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A technique that allows establishment of continuity between the right ventricle and the hypoplastic pulmonary confluence without the use of extracorporeal circulation in patients with pulmonary atresia and ventricular septal defect has been applied successfully in six consecutive patients. Exposure is achieved by an anterolateral thoracotomy through the left third intercostal space. A Dacron tubular graft of appropriate size is anastomosed to the hypoplastic but confluent pulmonary artery bifurcation. A fine, stranded, steel wire is passed through the anterior wall of the outflow portion of the right ventricle so that a 2 to 3 cm loop lies in the right ventricular cavity. The proximal end of the nonvalved tubular graft is anastomosed to the epicardial surface of the right ventricle around the exit points of the wire. The ventricular incision is achieved by sawing through the right ventricular wall with the wire as one would with a Gigli saw. No systemic heparinization is used. Six consecutive patients have undergone this procedure. All had confluent but hypoplastic pulmonary arteries of 6, 5, 5, 3, 3, and 4 mm in diameter. There were no surgical deaths. Average blood loss was 366 ml, and all patients had an increase in peripheral arterial oxygen saturation. All patients underwent postoperative cardiac catheterization and angiography. All patients had patent conduits and pulmonary arteries that had increased in diameter. Advantages of the procedure are avoidance of the median sternotomy, which may simplify future closure of the ventricular septal defect: simplification of an effective technique which, under extracorporeal circulation, is complicated by profuse collateral flow that tends to obscure the operative field and distend the heart; minimal bleeding resulting from avoidance of systemic heparinization, which in these very cyanotic patients can lead to severe bleeding diathesis; and a possible decrease in the surgical risk.

Twenty-seven patients underwent reoperation because of thrombotic obstruction of a disc-typs cardiac valve prosthesis. Preoperative clinical features included effort dyspnea in 81%, new-onset angina in 44%, a new murmur in 89%, and an abnormal opening or closing sound associated with the prosthetic valve in 56%. Symptoms were present for 1 week or more before reoperation in 86%, although many patients were referred only after acute exacerbation of heart failure and development of pulmonary edema. Noninvasive studies confirmed prosthetic valve malfunction in only 33%, but cardiac catheterization documented thrombotic obstruction in all 15 patients in whom it was performed. In 14 of the 27 patients, prothrombin time was in the therapeutic range at the time of admission. Prompt reoperation for valve replacement or thrombectomy was performed with an operative mortality of 11%, and long-term outcome was satisfactory in all but 1 hospital survivor. These findings emphasize the importance of considering the diagnosis of thrombosed heart valves in patients with mechanical heart valves who are seen with nonspecific symptoms.

Obstruction of pulmonary ventricle-pulmonary artery conduits can result from neointimal peel formation or valvular degeneration and calcification. To determine the risks and outcome of reoperation, we reviewed the records of 100 consecutive patients who had replacement of severely stenotic pulmonary ventricle-pulmonary artery conduits. At reoperation, the 70 male and 30 female patients had a mean age of 13.3 ± 4.8 years. During operation, 37 homografts, 62 Dacron grafts with integral xenograft valves, and one nonvalved conduit were replaced with valved (80) or nonvahed (17) prostheses. The mean transconduit pressure gradient decreased from 81 ± 26 mm Hg preoperativehy to 7 ± .8 mm Hg postoperatively (p

Definitive operation was performed on 20 patients (aged 25 to 178 months) with pulmonary atresia and intact ventricular septum. All patients had one or more prior preliminary palliative procedures. Right ventricular outflow tract reconstruction with atrial septal defect closure and shunt removal was done on 10 patients. Tricuspid annular circumference was at least 70% of normal in seven patients and between 55% and 70% in three patients. Two patients died during hospitalization. The eight surviving patients were asymptomatic 3 to 145 months after operation. The modified Fontan operation was performed on 10 patients. None of these patients had a tricuspid annular circumference greater than 70% of normal; the circumference was less than 55% in nine patients and between 55% and 70% in one patient. One patient died during hospitalization and one died later. Follow-up 6 to 48 months after operation showed that six patients were in the New York Heart Association Class I and two were in Class II. After effective preliminary palliation of pulmonary atresia with intact ventricular septum, definitive operation can be done with an operative risk of 15% (three of 20 patients) and excellent late results. Right ventricular outflow tract reconstruction can be done as a complete repair for patients who have adequate tricuspid annular size. The modified Fontan operation is the only option for definitive repair when the tricuspid anulus is severely hypoplastic.

Age-related changes in left ventricular wall thickness were studied in 92 autopsy specimens of complete transposition of the great arteries (TGA) and in 189 normal hearts. By means of morphologic and clinical hemodynamic criteria, three groups were defined: Group II, TGA with intact ventricular septum (low left ventricular pressure): Group II, TGA with ventricular septal defect but without pulmonary stenosis (systemic left ventricular pressure combined with volume overload); and Group III, TGA with ventricular septal defect and pulmonary stenosis (systemic left ventricular pressure). At birth, the left ventricular thickness for the three groups did not significantly differ from normal. In group I, the left ventricular thickness remained constant with age up to 4 years and, accordingly, was significantly less after 4 months of age than that both in normals and in Groups II and III. In those Group II specimens from patients without irreversible pulmonary vascular disease, the left ventricular thickness was similar to that of normal hearts. The left ventricular thickness in Group III increased, with age in a manner similar to that of normal hearts. If left ventricular wall thickness correlates with potential ventricular function, then this measurement, combined with other clinical data, may help to predict the ability of the left ventricle to perform systemic work following one of the arterial switch operations. Sequential determinations of wall thickness may be attained noninvasively by echocardiography.

Intraoperative two-dimensional echocardiograms were performed in 30 patients (group I) and two-dimensional Doppler color flow imaging was performed in 30 additional patients (group II) with various forms of congenital heart disease. A comparative complete two-dimensional Doppler and color flow examination was performed in group II patients 10 to 14 days postoperatively. Standard intraoperative two-dimensional echocardiograms demonstrated excellent correlation with preoperative findings and allowed assessment of valvular regurgitation or shunt when combined with echocardiographic contrast injections. However, intraoperative and postoperative two-dimensional color flow imaging was obtained more easily and rapidly and allowed recognition of more postoperative residual defects. Color flow imaging appears to be a useful method for intraoperative assessment of surgical repair of congenital cardiac defects. Twenty-one residual lesions were correctly diagnosed intraoperatively, whereas seven residual lesions were demonstrated only during later postoperative examination. This preliminary experience has also demonstrated several areas for future development and improvement of these techniques. Combined two-dimensional Doppler and contrast echocardiographic studies may allow better disclosure of residual defects.

We describe a patient who had tricuspid valve replacement and in whom dual-chamber pacing was accomplished by using a ventricular epicardial lead and by placing an atrial endocardial lead through the wall of the atrial appendage and positioning the tip against the endocardial surface of the atrial appendage. A ligature was placed around the atrial appendage where the lead passed through the wall of the right atrial appendage. This obviated the need for a second procedure to place the atrial lead in a transvenous fashion. After 5 years of follow-up the patient continues with normal DVI pacing.

From 1975 through 1986, 49 patients with asplenia (23 patients) or polysplenia (26 patients) syndromes underwent a modified Fontan operation. All patients had anomalous systemic venous return, and 43 (88%) had anomalous pulmonary venous return. The atrioventricular valve anatomy varied: 36 patients had a common atrial chamber and common atrioventricular valve, eight had mitral valve atresia, and five had severe mitral valve hypoplasia. Redirection of systemic venous return was accomplished by (1) atrial baffle (29 patients), (2) intraatrial conduit (19 patients), and (3) extraatrial conduit (one patient). There were 21 (43%) hospital deaths overall. However, since 1985, six of 22 patients (27%) have died. Increased mortality was seen in patients requiring atrioventricular valve repair or replacement (8/11, 73%) and in patients with asplenia (65%). Lower mortality was seen in patients with polysplenia (24%) and those receiving an intraatrial conduit (26%), although this decrease also represents the more recent experience. We conclude: (1) The Fontan operation for patients with asplenia or polysplenia syndromes has resulted in a significant (although recently declining) mortality; (2) mortality is higher in patients with asplenia; (3) patients with atrioventricular valve insufficiency requiring repair or replacement are at higher risk; and (4) intraatrial conduits seem to offer promise for successfully accomplishing this repair.

The cardiorespiratory response to exercise was measured in 27 children with functional single ventricle. All 27 patients had a significant reduction in exercise time, work performed, maximal exercise heart rate, maximal oxygen uptake and systemic arterial blood oxygen saturation. The reduction in exercise performance increased with increasing age of the patients. All patients ventilated excessively at rest and during exercise. This study documented the precise level of exercise intolerance in patients with functional single ventricle. The progressive deterioration in exercise performance with increasing patient age may lend credence to the concept that operation for physiologic correction of functional single ventricle should be considered during or before adolescence.

Between 1962 and 1979, 14 patients with complete atrioventricular canal and tetralogy of Fallot underwent repair of both anomalies. The ages of the patients ranged from 1 to 12 years. Six patients had Down’s syndrome. Five of the 14 had one or more previous systemic-pulmonary artery shunts. The correct diagnosis was established preoperatively in 11 of the patients. The ventricular septal defect, with its large anterior subaortic extension, was repaired by a combined atrial and right ventricular approach in five patients and by an atrial approach alone in nine. Outflow tract reconstruction (transannular patch) was performed in seven patients, without affecting the surgical mortality. Mortality was higher with associated Down’s syndrome, but not significantly so (p = 0.1), and was related to age less than 4 years (p = 0.04). The presence of complete atrioventricular canal should be considered in patients with tetralogy of Fallot, especially those having Down’s syndrome, electrocardiographic superior-axis deviation, and vectorcardiographic counterclockwise frontal QRS loop. This diagnosis can be confirmed preoperatively by right and left ventricular angiocardiography and two-dimensional echocardiography. The overall risk of repair has been high (29% early, 14% late mortality), but the mortality has been reduced to 17% during the last 10 years. No deaths have occurred in five recent patients who underwent closure of the ventricular septal defect by a combined atrial and ventricular approach.

Surgical drainage for effusive pericardial disease is usually accompanied by pericardial resection to obtain tissue for analysis and to lessen the chance of recurrent effusion or late constriction. The purpose of this study was to determine the relationship between the extent of resection and the development of late complications. From 1960 through 1983, 145 patients with pure pericardial effusive disease underwent operative drainage. The effusions were malignant in 72 patients (49.7%) and benign in 73 (50.3%). The patients were divided into three groups according to the extent of resection: complete in 72 patients (49.7%), partial in 36 (24.8%), and window in 37 (25.5%). The 30 day mortality was 19.4% for patients with malignant effusions and 5.5% for those with benign effusions (p less than 0.05). All survivors had immediate improvement in symptoms. The actuarial 1 year survival rate was 23.4% (mean 4.2 months) for patients with malignant disease and 85.6% for patients with idiopathic effusions (p less than 0.001). Survival was not influenced by the extent of resection. Fifteen patients (10.3%) had late constriction or recurrent effusion. Six of these required reoperation, all after having had a window procedure. Actuarial probability of reoperation or late complication was greater with window procedures than other resections, both for all patients (p = 0.0001) and for those with benign disease (p = 0.0001). Transthoracic complete pericardiectomy is the procedure of choice for effusive pericardial disease. Subxiphoid drainage has immediate advantages for selected patients but has a statistically greater chance of late complications.

From 1973 to 1980, 49 patients under 18 years of age survived cardiac valve replacement with Hancock porcine heterografts. Complete follow-up has been obtained on 44 patients (90%) in whom 46 valves were placed. There were 30 boys and 14 girls with an age range of 2 to 18 years (mean 10.0 years). Severe prosthetic valvular dysfunction requiring valve replacement occurred in eight valves in seven patients at 15 to 60 months postoperatively (mean 34.1 months), yielding a calculated replacement rate of 7.1% per patient-year. All eight valves demonstrated severe calcification with stenosis, two valves had significant insufficiency secondary to leaflet disruption, and one valve had a large leaflet perforation. Thirty-one patients with valves in place at 7 to 90 months (mean 38.4 months) are alive, but six have clinical evidence of progressive valvular dysfunction. The mean age at the time of the original Hancock valve placement of the group of patients having undergone replacement of a failed prosthesis together with those with clinical evidence of prosthetic dysfunction was 8.0 years, which is significantly less than that of the remaining group of patients with normally functioning valves (mean 11.2 years, p = 0.043). Actuarial curves demonstrate a predicted replacement-free rate of 87.4% ± 5.9% at 3 years, 82.3% ± 7.5% at 4 years, and 58.5% ± 15.7% at 5 years. On the basis of these data and other reports of early failure in the literature, we have discontinued the routine use of Hancock porcine heterografts for cardiac valve replacement in children in favor of mechanical prostheses.

The Fontan procedure has proved useful in the surgical treatment of patients with tricuspid atresia, univentricular heart, and other complicated cardiac anomalies. Previous palliation of these patients with ascending aorta-right pulmonary artery anastomosis (Waterston shunt) may impose severe restrictions in the operability of these patients because of severe distortion, narrowing, and scarring of the proximal right pulmonary artery. A modification of the Fontan operation is described in which repair is facilitated by transecting the right pulmonary artery at the site of anastomosis, trimming away the distorted narrowed segment, and anastomosing the resulting cuff to the lateral aspect of the superior vena cava. The right atrial appendage is anastomosed to the rudimentary right ventricle or the main pulmonary artery directly or via a tubular Dacron graft. The technique has been applied successfully in four consecutive cases.

Selection of types of prosthetic heart valves for children remains controversial. The case histories of 50 children surviving valve replacement with Starr-Edwards prostheses between 1963 and 1978 were reviewed to evaluate the long-term performance of mechanical valves. The 31 boys and 19 girls ranged from 6 months to 18 years in age (mean 10.4 years); 19 patients had had aortic valve replacement, 24 patients had had mitral valve replacement, and one patient had had both. Among the six patients who had had tricuspid valve replacement, four had corrected transposition, so that the tricuspid valve was the systemic atrioventricular valve. Mean (± standard deviation) follow-up interval was 7.9 ± 4.9 years (maximum 17 years). For all patients, the 5 year survival rate was 86% ± 6%. At 10 years postoperatively, the survival rate (± standard error) was 90% ± 7% after aortic valve replacement and 76% ± 8% after systemic atrioventricular valve replacement. At follow-up, 39 patients were alive, and 38 were in New York Heart Association Class I or II. Of the 11 deaths, four were valve-related. Seven patients had major (requiring hospitalization) thromboembolic events, and five patients had minor transient neurological symptoms suggesting thromboembolism; 50% of these patients were not taking warfarin (Coumadin) at the time of the thromboembolic event. The incidence of late (>30 days) thromboembolism was 5.3 per 100 patient-years after aortic and 2.0 per 100 patient-years after systemic atrioventricular valve replacement. At 10 years postoperatively, 66% ± 15% of patients who had had aortic valve replacement and 91% ± 6% of those who had had systemic atrioventricular valve replacement were free of thromboembolism. The excellent long-term survival, absence of mechanical failure, and relatively low rate of thromboembolism with this prosthesis contrast with our experience with biological valves, in which 41 % of children required reoperation in 5 years. Currently, mechanical valves, such as the Starr-Edwards prostheses, are our preferred valves for pediatric patients.

The gross surgical pathologic features of the pulmonary valve were reviewed in 116 patients (63 male and 53 female) who had undergone a cardiac operation with pulmonary valve excision at our institution during the period 1973 through 1987. Although the mean age was 12 years, subjects ranged in age from 3 months to 73 years, and 25 patients, including 19 with congenital heart disease, were older than 20 years of age. Among 105 patients who had pure pulmonary stenosis, 61 (58%) had tetralogy of Fallot, 18 had isolated pulmonary stenosis, 23 had other congenital cardiac anomalies, and 3 had carcinoid heart disease. Five patients had pure pulmonary regurgitation (four with tetralogy and one with infective endocarditis), and four had combined pulmonary stenosis and regurgitation (two with congenital cardiac anomalies and two with carcinoid heart disease). In two patients, the valve was neither stenotic nor regurgitant. Thus, congenital heart disease accounted for 110 of the 116 cases (95%), and tetralogy of Fallot was the most commonly observed form (65 cases). Bicuspid pulmonary valve was the most common anomaly and was present in 58% of patients with tetralogy but in only 17% of those with isolated pulmonary stenosis.

From 1975 through 1982, the Damus-Stansel-Kaye procedure was performed on 20 patients with complete transposition of the great arteries (TGA) and on 4 with double-outlet right ventricle (DORV) and subpulmonary ventricular septal defect (VSD). The patients ranged from 6 days to 20 years old (median age, 13 months). Associated anomalies included atrial septal defect (24 patients), VSD (14), and others (25). Thirteen patients had had palliative operations previously. Of the 14 hospital deaths (58%), 13 occurred among the 17 patients with one or more risk factors: age less than 18 months, weight less than 10 kg, and left ventricular peak systolic pressure less than 75% of systemic pressure. Follow-up ranged from 12 to 87 months (mean, 51 months). One patient died of cardiac failure two years postoperatively, and 2 required conduit replacement at 40 and 50 months because of stenosis. All 9 survivors are free from major symptoms. The Damus-Stansel-Kaye repair is most suitable for patients with TGA or DORV with subpulmonary VSD who are older than 18 months, weigh more than 10 kg, and have a "prepared left ventricle," and whose coronary artery anatomy precludes transplantation.

The results of operation in all patients with univentricular heart and an obstructed anterior subaortic outlet chamber who were operated on utilizing extracorporeal circulation at the Mayo Clinic from 1973 through 1983 were reviewed. Ten of the 18 patients died during the immediate postoperative period and there was one late death. Factors significantly related to operative and immediate postoperative mortality were age at operation, cardiothoracic ratio on X-ray examination, degree of ST depression on electrocardiogram and pressure gradient across the outlet foramen at catheterization. Autopsy in eight cases revealed significant hypertrophy of ventricular myocardium and a small outlet foramen that was considered stenotic relative to either body surface area or aortic root area. The ventricular myocardium showed histologic changes of chronic ischemia that predated the surgical procedure.

Our experience with pulmonary valve insertion during reoperation for residual lesions after initial open repair of tetralogy of Fallot in 15 patients is reported. Preoperatively, 14 patients were in moderate to severe congestive heart failure, and all 15 had decreased right ventricular (RV) function at cardiac catheterization. All 15 patients had pulmonary insufficiency but not as an isolated finding. The most common residual lesions encountered were ventricular septal defect in 9, tricuspid insufficiency in 11, and peripheral pulmonary arterial stenosis in 6. Tissue valves were inserted in all patients. Mean peak RV-left ventricular pressure ratio measured in the operating room decreased from 0.61 +/- 0.10 (+/- the standard deviation) to 0.47 +/- 0.17 (p less than 0.05). There were no operative deaths. At follow-up (mean, 33 months), all but 1 patient were in New York Heart Association Class I or II. Pulmonary valve insertion should be considered during reoperation for tetralogy of Fallot when pulmonary insufficiency and RV failure are present.

To characterize the exercise hemodynamic responses after definitive operation for patients with univentricular atrioventricular connection, we compared the cardiorespiratory response to exercise of 4 patients who had undergone the ventricular septation procedure and 9 patients who had undergone the Fontan operation with that of 38 patients who had univentricular atrioventricular connection but had not undergone definitive operation. Exercise duration and total work increased significantly after the Fontan procedure but not after the septation operation. Rest or exercise (or both) ventilation improved significantly after the septation operation but less so after the Fontan operation. Blood oxygen saturation (rest and exercise) improved significantly after either procedure. Cardiac output and stroke-volume response to exercise remained abnormal in both groups of patients after operation. Although definitive operation for univentricular atrioventricular connection results in improved cardiorespiratory function at rest and exercise, these variables remain abnormal when compared with those of normal subjects.

Anomalous origin of the left anterior descending coronary artery from the right coronary artery can interfere with the location of the usual ventriculotomy during repair of tetralogy of Fallot. The purpose of this study was to compare the results of two operative techniques: (1) a "tailored" right ventricular incision and outflow patch reconstruction and (2) placement of a conduit from the right ventricle to the main pulmonary artery. We reviewed the records of 416 patients who had complete repair of tetralogy of Fallot at the Mayo Clinic from 1973 through 1984. Twenty (5%) (median age 6.5 years) had anomalous origin of the left anterior descending coronary artery from the right coronary artery. Twelve of these patients had right ventricular outflow patch reconstruction, and eight had placement of a conduit from the right ventricle to the pulmonary artery. Three deaths occurred, all during hospitalization, two in the patch reconstruction group and one in the conduit group. The average reduction in right ventricular pressure postoperatively was slightly but not significantly greater for the conduit group. These data indicate that correction of tetralogy of Fallot with anomalous origin of the left anterior descending coronary artery can be done with either patch reconstruction or conduit placement. Selection of the more appropriate procedure depends on the exact location and degree of tortuosity of the anomalous artery and the level and severity of right ventricular outflow obstruction.

From 1965 until March, 1982, 167 patients underwent surgical repair of truncus arteriosus. The age at operation ranged from 18 days to 33 years (mean 6 years). There were 48 hospital deaths (28.7%). The following factors had a positive correlation with the possibility of a surgical death: age at operation less than 2 years (p

Between 1961 and 1978, 6,602 valves were replaced in 5,660 patients. Reoperation for periprosthetic leakage was performed in 105 patients (1.6% of the valves); early mortality was 5.7%. At reoperation, 52% of patients were in New York Heart Association Classes III and IV, whereas 72% had been in Classes III and IV prior to the primary valve replacement. Seventy-five patients had aortic periprosthetic leaks, which were distributed equally around the annulus. Among these patients, 41 (55%) had aortic valve rereplacement and 34 (45%) had suture repair. At 5 years, the survival was 94% and the event-free survival was 71%. Seventeen patients had multiple aortic valve reoperations. Hospital mortality for the second reoperation was 5.8%. At late follow-up, 19 patients had murmurs of residual or recurrent aortic periprosthetic leakage. Twenty-nine patients had mitral periprosthetic leaks, most often near the anterior leaflet. Eight patients had mitral valve rereplacement, and 21 had suture repair. At 5 years, the survival was 75% and the event-free survival was 52%. Four patients underwent multiple reoperations. At late follow-up, 5 of the 29 patients in the mitral valve group had murmurs of residual or recurrent periprosthetic leakage. One patient had tricuspid valve rereplacement. The low hospital mortality and the good late results have encouraged us to recommend an aggressive approach in the correction of periprosthetic leakage in all symptomatic and selected asymptomatic patients.

After the Fontan operation, patients who had a prior Glenn anastomosis should have less pleural drainage than patients without a prior Glenn anastomosis because innominate and pleural vein and thoracic duct pressures are unaltered in the former group. To test this hypothesis, we studied 92 patients who had had a Fontan operation between 1973 and 1986—46 with a prior Glenn anastomosis and 46 without a prior Glenn anastomosis (controls)—who were matched for age, gender, diagnosis, and number of prior shunt operations. The volume of pleural drainage was significantly less (p

Double-orifice mitral valve is an uncommon but surgically important condition. The experience in 25 cases of double-orifice mitral valve associated with atrioventricular canal defects was reviewed. This constituted 43 % of the 581 cases of atrioventricular canal defects operated upon between 1961 and July, 1984. The combined mitral orifice area ranged from 85% to 91 % of normal in those patients whose valves were sized intraoperatively. Ten associated cardiac defects were repaired in six patients. Of 23 patients having cleft mitral valve, 21 had partial closure of the cleft. There was one operative death (4.0 %), which occurred early in the series in a patient in whom the tissue bridge was severed and massive mitral regurgitation resulted. In the remaining 24 patients the tissue bridge was left intact, and all survived operation. No patient had clinically significant mitral stenosis during a follow-up of 1 to 14 years (mean 4.9 years). Two patients (8%) developed progressive mitral regurgitation and required mitral valve replacement 3 and 11 years postoperatively. One of these patients died and a second death occurred suddenly 2 years following operation. All survivors are in Functional Class I or II. The noncleft orifice of a double-orifice mitral valve usually is competent and rarely requires closure. The cleft, because it constitutes a type of parachute (single papillary muscle) valve, should be closed partially so as to relieve valve incompetence without causing undue stenosis. The incidence of late development of mitral regurgitation is similar to that of atrioventricular canal without double-orifice mitral valve. Repair of atrioventricular canal associated with double-orifice mitral valve can be achieved with a low operative mortality and excellent late results.

Records of 231 patients (171 males, 60 females; aged 10 months to 83 years [median 45 years]) who underwent operation for constrictive pericarditis at the Mayo Clinic from 1936 through 1982 were reviewed. All had had hemodynamically significant pericardial constriction preoperatively, and pericardial disease was confirmed at operation. Preoperatively, 69% were in New York Heart Association Class III or IV and 81% had peripheral edema or ascites. Pericardiectomy was performed through a left anterolateral thoracotomy (34%), a median sternotomy (27%), a U incision (Harrington) (21%), or a bilateral anterior thoracotomy (18%). Postoperatively, 28% of patients had evidence of low cardiac output; 70% of the 32 deaths within 30 days of operation were due to low cardiac output. Operative risk was significantly (p less than 0.001) related to preoperative disability (1% for Class I or II; 10% for class III; 46% for Class IV). Median postoperative follow-up was 9 years (longest was 43 years). Probability of survival for patients dismissed alive from the hospital was 84% at 5 years, 71% at 15 years, and 52% at 30 years. Long-term survival (excluding operative mortality) was not significantly influenced by the disability class preoperatively, the operative approach, or the development of low cardiac output in the immediate postoperative period. At the end of the follow-up interval, there were 141 patients in whom functional capacity could be assessed; 140 were in Class I or II. We conclude that a poor hemodynamic result after complete pericardiectomy relates to the preoperative degree of constriction and resultant cardiomyopathy. We recommend early pericardiectomy when pericardial constriction is diagnosed, and we continue to use a left anterolateral thoracotomy as the preferred approach for most patients.

The calcium transients associated with contraction in human working myocardium were recorded by use of the bioluminescent protein, aequorin, a substance that emits light when it combines with calcium ion (Ca++). Small amounts of aequorin were microinjected into superficial cells of human atrial and ventricular muscle obtained from tissue routinely excised and discarded at the time of cardiac surgery. Light output, an index of intracellular Ca++, and isometric tension development were recorded at 37.5 degrees C at 1 to 5 second intervals of stimulation. Light increases much more quickly than tension and decreases toward basal levels by the time that peak tension is reached. The configuration and time course of the aequorin signal in human myocardium and its responses to inotropic interventions are similar to those recorded in lower mammalian species. The calcium transient appears to be dominated by the release and uptake of Ca++ from intracellular stores under all conditions studied. These results indicate that aequorin is a useful tool for studying the effects of drugs and disease states on cardiac excitation-contraction coupling in human beings as well as in lower animals.

Five hundred fifty-two patients underwent a total of 617 reoperations for repair or replacement of a prosthetic heart valve. Operative mortality for first reoperation (530 patients) was 5.9% for the aortic position and 19.6% for the mitral position. Overall operative mortality was 14% for second reoperation (69 patients) and 7% for third reoperation (14 patients). In addition to valve position, operative mortality for first reoperation appeared to be related to pre-reoperation functional class and urgency of operation. First reoperation for mitral valve patients in New York Heart Association (NYHA) Class II was 4.2%; for Class III. 9.3%; and for Class IV, 41%. In the aortic position, operative mortality was 2.4% for Class I, 1.6% for Class II, 6.3% for Class III, and 20.8% for Class IV. The mortality for elective mitral valve reoperation was 0%; for urgent operation, 20.3%; and for emergency procedures, 54.5%. Elective aortic valve reoperation carried a 1.4% mortality; urgent procedures, 8%; and emergency procedures, 37.5%. No significant differences in bleeding complications were noted between reoperations and initial valve replacement. The data appear to suggest that when significant valve dysfunction is first noted, reoperation should be undertaken to minimize operative risk.

An alternative technique for creation of a Drapanas shunt was used in a 12-year-old boy with upper gastrointestinal bleeding. Dissatisfaction with available prosthetic grafts and the inherent limitations of other autogenous materials led to the use of a spiral saphenous vein graft to bridge the superior mesenteric vein and the inferior vena cava. Patency of the graft was demonstrated 1 year postoperatively, and the patient has not had further bleeding episodes for 2 years postoperatively. Continued use of this operation is necessary to determine its usefulness.

To determine late survival and functional status after second revascularization procedures for coronary artery disease, we studied 106 consecutive patients operated on between June, 1969, and December, 1980. The mean age of the 96 men and 10 women was 49 ± 8 years (range 22 to 65 years). Before reoperation, 101 patients (95%) were judged to be in New York Heart Association Class III or IV with angina, and 81 patients (76%) had three-vessel involvement. Angina recurrence was most commonly caused by bypass graft occlusion alone and in combination with progressive disease of the native arteries (60 patients, 57%). Three patients (2.8%) died within 30 days of reoperation; each death resulted from myocardial infarction. An average of 2.2 coronary arteries were bypassed in each patient. Complete follow-up data (mean 43 months) were available for 105 patients. Actuarial survival of patients dismissed alive is 94% at 5 years and 89% at 7 years. All late cardiac-related deaths occurred in patients with three-vessel disease. When recurrence of any angina, need for a third operation, and myocardial infarction are included with cardiac-related deaths, event-free survival is 28% at 5 years and 26% at 7 years. Late survival and functional status could not be predicted by the cause of recurrent angina or the presence of risk factors. Repeat myocardial revascularization can apparently be undertaken with low risk and with prospects for excellent long-term survival. After reoperation, recurrence of mild angina is not uncommon, but freedom from serious cardiac events and relief of severe symptoms were noted in more than 60% of patients 5 years later.

From 1982 to 1987, 38 consecutive patients with pulmonary atresia and ventricular septal defect underwent staged unifocalization procedures in preparation for final intracardiac repair of the anomaly. Thirty-six patients had concordant visceroatrial, atrioventricular, and ventriculoarterial connections. A central pulmonary artery confluence was present in 19 patients and absent in the remaining group. All patients with central pulmonary arteries had inadequate peripheral pulmonary arterial arborization. Systemic collateral arteries were present in all 38 patients. The objectives of the unifocalization procedures were the interruption of extracardiac sources of pulmonary arterial blood flow, the restoration of segmental, lobar, and pulmonary arterial confluence, the replacement of missing central pulmonary arterial branches, and the creation of a central, accessible source of pulmonary arterial blood flow. A total of 54 unifocalization procedures were performed in the 38 patients. These procedures included 85 permanent connecting anastomoses, 15 temporary anastomoses to the ascending aorta, 13 angioplasty procedures, and 15 modified Blalock-Taussig shunts. Three patients died after unifocalization (two early and one late). By the end of the study, eight patients were still waiting for further unifocalization procedures or angiographic assessment. Four patients were rejected for further surgical treatment because of persistent, uncorrectable defects of the pulmonary arterial arborization pattern. Twenty-three patients underwent complete intracardiac repair with two deaths (one early and one late). Postrepair, intraoperative right ventricular/left ventricular systolic pressure ratio after complete surgical repair ranged from 0.4 to 1.0 (mean = 0.63, standard deviation = 0.14). At the end of follow-up, 21 survivors of complete repair were free of significant symptoms. Unifocalization procedures designed to improve the pulmonary arterial arborization pattern of patients with pulmonary atresia and ventricular septal defect with or without central pulmonary arteries can prepare a significant number of these patients for successful intracardiac repair of the anomaly.

A patient with unruptured aneurysm of the sinus of Valsalva presented because of ventricular tachycardia refractory to medical therapy. The underlying problem was not suspected until cardiac catheterization. Once the aneurysm was repaired, the tachycardia was abolished; the patient required no antiarrhythmic drugs. Two points are emphasized: First, cardiac catheterization is often indicated early in cases of ventricular tachycardia without obvious cause. Second, recurrent ventricular tachycardia is a hitherto unreported but important complication of sinus of Valsalva aneurysm.

Between 1961 and 1984, 91 patients underwent simultaneous triple valve replacement at the Mayo Clinic. Of the 273 prosthetic valves used, 77% were Starr-Edwards. Perioperative (30 day) mortality was 24% to 27% between 1962 and 1974 and 7% between 1975 and 1983 (p = .17). In patients with NYHA class IV symptoms, perioperative mortality was 44%, and in those with milder symptoms, it was 8% (p less than .0001). The median follow-up was 7.5 years (range, 6 weeks to 20 years). Cumulative survival, which was calculated taking into consideration perioperative mortality, was 64% at 1 year, 55% at 5 years, 40% at 10 years, and 25% at 15 years. Multivariate analysis identified preoperative functional class and age as predictors of late survival. Among causes of late mortality were sudden death in 32.5%, congestive heart failure in 15%, thromboembolism in 12.5%, prosthetic valve dysfunction in 7.5%, and infective endocarditis in 5%. Late complications included systemic emboli in 42% (embolic rate, 12.3 events per 100 patient-years), bleeding in 22%, myocardial infarction in 16%, and infective endocarditis in 6%. Eight patients required reoperation for prosthetic valve dysfunction, and 12 patients had permanent pacemakers. Of the 29 patients still alive, 79% are in NYHA class I or II. In summary, perioperative mortality after triple valve replacement appears to be declining; long-term survival in 30 day survivors is similar to that after single valve replacement and excellent symptomatic improvement can be obtained, although morbidity is high.

Operative treatment of dissections of the ascending aorta differs from that for the descending aorta, not only because of the need for cardiopulmonary bypass, but also because of the frequent occurrence of aortic valve insufficiency. To determine the early and late results of operative repair, we have reviewed the case histories of 121 consecutive patients who underwent repair of ascending aortic dissections between 1962 and 1985. Ages ranged from 16 to 79 years (mean 56 ± 14 years); 54 patients had operation within 2 weeks of onset of symptoms (acute), and the remainder had later repair (chronic). Seventy patients (58%) had clinical evidence of aortic insufficiency at the time of admission. During repair of acute dissection, 10 patients (19%) had aortic valve resuspension and 15 patients (28%) had aortic valve replacement During repair of chronic dissection, eight patients (12%) had resuspension and 43 patients (64 %) had replacement Overall operative mortality was 22 %, significantly higher for patients with acute than for those with chronic dissections (39 % versus 9 %, p

From 1965 through 1983, 43 patients underwent concomitant cardiac and pulmonary procedures at our institution. Most patients presented with cardiac symptoms and were incidentally found to have a roentgenographically indeterminate lung nodule. The pulmonary diagnosis of 38 patients was unknown preoperatively, and nine of these had a malignant lesion. All 43 cardiac procedures necessitated extracorporeal circulation. Thirty-one patients had benign pulmonary disease, 10 had bronchogenic carcinoma, and two had metastatic carcinoma. Concomitant pulmonary procedures were performed via median sternotomy and included single wedge resections in 32 patients, lobectomy in seven, multiple wedge resections in three, and pneumonectomy in one. Most resections were performed either before or after institution of bypass, without systemic anticoagulation. Of the two operative deaths (4.6 %), one was related to intraparenchymal pulmonary hemorrhage after multiple wedge resections during anticoagulation. Thus, pulmonary resections performed during anticoagulation may be associated with increased risk and probably should be avoided. The second death was cardiac in origin and not related to pulmonary resection. The remaining patients recovered uneventfully. Definitive correction of both cardiac and pulmonary disease can be performed at one operation via a single incision with safety and benefit to the carefully selected patient

In patients with pulmonary atresia and ventricular septal defect, hypoplasia of the central pulmonary arteries prevents single-stage complete repair. Over an interval of 8 1/2 years, 105 patients underwent establishment of continuity between the right ventricle and a hypoplastic central pulmonary arterial confluence (first stage). There were 12 hospital deaths (11%) and 11 late deaths before second-stage (complete) repair. Twenty-five patients await late evaluation. The remaining 57 individuals have had follow-up cardiac catheterization a mean of 33 months postoperatively. In 31 of these, final repair was deferred because of insufficient pulmonary arterial enlargement (14), restricted peripheral arborization (nine), or both (eight). The final 26 patients were accepted for second-stage repair, which has been performed in 24. Complete repair included ventricular septal defect closure (24), right ventricular outflow tract reconstruction (18), relief of central pulmonary arterial stenosis (14), and ligation of systemic-pulmonary collateral arteries (10). The mean postrepair peak systolic right ventricular-left ventricular pressure ratio was 0.67 (range 0.32 to 1.0). One of these patients (4%) died in the hospital and there was one late death (4%) from sepsis after tricuspid valve replacement. Three patients were lost to follow-up; the remaining 19 patients are in functional Class I or II. A two-stage surgical approach is highly successful in those patients whose pulmonary arteries are too hypoplastic to allow a single-stage repair.

Nineteen patients with truncus arteriosus and single pulmonary artery had corrective operations at the Mayo Clinic from 1969 to 1983. At operation, their ages ranged from 4 months to 20 years (mean 8.1 years). The preoperative pulmonary resistance divided by 2 was used to predict the degree of pulmonary vascular obstructive disease at operation. The influence of elevated pulmonary resistance and the intraoperative postrepair ratio of pulmonary artery to left ventricular pressure on operative and late mortality were examined. The outcome of patients with single pulmonary artery was compared with the outcome of 148 patients with truncus arteriosus and two pulmonary arteries operated on during the same period. Patients with a single pulmonary artery had an operative mortality similar to that of patients with two pulmonary arteries (32 versus 28%, p greater than 0.05). Late mortality was, however, significantly greater (p less than 0.001) for patients with a single pulmonary artery. Elevated ratios of intraoperative postrepair pulmonary artery to left ventricular pressure were associated with significantly higher (p less than 0.02) operative and late mortality, but elevated preoperative pulmonary resistance was not (p greater than 0.10). Truncus arteriosus with single pulmonary artery is associated with poor postoperative survival, and although elevated pulmonary resistances preoperatively did not predict outcome, elevated intraoperative postrepair pulmonary artery to left ventricular pressure ratios were associated with increased operative and late survival, suggesting a deleterious role of pulmonary hypertension.

From 1973 through 1979, 16 patients with pulmonary atresia, two normal-sized ventricles, and bilateral but nonconfluent pulmonary arteries underwent complete repair at the Mayo Clinic. Mean age at operation was 9.1 years (standard deviation [SD] 5.2 years). Sources of pulmonary flow were previous surgical shunts, patent ductus arteriosus, and discrete systemic-pulmonary arterial collaterals. The complete surgical repair included interruption of extracardiac shunts, closure of ventricular septal defect (15 patients), closure of atrial septal defect (3 patients), and establishment of right ventricular-pulmonary arterial continuity with a porcine-valved extracardiac conduit anastomosed to a transverse limb (T graft in 12 patients) or to a side-limb (Y graft in 4 patients). There were no operative deaths. Morbidity included reoperation for bleeding in 3 patients and compression of the prosthetic graft by the sternal closure in 1. The mean postrepair ratio of right ventricular peak systolic pressure to left ventricular peak systolic pressure (pRV/pLV) was 0.64 (SD, 0.23). Follow-up ranged from 12 to 72 months (mean, 34.6 months; SD, 20.7 months). One patient died 12 months after operation (postrepair pRV/pLV, 1.3). Conduit obstruction has been proved in 4 patients, of whom 3 underwent reoperation for extracardiac conduit obstruction at 46, 47, and 48 months. The remaining 11 patients are alive and free of major symptoms.

The course and management of 40 consecutive newborns (aged less than 2 weeks) who presented with signs and symptoms of congenital heart disease were reviewed to determine the impact of 2-dimensional (2-D) echocardiography on their subsequent management. Of the 40 patients with congenital heart disease, 60% did not undergo cardiac catheterization. Forty-two percent of the patients who were treated surgically went directly to operation without preoperative cardiac catheterization. Only 40% of the patients with congenital heart disease required cardiac catheterization in the newborn period, and 43% of these procedures were primarily therapeutic (that is, balloon atrial septostomy). In each patient 2-D echocardiography correctly identified the major cardiac malformation and there was good agreement with angiographic, surgical, and autopsy findings. The most commonly overlooked defect was a patent ductus arteriosus. Thus, 2-D echocardiography not only allows diagnosis of congenital heart disease in the newborn but can expedite clinical management. No longer is cardiac catheterization necessarily the primary means for an anatomic diagnosis of congenital cardiac malformations in the newborn.

Depressed contractility with a paradoxically increased myocardial oxygen consumption has been associated with pressure-overload hypertrophy. The present experiments investigated myocardial hypertrophy induced by volume overload. Right ventricular volume overload was produced in 19 cats by surgically creating atrial septal defects (ASD); these cats were compared with 10 sham-operated control cats. The ASD cats showed an increase in the ratio of pulmonary blood flow to systemic blood flow from 1.04 ± 0.01 ( SE ) (control) to 3.30 ± 0.28 (ASD) ( P < 0.001). Hypertrophy was evidenced by a ratio of right ventricular weight to body weight of 0.59 ± 0.03 g/kg for control cats and 0.97 ± 0.03 for ASD cats ( P < 0.001). A polarographic muscle bath was used to study papillary muscles from 8 control and 8 ASD cats. ASD muscles demonstrated normal force-velocity curves, with maximal measured preload velocities of 1.32 ± 0.05 muscle lengths/sec: control velocities were 1.33 ± 0.05 muscle lengths/sec ( P > 0.9). The myocardial oxygen consumption of isotonic contractions was normal for ASD muscles. The length-tension curves were comparable, with developed tensions at Lmax of 6.20 ± 0.31 g/mm 2 for ASD muscles and 6.34 ± 0.23 g/mm 2 for control muscles ( P > 0.7). Myocardial oxygen consumption pergram of tension development at Lmax was 0.66 ± 0.06 µliters/mg beat -1 x 10 -3 in the ASD muscles and 0.65 ± 0.05 µliters/mg beat -1 x 10 -3 in the control muscles ( P > 0.8). The mitochondrial oxidative indexes from control and hypertrophied right ventricles were similar, with respiratory control indexes of 14.3 ± 0.8 for ASD hearts and 12.8 ± 1.6 for control hearts ( P > 0.1). These data demonstrate that contractility and energetics are normal in volume-overload hypertrophy, although these same factors are abnormal in pressure-overload hypertrophy. Thus, hypertrophy alone is not a common denominator for abnormal myocardial function and energetics.

Background: We describe the long-term outcome of repair of partial atrioventricular septal defect by determining the rates of survival, reoperation, and occurrence of left atrioventricular valve regurgitation, left atrioventricular valve stenosis, left ventricular outflow tract obstruction, and arrhythmia. Methods: We studied 334 patients who underwent repair of partial atrioventricular septal defect before 1995. Results: The 30-day and 5-, 10-, 20-, and 40-year survival were 98%, 94%, 93%, 87%, and 76%, respectively. Closure of the left atrioventricular valve cleft (P = .03) and age less than 20 years at operation (P < .001) were associated with better survival. Reoperation was performed for 38 patients (11%). Repair of residual/recurrent left atrioventricular valve regurgitation or stenosis was the most common reason for reoperation. Left ventricular outflow tract obstruction occurred in 36 patients, and 7 patients underwent reoperation to relieve this obstruction. Supraventricular arrhythmias were observed in 58 patients (16%) after the operation. Supraventricular arrhythmias increased with increasing age at primary operation (P = .001). Complete atrioventricular block occurred in 9 patients (3%). Permanent pacemakers were implanted in 11 patients. Conclusions: Long-term survival after repair of partial atrioventricular septal defect is good. It is important to close the cleft in the left atrioventricular valve. Reoperation for persistent or recurrent left atrioventricular valve malfunction and relief of left ventricular outflow tract obstruction is necessary in approximately 11% of patients. (J Thorac Cardiovasc Surg 2000;119:880-90)

ObjectivesFreedom from anticoagulation is the principal advantage of bioprosthesis; however, the American Heart Association/American College of Cardiology and the American College of Chest Physicians guidelines recommend early anticoagulation with heparin, followed by warfarin for 3 months after bioprosthetic aortic valve replacement. We examined neurologic events within 90 days of bioprosthetic aortic valve replacement at our institution.MethodsBetween 1993 and 2000, 1151 patients underwent bioprosthetic aortic valve replacement with (641) or without (510) associated coronary artery bypass. By surgeon preference, 624 had early postoperative anticoagulation (AC+) and 527 did not (AC−). In the AC− group, 410 patients (78%) received antiplatelet therapy. Groups were similar with respect to gender (female, 36% AC+ vs 40% AC−, P = .21), hypertension (64% AC+ vs 61%, P = .27), and prior stroke (7.6% AC+ vs 8.5% AC−, P = .54). The AC+ group was slightly younger than the AC− group (median, 76 years vs 78 years, P = .006).ResultsOperative mortality was 4.1% with 43 (3.7%) cerebrovascular events within 90 days. Excluding 18 deficits apparent upon emergence from anesthesia, we found that postoperative cerebrovascular accident occurred in 2.4% of AC+ and 1.9% AC− patients. By multivariable analysis, the only predictor of operative mortality was hypertension (P < .0001). Postoperative cerebrovascular accident was unrelated to warfarin use (P = .32). The incidence of mediastinal bleeding requiring reexploration was similar (5.0% vs 7.4%), as were other bleeding complications in the first 90 days (1.1% vs 0.8%). No variables were predictive of bleeding by multivariate analysis.ConclusionsAlthough these data do not address the role of antiplatelet agents, early anticoagulation with warfarin after bioprosthetic aortic valve replacement did not appear to protect against neurologic events.

To determine late patient outcome and homograft durability, we reviewed 326 patients who received aortic ( n = 230) or pulmonary ( n = 118) cryopreserved homografts for right ventricular outflow reconstruction between January 1985 and October 1993. Patient survival, including operative mortality, 5 years after the operation was similar between the two groups (ulmonary homograft 86%, aortic homograft 80%; p = not significant by log-rank test). However, 5-year freedom from homograft failure was significantly better for pulmonary homografts (94% versus 70%), p < 0.01 by log-rank test). Late calcification was evaluated by chest roentgenography and echocardiography. Overall, 20% of aortic homografts became moderately or severely calcified compared with 4% of pulmonary homografts ( p < 0.001). Twenty-six percent of aortic homografts in children 4 years old or younger had moderate or severe obstruction associated with calcification, whereas only 11% of aortic homografts in patients over 4 years of age had calcific obstruction ( p < 0.01). No late deaths among patients receiving pulmonary homografts were related to graft failure; two late deaths in the aortic homograft group were homograft related. Risk factors for patient mortality and homograft failure (defined as either need for homograft replacement because of homograft failure ( p < 0.0001), but type of homograft was not correlated with patient mortality. Age 4 years or younger was a significant risk factor for homograft failure ( p < 0.0001), but type of homograft was not correlated with patient mortality. Age 4 years or younger was a significant risk factor for both mortality ( p < 0.01) and homograft failure ( p = 0.03) in aortic homograft recipients but not in pulmonary homograft recipients. These results indicate that both aortic and pulmonary homografts provided excellent intermediate-term patient survival after right ventricular outflow tract reconstruction, but pulmonary homografts are more durable than aortic homografts with less calcification and obstruction, especially among children 4 years old or younger. (J T HORAC C ARDIOVASC SURG 1995; 109: 509-18)

Between May 1974 and March 1989, 155 patients with double-inlet left ventricle had the Fontan procedure performed at the Mayo Clinic. Age at operation ranged from nearly 2 to 41 years (median 10). The operative mortality rate from 1974 through 1980 (39 patients) was 21%, but from 1981 through 1989 (116 patients) it was reduced to 9%. The 17 late deaths were secondary to reoperation (n = 8), progressive myocardial failure (n = 5), sudden arrhythmia (n = 3) and bleeding varices (n = 1). Neither operative nor late mortality rate was significantly related to age at operation. At follow-up of 6 months to 11 years (mean 4.9 years) in 111 patients, 88% were in good or excellent condition and 12% were in fair or poor condition. The Fontan operation can be performed with a mortality risk of less than 10% in properly selected patients with double-inlet left ventricle. Late results are encouraging when contrasted with the clinical course of patients before this operative approach was utilized.

OBJECTIVE: The contemporary risk of reoperative aortic valve replacement is ill-defined. We therefore compared the recent early results of reoperative and primary aortic valve replacement in our institution. METHODS: Between January 1993 and January 2001, a total of 162 patients underwent reoperative aortic valve replacement with or without coronary artery bypass grafting, and 2290 underwent primary aortic valve replacement with or without coronary artery bypass grafting. The reoperative and primary groups were similar with regard to gender (37% female in both), preoperative New York Heart Association functional class (2.8 +/- 1 vs 2.8 +/- 1), and ejection fraction (58% +/- 15% vs 57% +/- 15%). Patients undergoing reoperative aortic valve replacement were younger than those undergoing primary aortic valve replacement (64 +/- 15 years vs 70 +/- 13 years, P < .001). Previous prostheses were xenografts in 77 patients (48%), homografts and autografts in 25 (15%), and mechanical prostheses in 60 (37%). Mean time to reoperation was 9.7 +/- 6.8 years. RESULTS: Early mortality for reoperative aortic valve replacement (8/162, 5%) was not statistically different from that for primary aortic valve replacement (71/2290, 3%, P = .20). Endocarditis was more common in the reoperative group (22% vs 3%, P < .001); when endocarditis was excluded from the analysis, early mortality was 3% in both groups. Multivariate predictors for early mortality were prosthetic valve endocarditis ( P < .001, odds ratio 9.8), advanced preoperative functional class ( P < .001, odds ratio 2.0), peripheral vascular disease ( P = .008, odds ratio 2.0), preserved left ventricular ejection fraction ( P = .004, odds ratio 0.98), and male gender ( P = .009, odds ratio 0.49). After adjustment for these factors, there was no difference in early mortality between the groups ( P = .095). CONCLUSION: The risk of reoperative aortic valve replacement is similar to that for primary aortic valve replacement. These data support the expanded use of bioprosthetic valves in younger patients.

OBJECTIVES We assessed the operative and late mortality and the present clinical status of 216 patients with tricuspid atresia who had a nonfenestrated Fontan procedure performed at the Mayo Clinic in the 25-year period 1973 to 1998. BACKGROUND The Fontan operation eliminates the systemic hypoxemia and ventricular volume overload characteristic of prior forms of palliation. However, it originally did so at the cost of systemic venous and right atrial hypertension, and the long-term effects of this “price” were unknown when the procedure was initially proposed. METHODS We reviewed the clinical records of the 216 patients retrospectively. These were arbitrarily grouped into early (1973 through 1980), middle (1981 through 1987) and late (1988 through 1997) surgical eras. Patient outcome was also analyzed according to age at surgery. Operative and late mortality rates were determined and present clinical status was ascertained in 167 of 171 surviving patients. RESULTS Overall survival was 79%. Operative mortality steadily declined and was 2% (one of 58 patients) during the most recent decade. Late survival also continues to improve. Age at operation had no effect on operative mortality, and late mortality was significantly increased only in patients who were operated on at age 18 years or older. Eighty-nine percent of surviving patients are currently in New York Heart Association class I or II. CONCLUSIONS The initial 25-year experience with the nonfenestrated Fontan procedure for tricuspid atresia has been gratifying, with most survivors now leading lives of good quality into adulthood. These results justify continued application of this procedure for children born with tricuspid atresia.

Between May 1983 and March 1, 1995, 50 patients had replacement of an obstructed pulmonary ventricle–pulmonary artery conduit with an autologous tissue reconstruction in which a prosthetic roof was placed over the fibrous tissue bed of the explanted conduit. The roof was constructed with xenograft pericardium (most recently) ( n = 42), homograft dura mater ( n = 5), or Dacron fabric ( n = 3). Patient ages ranged from 5 to 34 years (median 16 years). The explanted conduits were Hancock conduits ( n = 33), Tascon conduits ( n = 6), homograft ( n = 4), Dacron tube ( n = 3), and others ( n = 4). Preoperative maximum systolic gradients ranged from 44 to 144 mm Hg (median 78 mm Hg). Thirty-seven concomitant cardiac procedures were done in 29 patients. When a valve was necessary ( n = 15), it was possible to place a large-sized valve in the autologous tissue reconstructions (range 22 to 29 mm, median 26 mm). Cardiopulmonary bypass times ranged from 34 to 223 minutes (median 84 minutes), and aortic crossclamp times ranged from 0 (in 32 patients) to 109 minutes (median 0 minutes). Intraoperative postrepair peak systolic gradients from pulmonary ventricle to pulmonary artery ranged from 0 to 33 mm Hg (median 13 mm Hg). There was one early death (2%) in a patient who had additional cardiac procedures. Follow-up was complete in all patients and ranged from 1 month to 11.8 years (median 7.5 years). There were two sudden late deaths: conduits in both were known to be free from obstruction. Forty-four of the 47 surviving patients had evaluation of the gradient by echocardiography or cardiac catheterization 1 month to 11 years (median 7 years) after operation. The gradients ranged from 5 to 45 mm Hg (median 20 mm Hg). None of the conduits developed an obstructive peel, valve obstruction, or valve incompetence. At 10 years, the freedom from reoperation for conduit obstruction was 100%, and freedom from reoperation for any cause was 81%. This technique simplifies conduit replacement, allows for a generous-sized outflow tract, has a low risk, and yields late results that appear superior to those of cryopreserved homografts or other types of extracardiac conduits. (J THORAC CARDIOVASC SURG 1995;110:1359-68)

Background: Pulmonary regurgitation appears to be well tolerated early after repair of tetralogy of Fallot; however, it may result in progressive right ventricular dilatation and dysfunction necessitating eventual valve replacement. Our objective was to review our experience with late pulmonary valve replacement after complete repair of tetralogy of Fallot. Methods and results: A total of 42 patients (16 female and 26 male) were operated on between July 1, 1974, and January 1, 1998. Mean age was 22 years (range 2-65 years). The mean interval between tetralogy repair and pulmonary valve replacement was 10.8 years (range 1.6 months–33 years). Mean follow-up was 7.8 ± 6.0 years (maximum 23 years). Indications for pulmonary valve replacement included decreased exercise tolerance in 58%, right heart failure in 21%, arrhythmia in 14%, syncope in 10%, and progressive isolated right ventricular dilatation in 7%. Heterograft prostheses were used in 33 patients and homografts in 9. Five patients underwent isolated pulmonary valve replacement; concomitant procedures performed in 37 patients included tricuspid valve repair/replacement (n = 18), residual ventricular septal defect repair (n = 12), atrial septal defect closure (n = 4), pulmonary artery patch angioplasty (n = 17), and right ventricular outflow tract enlargement (n = 13). One patient died early (2%) of multiorgan failure. There were 6 late deaths, 3 of which were cardiac related. Survival was 95.1% ± 3.4% and 76.4% ± 8.9% at 5 and 10 years, respectively. Functional class of patients was improved significantly; preoperatively, 76% of patients were in New York Heart Association class III-IV, and after pulmonary valve replacement, 97% of surviving patients were in class I-II ( P =.0001). Moderate to severe reduction in right ventricular function was noted on preoperative echocardiography in 59% and on late echocardiography in 18% ( P =.03). Of the 5 patients who had supraventricular arrhythmias before pulmonary valve replacement, 1 had postoperative recurrence and the arrhythmia is controlled with antiarrhythmic therapy; the other 4 are in normal sinus rhythm at late follow-up. Eight patients subsequently underwent pulmonary valve re-replacement without early mortality at a mean interval of 9.0 ± 4.2 years (range 3.8-16.8 years). Freedom from pulmonary valve re-replacement was 93.1% ± 4.7% and 69.8% ± 10.7% at 5 and 10 years, respectively. The only significant risk factor for re-replacement was young age at the time of the initial pulmonary valve replacement ( P =.023). Conclusion: Late pulmonary valve replacement after tetralogy repair significantly improves right ventricular function, functional class, and atrial arrhythmias, and it can be performed with low mortality. Subsequent re-replacement may be necessary to maintain functional improvement. (J Thorac Cardiovasc Surg 2001;121:344-51)