmed electrical stimulation. A trial of conventional antiarrhythmics had failed in all 10 patients; seven patients required frequent cardioversion, and three patients required overdrive suppression with temporary transvenous pacing. Encircling endocardial resection was performed in all patients, with complete removal of endocardial scar; partial reimplantation of the mitral apparatus was required in nine patients. Eight patients underwent aneurysmectomy, and the nine patients who required concomitant aorta-coronary bypass received a total of 13 grafts (mean 1.3 grafts per patient). There were no spontaneous postoperative arrhythmias. One patient without postoperative clinical arrhythmias, who had required daily preoperative cardioversion, had inducible ventricular tachycardia with postoperative programmed electrical stimulation, but not after loading with procainamide. Mean follow-up was 17.3 months. Eight patients are alive and well. There were two late deaths. One patient died with recurrent ventricular septal defects 2.5 months following extensive septal encircling endocardial resection, and one patient was readmitted after 4 months with massive pulmonary embolus and right-sided heart failure. This early experience suggests that this procedure, with complete removal of endocardial scar, successfully ablates reentrant ventricular tachycardia. We believe that the procedure will prove to be more effective than localized endocardial resection because the encircling procedure removes all ventricular sites that have the potential to generate reentrant ventricular tachycardia.

Myocardial protection in infant open heart surgery.

Myocardial protection was evaluated in 2 groups of 5 infants each undergoing correction of either tetralogy of Fallot (TOF) or subcristal ventricular septal defect (VSD). In group A, profound hypothermia and total circulatory arrest (PHTCA) was utilized. In group B, profound hypothermia and total circulatory arrest combined with potassium cardioplegia (PHTCA + K) was the method of protection used. The analysis was carried out by sequential measurements of clinical, electrocardiographic, enzymatic (CK-MB) and ultrastructural parameters. There were no operative deaths. One infant had a second operation for recurrent VSD. The average anoxic time was 35.4 min in group A (PHTCA) and 32.6 min in group B (PHTCA + K). Analysis of our data demonstrated that when potassium cardioplegia was added to PHTCA, there was less intraoperative myocardial damage according to physiological, ultrastructural and biochemical parameters than when profound hypothermia and total circulatory arrest was applied alone.

Transposition of the great arteries, ventricular septal defect, and left ventricular outflow obstruction: results of conservative correction.

Summary Sixteen children with transposition of the great arteries (TGA), ventricular septal defect (VSD), and left ventricular outflow obstruction (LVOO) underwent intracardiac correction. The atrio-ventricular relationship was concordant in all instances. The VSD was single in 1 3 and multiple in 2 patients. In one child a common ventricle was found. LVOO presented as valvular stenosis in 2 cases, subvalvular stenosis in 9 cases, and combined valvular and subvalvular stenosis in one case. Three patients had previously undergone banding of the pulmonary artery. Intracardiac correction consisted in atrial inversion according to the Mustard technique. In 11 cases complete closure of the VSD was achieved. Because of incomplete subpulmonary resection, in 4 instances the VSD remained only partially closed. In the child with a common ventricle, atrial inversion without closure of the ventricular communication was performed. LVOO was treated by valvulotomy, resection of subpulmonary stenosis, or debanding of the pulmonary artery. There were two early deaths and one late death. Because of a recurrent VSD and severe tricuspid incompetence, reintervention with VSD closure and tricuspid valve replacement was necessary in one case. All surviving patients (81%) are in good clinical condition, although only in 7 of them had the VSD initially been totally closed. The presented results of conservative correction are comparable to those after the Rastelli operation for TGA, VSD, and LVOO. It may be advantageous, particularly in the younger children, that with this hemodynamic repair no extracardiac conduit is required.

Surgical repair of isolated ventricular septal defects in the first year of life.

Since October 1975, 6 infants ranging in age from 5 to 9 months and weighing from 5.2 to 7.8 kg have been treated with primary closure of ventricular septal defect (VSD) at Ullevål Hospital. The indications for operation were large left-to-right shunts combined with persistence of heart failure in 4 patients, a large left-to-right shunt only in one and elevated pulmonary arterial resistance in one patient. Conventional cardiopulmonary bypass was used in all cases. There were no early or late deaths during the mean observation period of 17.3 months (range 3--25 months). One patient developed a recurrent VSD and was successfully re-operated on 8 months after the first operation; otherwise no signs of recurrence were found. The growth and weight gains have been satisfactory and the psychosomatic development of all the infants has been normal. All are in sinus rhythm with right bundle branch block in 4. Cardiac arrhythmias have not been in evidence.

Left ventriculotomy for closure of muscular ventricular septal defects. Treatment of choice.

Closure of muscular ventricular septal defects (VSDs) through the right atriotomy or right ventriculotomy may be difficult. These VSDs are often located behind the hypertrophied trabeculae carnae or papillary muscle. Residual or recurrent VSD may result from the difficult approach. Between March 1971 and December 1975, we have used the left ventriculotomy near the apex for closure of muscular VSDs in ten children. The patients' ages ranged from five months to eight years and three months. The diagnosis was established by cardiac catheterisation and left ventricular angiocardiogram in all patients. Six patients had multiple VSDs; in four patients VSD in the muscular septum was present (three apical, one midseptal). Operations were performed on cardiopulmonary bypass with moderate hypothermia and intermittent anoxic arrest. VSDs in the membranous septum were closed through the right atrium. Muscular VSDs were approached through a small vertical incision in the left ventricle near the apex. The postoperative course was uneventful in eight patients. Two patients, aged 16 months and eight years, died; histology showed grade IV pulmonary vascular disease in both. All survivors are well four months to five years after the operation, without clinical evidence of residual or recurrent VSD.

Aneurysm of Pericardial Right Ventricular Outflow Tract Patches

Among 1,022 patients who underwent repair of tetralogy of Fallot, 252 received a pericardial patch of the right ventricular outflow tract; of these, 10 subsequently developed an aneurysm of the right ventricular outflow tract. Cardiac catheterization and angiography revealed moderate pulmonary insufficiency in all patients, a residual pressure gradient in the right ventricular outflow tract in 7, and a residual ventricular septal defect in 2 patients. Reoperation was indicated in 8 patients because of progressive distention of the aneurysm, residual infundibular or pulmonary artery stenosis, and recurrent ventricular septal defect. Reconstruction of the right ventricular outflow tract was accomplished by resection of the aneurysm and insertion of a woven Dacron patch in 5 patients, primary suture of the pulmonary artery in 2, and implantation of a woven Dacron conduit containing a Björk-Shiley cardiac valve prosthesis in 1 patient. There were no early or late deaths. When reconstruction of the right ventricular outflow tract is necessary, we recommend a woven Dacron patch because pericardium may form an aneurysm.

Reoperation after total correction of tetralogy of Fallot

Fifteen patients have required repeat heart surgery after total correction of tetralogy of Fallot. Indications for reoperation included recurrent ventricular septal defect (VSD), 9 patients; tricuspid regurgitation, 2 patients; residual right ventricular hypertension, 1 patient; and infection of the right ventriculotomy, 3 patients. From this experience, we have drawn the following conclusions: (1) The need for reoperation after correction of Fallot's tetralogy is unusual; (2) although technically more difficult than the primary operation, the second operation does not cause an excessive mortality rate (13 of 15 survived), and (3) properly selected patients derive substantial benefit from reoperation.

Surgical Experience with Recurrent Ventricular Septal Defect

Twenty-two of 370 patients undergoing closure of ventricular septal defect required reoperation to close a residual defect. These defects tended to be in the posteroinferior angle of the defect, and the recurrence was never due to tearing of the prosthetic patch but always to failure of the sutures to hold securely in the perimeter of the defect. Closure of the recurrent defect was advised when the left-to-right shunt exceeded 2:1 or when significant right ventricular outflow obstruction remained due to unrelieved obstruction in Fallot's anomaly or to cicatricial stenosis following removal of a pulmonary artery band. The second operations were less hazardous than had been feared and yielded satisfactory results in all but 1 of the survivors.

Aortic Sinus Fistula—Surgical Considerations and Results of Operation

From 1956 to 1971, 21 Mayo Clinic patients underwent surgical correction of aortic sinus fistula. The 12 male and 9 female patients were from 3 to 52 years old (median 27 years). In 16 patients the right aortic sinus had ruptured into the right ventricle, and in 1, into the right atrium; in 4 patients a noncoronary sinus fistula communicated with the right atrium. The appearance of 4 fistulas was related to trauma, but all 21 fistulas were basically congenital in origin. Associated lesions were common; 15 patients had one or more of the following: ventricular septal defect (VSD) (14 patients), aortic insufficiency (7 patients), and pulmonary stenosis (3 patients). All patients survived operation. Three required reoperation: 1 for closure of a recurrent VSD (deterioration of an Ivalon sponge patch), 1 for recurrence of the fistula and VSD, and 1 to replace a malfunctioning Teflon cusp with a prosthetic valve. Follow-up has been carried out for as long as fourteen years (median seven years) after operation. One patient has moderate aortic insufficiency but remains well compensated; the remaining patients are free of symptoms and clinical signs of cardiac dysfunction. Currently, an aortic sinus fistula should be repaired when it is diagnosed because the disability is progressive, operative risk is negligible, and long-term results are excellent.

On the problem of recurrent ventricular septal defect

On the problem of recurrent ventricular septal defect