Biomedical subjects
Publications and source records attributed to A R Castaneda.
Repair of atrial septal defect primum (ASD primum) continues to be a challenge to the surgeon. The most common problems involve reconstructing the mitral valve and avoiding rhythm disturbances after the operation. In this report we describe our results in 92 patients with ASD primum who were operated upon between 1955 and 1975.
The course and prognosis of 208 patients with an ascending aorta to pulmonary artery anastomosis is reviewed. Mortality rate during, or within one month, of surgery was 24 per cent (50/208) and late mortality rate, prior to repair, was 10 per cent (21/208). An additional 5 per cent (10/208) died during subsequent intracardiac repair. Congestive heart failure developed in 25 per cent (53/208), pulmonary artery hypertension in 17 per cent (12/72), and pulmonary vascular obstruction in 6 per cent (4/72). An increase in orifice size of the stoma with time was documented in eight patients. Additional subsequent palliative surgery was required in 22 per cent (45/208). Mortality rate was directly related to age at operation and was highest in neonates less than one week of age. In infants with tetralogy of Fallot, a preliminary comparison of mortality rate between palliative surgery and primary repair clearly suggests that the latter is the preferred method of treatment.
Dacron valved conduits or aortic allografts were placed between the right heart and the pulmonary artery for repair of various complex congenital cardiac anomalies in 56 patients (aged 15 days to 33 years; median, 11 years). Forty-four patients had a total of 56 previous palliative procedures, which contributed to postoperative morbidity and mortality. Six patients had a total of seven episodes of early or late sepsis involving the conduit. One patient, treated for early sepsis, again developed infection in the Hancock graft 1 year postoperatively and died. Three other patients, 2 with calcified allografts, developed infections 4 months to 7 years following repair and required graft replacement. Hemodynamic data 1 month to 5 years (mean, 1.6 years) following repair revealed mild to moderate obstruction (less than 45 mm Hg gradient) at the Hancock conduit valve ring in 13 of 19 patients, while 5 had large pressure gradients (greater than 75 mm Hg). All aortic allografts had severe obstruction and calcification necessitating graft replacement. It is anticipated that improved technique and appropriate timing of palliative and corrective operations will substantially reduce or eliminate these problems.
Thirty-eight corrective operations have been performed in patients with tetralogy of Fallot and a functioning aortopulmonary shunt. There were 3 operative deaths (7.9%) and 1 late death (2.6%), and 3 patients have required reoperation for significant residual defects. Only 1 of 10 patients studied postoperatively by radionuclide scanning has a significant reduction in blood flow to the lung on the side of the closed shunt. We conclude that the presence of an aortopulmonary shunt does not add to the risk of repair in patients with tetralogy of Fallot and that mortality after such operations is related to the complex anatomy often present in patients of this group.
Surgical repair was performed on 8 patients with tetralogy of Fallot and congenital or acquired absence of the left pulmonary artery. Prior palliative systemic-pulmonary artery shunts had been performed in the 5 patients with acquired absence of the pulmonary artery, and in none was repair of the damaged pulmonary artery possible. A valve-containing conduit (Hancock) was used in each patient to prevent pulmonary valvular regurgitation during the early postoperative period. All patients survived operation and have exhibited marked symptomatic and hemodynamic improvement. This contrasts with the poor results of corrective operation previously reported in patients in this diagnostic category. We believe that the present improved results are due in large part to the valved conduit, and we therefore recommend its use during repair in children or adults with tetralogy and a single pulmonary artery.
Fifty infants ranging in age from 13 days to 18 months (mean age 6 months) and weighing from 1.7 to 8.2 kg (mean weight 4.5 kg) underwent patch closure of a ventricular septal defect (VSD) with use of deep hypothermic circulatory arrest. Seventeen infants were under 3 months of age. The principal indication for operation was intractable chronic congestive heart failure; All infants were below the third percentile for weight preoperatively; Three patients (6%) died postoperatively within the second month of life. There was no late mortality. Seven infants (14%) had seizures; these were associated with a low output state in 2 infants, with hypoxic episodes in 4 infants, and occurred postoperatively in 1 infant. Postoperatively, 8 (17%) of the surviving infants developed right bundle-branch block and left anterior hemiblock, and 16 (32%) developed right bundle-branch block alone. One year postoperatively, catheterization studies in 24 children revealed normal pulmonary artery pressure and pulmonary vascular resistance in all; there were no significant residual ventricular septal defects. Because of these results we continue to be enthusiastic about primary closure of VSD irrespective of age or weightk0
Infusion of prostaglandin E1 into the main pulmonary artery of an infant with interruption of the aortic arch and a closing ductus arteriosus resulted in dilation of the ductus arteriosus and improved systemic perfusion. Treatment with prostaglandin E1 is recommended for infants with interruption of the aortic arch, critical coarctation of the aorta, and other lesions in which systemic perfusion is limited by a restrictive ductus arteriosus.
Electrophysiologic delineation of the atrioventricular conduction system at surgery is described in two patients with corrected transpostion of the great arteries in situs inversus. Intra-atrial electrograms were recorded in one patient from sites immediately adjacent to the coronary sinus located in the left-sided right atrium. The intraventricular portion of the atrioventricular conduction system was identified in both patients along the posterior and inferior margin of the ventricular septal defect, in contrast to the superior and anterior location found in corrected transposition of the great arteries in situs solitus. In contrast to the superior and anterior location found in corrected transposition of the great arteries in situs solitus. The course of the conduction system in the hearts of these two patients and a possible relationship to the cardiac loop and dual origin of the atrioventricular node is discussed. These cases illustrate the usefulness of segmental diagnosis of congenital heart disease and of electrophysiologic identification of the specialized atrioventricular conduction system at surgery.
The etiology of chronic congestive heart failure (CHF) after repair of tetralogy of Fallot was determined in 102 patients consecutively catheterized 1 to 12 years postoperatively. Chronic CHF was observed in 36/102 patients. The most prevalent abnormality leading to congestive failure (31/36) was a large residual ventricular septal defect alone or in combination with other lesions. All postoperative patients with pulmonary to systemic flow ratios greater than 2:1 (25/102) had congestive failure and evidence of biventricular dysfunction. Significant tricuspid regurgitation (N = 11) and persistent systemic to pulmonary artery shunts (N = 6) contributed to volume overload and congestive failure in the patients with large residual ventricular septal defect. Isolated severe residual right ventricular outflow tract obstruction was a common cause of chronic CHF. Pulmonary artery hypertension was present in 20/36 patients with CHF. The increased pulmonary pressure was not wholly due to an increased pulmonary flow since 7/20 patients had pulmonary vascular resistance greater than 3 mm Hg/L/min/m2. Our findings indicate that persistent or chronic congestive heart failure in postoperative tetralogy of Fallot patients requires bilateral cardiac catherterization since an identifiable and surgically correctable lesion is nearly always present.
The clinical course of 38 patients with congenital mitral stenosis (MS) is reviewed. Associated cardiac defects were present in 28 patients, including tetralogy of Fallot in five. In all but one of the eight patients with supravalvar mitral ring (SVR), there were concomitant abnormalities of the mitral valve. Delay in the diagnosis of MS was common. Serial cardiac catheterizations and pulmonary pathologic examination indicated that pulmonary vascular obstructive disease develops during childhood. Mitral valve surgery was performed in 19 of 38 patients: valvotomy alone in eight, excision of SVR in five (two ofwhom also had valvotomy) and mitral valve replacemtnt in seven. Additional non-mitral cardiac surgery was performed in 18 patients. Overall surgical mortality was 49%; mortality for surgery on the mitral valve was 26%. Only patients having mitral valve replacement or with isolated SVR which was then resected became asymptomatic and had normal hemodynamics on postoperative catheterization.
Thirty-nine ventilation and perfusion lung studies with xenon 313 were perfomed in 29 patients with D-transposition of the great arteries (DTGA). Fifteen patients had simple DTGA and 14 more complex anatomic features. Inequalitiies of ventilation (V) were present in 23% (9/39) and perfusion (Q) in 44% (17/39) of studies. Six patients with simple DTGA showed abnormal distribution of perfusion, all with increased flow to the right lung. Among the 14 patients with complex DTGA, eight (57%) had abnormal distribution of perfusion. In patients with pulmonary artery band, increased flow was directed toward the left lung, and in those with an aorticopulmonary anastomosis, increased flow was to the side of the shunt. Radionuclide angiograms were performed in 17 patients with DTGA, both before and after surgical repair. In all, an abnormal circulatory pattern was noted. Complete superior vena cava obstruction present in four patients and residual left to right shunt (Qp/qs greater than 1.7/liter) in three was confirmed at cardiac catheterization. Ventilation perfusion studies with xenon-313 and technetium-99m radionuclide angiogram were effective noninvasive techniques in assessing pulmonary function and hemodynamics in patients with DTGA.
A 3-year-old boy underwent successful surgical correction of double-outlet right ventricle (S, D, D), noncommitted ventricular septal defect (VSD) of the endocardial cushion type, and pulmonary stenosis. The operation consisted of an internal baffle connecting the left ventricle to the aorta through the VSD. The pulmonary outflow tract was widened with a Dacron patch. Surgical options in this and other subsets of DORV are discussed.
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The association of aorticopulmonary window and tetralogy of Fallot is rare. In this report, we describe two cases in which this combination of anomalies was repaired successfully. Both patients made uneventful recoveries.
It is now possible to construct vascular grafts of expanded polytetrafluoroethylene having complex configurations. In this series of experiments a double tapered graft was used to create a bypass shunt between the aorta and the pulmonary artery in rhesus monkeys and between the aorta and the iliac artery in dogs. When the synthetic material was placed under a slight degree of tension, a high degree of patency was achieved in animals killed three to six months following implantation. The use of this approach in neonates with cyanotic congenital heart disease necessitating the creation of systemic-pulmonary artery shunts is suggested as a new method to achieve a controlled lumen size and an increased patency rate, while simultaneously decreasing the incidence of congestive heart failure or of late stricture of the pulmonary artery.
Data from 30 infants with interrupted aortic arch in the New England Regional Infant Cardiac Program, 1968 to 1974, were reviewed. All patients had major associated cardiac abnormalities: approximately one third had ventricular septal defect with patent ductus arteriosus, one third had complex ventricular septal defect with left ventricular outflow obstruction, and one third had complex intracardiac lesions incompatible with survival. Twenty-one of the patients had either palliative or reconstructive surgery, with a hospital mortality rate of 76%. Nine patients did not have surgery; eight of them died at a median age of four days. One-stage primary repair of interrupted aortic arch including the associated cardiac defects, using deep hypothermia and circulatory arrest, is proposed as the current method of treatment in such infants.
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The pathogenesis of paradoxical hypertension after resection of coarctation of the aorta was investigated by comparing the course of seven children undergoing repair of coarctation with five acyanotic children undergoing elective cardiovascular surgery. During the first 24 hours after surgery, all coarctation patients demonstrated a rise in systolic blood pressure (35 +/- 15.5 mm Hg; P less than 0.001), a significant depression in cold pressor test response, and only a slight elevation in plasma renin activity. In the next 24-72 hours, coarctation patients developed a rise in diastolic blood pressure (26.8 +/- 10.6 mm Hg; P less than 0.001), plasma renin activity (22.9 +/- 10.2/ml/hr; P less than 0.001) and fluid retention. By contrast, control patients had no significant postoperative changes. Abdominal pain occurred in five coarctation patients during the period of maximal plasma renin activity. The data suggest that the sympathetic nervous system may be responsible for the initial phase of hypertension after coarctation resection and that the renin angiotension system plays a major role in the second phase of hypertension and in the pathogenesis of mesenteric arteritis.