Comparison of the aortic homograft and the pulmonary autograft for aortic valve or root replacement in children

To assess late results of aortic homograft and pulmonary autograft valves implanted into the left ventricular outflow tract of children, we reviewed the case histories of 146 patients 18 years of age or younger who underwent aortic valve or root replacement between November 1964 and April 1990. One hundred three patients (mean, 12 +/- 3.9 years) received an aortic homograft and 43 (mean, 14 +/- 4.1 years) had their own pulmonary valve transferred to the aortic position. There were 54 valve and 49 root replacements with homografts and 36 valve and seven root replacements with autografts. Hospital mortality rate was 15.5% (16 patients) in the homograft group and 11.6% (five patients) in the autograft group. Survivors were followed up for a total of 867 (homograft) and 297 (autograft) patient-years. The late mortality rate was 16.7% (1.9% per patient-year) for patients with homografts and 13.2% (4.4% per patient-year) for patients with autografts, whereas the incidence for reoperation per patient-year was 2.9% and 2.0%, respectively. At 15 years actuarial rates for homografts and autografts for freedom from reoperation were 54% +/- 8.1% and 68% +/- 11.1%; freedom from endocarditis, 97% +/- 2.4% and 75% +/- 10.2%; and freedom from any complication, 41% +/- 6.5% and 50% +/- 10.3%. Valve degeneration occurred in 19 homografts (2.2% per patient-year), whereas there was no definite instance of primary tissue failure among the pulmonary autografts. This experience would indicate that either the homograft or the autograft valve can be used with acceptable results in children. However, the pulmonary autograft gives better long-term performance and, if growth potential is realized, may be the ideal valve substitute in children.     

Repair of tetralogy of Fallot in infancy with a transventricular or a transatrial approach.

OBJECTIVE: The optimal time and approach of repair of tetralogy of Fallot (TOF) remain controversial. The purpose of this study was to evaluate the outcome following repair of TOF in infants with particular regard to the surgical approach used. PATIENTS: One hundred and sixty infants (mean age 195+/-89 days, range 11-364 days) undergoing repair of a simple TOF were studied. Between 1974 and 2000, a transventricular approach (RV) was used in 91 and between 1988 and 2000, a transatrial (RA) approach in 69 infants. Ten of these infants (6.2%) had a previous palliative shunt (four in the RV versus six in the RA group). A transannular patch (TAP) was inserted in 96 (60%) infants (76 versus 20). Follow-up was complete (mean 14.5+/-5.2 versus 6+/-1 years). RESULTS: There were three operative deaths (1.9%), (two in RV versus one in RA group). A re-operation for right ventricular outflow tract obstruction (RVOTO) was performed in 19 patients (3 versus 16). Ten-year freedom from re-operation for RVOTO (+/-standard error of the mean) was 88+/-4% (98+/-2 versus 72+/-6%, P<0.0001). Within the RA group, 5-year freedom from re-operation for RVOTO for those who had a TAP was 79+/-9% and it was 75+/-4% for those having a simple repair. Six patients in the RV group required pulmonary valve replacement (PVR). Ten-year freedom from PVR was 98+/-1% (97+/-2 versus 100%, P=0.3). There were two late deaths, one in each group. Ten-year survival was 97+/-1%. One patient in the RV group developed late recurrent ventricular tachycardia requiring the implantation of a defibrillator. At most recent echocardiography, all but the patient who had the defibrillator had good right and left ventricular function. CONCLUSIONS: Transventricular and transatrial repair of TOF in infancy, are associated with an acceptable operative risk, low incidence of late arrhythmia, good bi-ventricular function and excellent survival. In our experience, however, transatrial repair has a disturbing incidence of early and mid-term residual or recurrent RVOTO, even when a TAP has been used.     

Stentless xenografts and homografts for right ventricular outflow tract reconstruction during the Ross operation

BACKGROUND: Shortage of homografts prompted us to replace the transplanted pulmonary trunk with stentless xenografts during the Ross procedure. The 5-year follow-up in comparison with pulmonary homografts is presented. METHODS: From April 1997 to March 2002, of 51 patients undergoing a modified Ross procedure 15 patients (age range 55 to 65 years, mean 59 +/- 5) received a stentless xenograft, and 36 patients (15 to 56 years, mean 36 +/- 11) a pulmonary homograft for right ventricular outflow tract (RVOT) reconstruction. Follow-up was complete for a mean of 3.1 years (range 6 to 60). Regularly performed echocardiography included determination of valve annulus, peak instantaneous gradient, leaflet performance, location of obstruction, and degree of regurgitation. RESULTS: There was 1 late death and 1 reoperation for homograft stenosis. The homograft annulus diameter decreased by a mean of 10% (range 3 to 10 mm; p < 0.01), and peak Doppler gradient increased significantly (p < 0.001). All patients except 1 had gradients less than 25 mm Hg. Gradients in xenograft patients were stable at a low level (6.5 +/- 4.3 mm Hg to 8.8 +/- 7.4 mm Hg at the latest follow-up). Mild pulmonary regurgitation was noted in 46.6% (xenografts) and 19.5% (homografts). Leaflet quality and mobility were maintained in all patients. CONCLUSIONS: Pulmonary homografts underlie a process of annular reduction after the Ross procedure, which is usually not associated with graft stenosis. Mild pulmonary regurgitation is more common in xenografts than in homografts. RVOT reconstruction using stentless xenografts represents a satisfactory treatment modality for aged patients.     

Geometric mismatch between homograft (allograft) and native aortic root: a 14-year clinical experience.

OBJECTIVES: We evaluated the effect of homograft/native aortic root geometric matching and mismatching on valve survival and myocardial remodeling. METHODS: Between January 1, 1987 and March 2000, a total of 292 patients, aged 1.5-78 years (mean, 46.2 years), underwent freehand subcoronary aortic valve (AVR; n=207) and root (ARR; n=85) replacement with matched and mismatched cryopreserved homografts. All patients had pre- and postoperative two-dimensional Doppler echocardiographic studies. Two-hundred and forty-three survivors, excluding children with complete data on sizing, were followed at a total follow-up time of 1269 patient-years. Seventy percent received matched and 30% received mismatched aortic homografts. The homograft valve sizes ranged from 19 to 28 mm. RESULTS: Hospital death for elective first operation was 2.3%, and late death after a mean follow-up of 52 months was 7.9%. The patient survival at 14 years was 92+/-2%. By linear regression analysis, matched homografts were equal to or 1-2 mm less than the native aortic annulus (r(2)=0.73). The valve survival in patients with AVR and ARR was 72+/-4 and 80+/-8% at 14 years, respectively. The freedom from reoperation was 92+/-5, 77+/-4 and 48+/-10% at 14 years for matched, oversized and undersized homografts, respectively (P=0.001). The postoperative cardiac index of patients with 22 and 24 mm homografts was 3.8-4.1 l/m(2), and there was a regression of the left ventricular mass and end-diastolic diameter (P=0.001). CONCLUSIONS: The aortic homograft offers an excellent long-term clinical result. A mismatched homograft is a risk factor for postoperative aortic incompetence, reinfection with pseudoaneurysmal formation and reoperation for the freehand subcoronary implantation technique during the first 7 years of the postoperative period. It is prudent therefore to avoid mismatched homografts and use rather a properly sized stentless xenograft if a root replacement is not indicated.     

Homograft mitral valve replacement: five years' results

OBJECTIVE: Results of mitral valve replacement with a mitral homograft were evaluated at 5 years to assess the suitability of the procedure. METHODS: Thirty-seven patients (25 male subjects) aged 10 to 49 years (mean, 32 +/- 10 years) with rheumatic mitral valve disease underwent total (n = 35) or partial (n = 2) mitral valve replacement with a fresh antibiotic-preserved (n = 23) or cryopreserved (n = 14) mitral homograft. The predominant lesion was mitral stenosis (n = 30). RESULTS: There were 5 early deaths. Operative survivors were followed up for 1 to 60 months (mean, 26.6 +/- 12 months). Among these, 21 patients had severe mitral regurgitation during the follow-up period; 3 died and 8 underwent reoperation. The homograft failure rate was not affected by preoperative physiologic lesion (stenosis vs regurgitation, P =.4), type of homograft (antibiotic-preserved vs cryopreserved homograft, P =.9), papillary muscle pretreatment (yes vs no, P =.9), or addition of posterior collar annuloplasty (yes vs no, P =.2). Among the remaining patients, 5 had moderate mitral regurgitation, 4 had either trivial or mild mitral regurgitation, and 2 were lost to follow-up. Study of the explanted mitral homografts (n = 8) revealed that disruption of one of the donor papillary muscles was responsible for early failures (n = 2), whereas cuspal and chordal degeneration was responsible for late failures (n = 6). Microscopically, the explanted valve lacked any viable cellular elements, and there was no evidence of immunologic injury to the homografts. CONCLUSION: The mitral homograft did not fulfill our expectations as a suitable substitute for the diseased mitral valve.     

Late pulmonary valve replacement after repair of tetralogy of Fallot

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.     

Aortic valve homografts in the surgical treatment of complex cardiac malformations

From April of 1968 to March of 1983, the surgical treatment of complex congenital cardiac malformations requiring an extracardiac conduit for their correction was performed with aortic valve homografts or aortic valved homograft conduits sterilized and preserved in our hospital. Our experience concerns 93 patients in whom a total of 103 aortic valve homografts were implanted. Ages of the patients ranged from 7 months to 36 years (mean 11.6 years). The aortic valve homografts were used from the right atrium to the pulmonary arteries or right ventricle (right atrium-dependent conduit), from the venous ventricle to the pulmonary arteries (ventricle-dependent conduit), or in the pulmonary orifice and in the superior and/or inferior venae cavae. There were 25 early and nine late deaths (36.5%), none of them related to the aortic valve homograft. The clinical follow-up of the 59 survivors (1 month to 15 years, mean 4.3 years) evidenced neither dysfunction of the aortic valve homograft nor thromboembolism or hemolysis; 93% of the patients are in New York Heart Association Class I or II. Control cardiac catheterization in 53 patients evidenced a pressure gradient in only 14 ventricle-dependent conduits. In seven patients with serial control catheterizations after 5 to 10 years, the pressure gradient had not increased.     

Early results of right ventricular-pulmonary artery conduits in patients under 1 year of age.

OBJECTIVES: Management strategies for the repair of many complex heart defects require the implantation of a valved conduit between the right ventricle (RV) and the pulmonary artery (PA), often using aortic or pulmonary homograft valves. Their limited availability, however, has led to the development and use of new conduits. We retrospectively compared our experience with small homografts in patients of less than 1 year of age with the TissueMed bioprosthetic valved conduit. METHODS: From March 1994 to November 1997 29 patients in their first year of life underwent conduit implantation for complex heart defects. These were retrospectively reviewed in order to determine the incidence of death or conduit stenosis. Seventeen patients received homografts and 12 TissueMed conduits. RESULTS: Diagnoses and operative details including conduit size were similar in the two groups and in all cases complete repair of the underlying defect was carried out. Early post-operative mortality was 4/17 (23.5%) in the homograft group and 3/12 (25%) in the TissueMed group. Echo Doppler evaluation within 1 month of operation showed no right ventricular outflow tract (RVOT) obstruction in any of the survivors. In the TissueMed group 8/9 (77%) survivors have gone on to develop significant RVOT obstruction within 12 months of operation. There have been three late deaths in this group all related to severe RVOT obstruction. Two patients died during an attempt at balloon dilatation and one patient died of progressive right heart failure. Five patients had successful replacement of the TissueMed conduit. One child remains well with no evidence of RVOT obstruction. At operation to replace conduit, or at autopsy, the stenoses were related to the deposition of fibrous tissue at the anastomotic suture lines. In the homograft group none of the survivors developed RVOT obstruction during the first 12 months post-operatively. There was one late death (non-cardiac in origin) and one child is awaiting conduit replacement 40 months after initial implantation for obstruction. CONCLUSIONS: The homograft is a satisfactory conduit for re-establishment of RV-PA continuity in infancy. Further work needs to be undertaken in order to elucidate the mechanisms of early graft failure in bioprosthetic conduits if these are to be a suitable alternative for RV outflow reconstruction in infants.     

Current approaches to pulmonary regurgitation

Objective: To evaluate the effects on ventricular function and volumes following right ventricular outflow tract reconstruction (RVOTR) with pulmonary homograft replacement (PVR) and percutaneous pulmonary valve implantation (PPVI) for predominant pulmonary regurgitation. This study was not intended to compare the two approaches. Methods: We prospectively examined 25 patients (mean age 21+/-13 years, 96% tetralogy of Fallot, 1/25 with conduit dysfunction) who had PVR with RVOTR for severe pulmonary regurgitation (PR), and 11 patients (mean age 20+/-9 years, 64% tetralogy of Fallot, 9/11 with conduit dysfunction) who underwent PPVI for predominant PR. Mean age at primary repair in both groups was 4.3+/-6.6 years. Magnetic resonance imaging was performed prior to, and 1 year following, interventions. Results: Before procedure, NYHA classification was similar in both groups 2.1+/-0.5. Following interventions, there was a significant reduction in RV volumes in both groups. In the surgical (PVR) group, RV end-diastolic volume (EDV) decreased from 151+/-49 to 97+/-32ml/m(2) (p<0.0001) whereas end-systolic volume (ESV) decreased from 80+/-43 to 46+/-23ml/m(2) (p<0.0001). In the PPVI group, RV EDV decreased from 106+/-27 to 89+/-25ml/m(2) (p=0.002) and RV ESV from 49+/-20 to 40+/-16ml/m(2) (p=0.034). Both groups had a significant improvement in RV (63+/-20 to 72+/-16ml/beat, p=0.003 (PVR group), 53+/-14 to 67+/-16ml/beat, p=0.030 (PPVI group)) and LV effective stroke volume (61+/-18 to 73+/-16ml/beat, p=0.001 (PVR group); 59+/-24 to 75+/-16ml/beat, p=0.009 (PPVI group)). Conclusions: Following either PVR with RVOTR or PPVI, there was a significant reduction in RV volumes and an improvement in RV function. Importantly, in both groups, LV effective SV increased, and this may be the parameter to judge the benefit of the procedure. These results also support PPVI as an extra dimension in complex RVOT management.     

Blood group incompatibility and accelerated homograft fibrocalcifications

OBJECTIVE: Cryopreserved valved homograft has become the conduit of choice for right ventricular outflow tract reconstruction in pediatric cardiac surgery. Aortic homografts have been frequently used in pulmonary position, but accelerated aortic homograft fibrocalcification may occur. Blood group incompatibility between receiver and homograft donor may play a central role in this context. METHODS: Between 1993 and 2000, 59 children (mean age 6.4 +/- 4.4 years) received cryopreserved valved homografts for right ventricular outflow tract reconstruction and were followed from 2 to 10 years clinically, with echocardiography and chest radiography for detection of development of homograft calcifications. Seventeen patients were 3 years or younger. Fifty aortic (85%) and 9 pulmonary homografts were all used in pulmonary position. Thirty-three patients (56%) had the same blood group (ABO) as the homograft donor (iso group), and 26 were blood group-incompatible (non-iso group). RESULTS: No deaths occurred during follow-up. Six patients (10.2%) required homograft replacement because of severe fibrocalcifications, and another 3 showed moderate homograft calcifications (5.1%) at last examination. Freedom from moderate to severe homograft calcification at 8 years (Kaplan-Meier) was 95.2% for the iso group and 72.9% for the non-iso group (P <.0001). Homograft calcifications occurred within 2 years of implantation in 6/9 patients (67%) in the non-iso group. CONCLUSIONS: Blood group incompatibility between receiver and homograft donor seems to play an important role in the development of accelerated fibrocalcifications in cryopreserved homografts, particularly in the very young (3 years old or younger). Blood group compatibility should therefore be respected to avoid accelerated homograft fibrocalcifications.     

Right ventricular outflow tract reconstruction for pulmonary regurgitation after repair of tetralogy of Fallot. Preliminary results.

BACKGROUND: Pulmonary regurgitation after tetralogy of Fallot (ToF) repair is associated with right ventricular dilatation, failure and arrhythmia. Timing and technique for re-intervention remain controversial. METHODS: Our recent approach is to reconstruct the dilated right ventricle outflow tract (RVOT) as a fibro-muscular sleeve to support a pulmonary homograft valve conduit in orthotopic position. Indication is based on clinical and magnetic resonance (MR) criteria. We reviewed all patients who underwent RVOT reconstruction between January 2004 and February 2005. There were seven children (mean age 14+/-2 years) operated 13+/-2 years after ToF repair, and 12 adults (mean age 30+/-15 years) operated 23+/-10 years after ToF repair. Exercise testing and MR evaluation prior to surgery and at 1 year postoperative follow-up were compared. RESULTS: There was no operative mortality. At 1 year, pulmonary regurgitation was mild or less in 16/19 patients. Right ventricular (RV) end-diastolic (158+/-51 to 103+/-36ml/m(2), p<0.001) and end-systolic volumes (85+/-42 to 49+/-24ml/m(2), p=0.001) fell significantly. Importantly, effective RV stroke volume (43+/-10 to 48+/-7ml/m(2), p=0.019) and left ventricular (LV) stroke volume (43+/-7 to 47+/-7ml/m(2), p=0.009) increased significantly. The mean RV/LV end-diastolic volume ratio fell markedly in both children and adults (2.22+/-0.62 to 1.38+/-0.52). However, no improvement in maximal VO(2) on exercise was noted in either group. CONCLUSIONS: RVOT reconstruction restored valve function, improved RV dimensions and left and right stroke volumes. Maximal exercise capacity did not improve in either children or adults.     

Expanding the indications for pulmonary valve replacement after repair of tetralogy of fallot

BACKGROUND: Insertion of a competent pulmonary valve has been advocated to reduce right ventricular volume overload associated with pulmonary regurgitation (PR) after repair of tetralogy of Fallot. However the indications, proper timing, and long-term benefits of restoring pulmonary valve function remain controversial. METHODS: Thirty-six patients (aged 15.2 +/- 9.2 years) underwent pulmonary valve implantation (31 homografts, 5 heterografts) 12.2 +/- 6.9 years after tetralogy repair. Additional surgical procedures included pulmonary artery augmentation (n = 14), closure of septal defects (n = 10), and cryoablation and endocardial resection of ventricular tachycardia (n = 2). RESULTS: All patients have had clinical improvement in their exercise capacity. Preoperative and postoperative bicycle ergometry tests in 6 patients demonstrated significant improvement in the percent of predicted peak workload (68.5% +/- 19.8% to 80.7% +/- 17.4%, p < 0.015). One midterm death occurred in a 38-year-old patient with a history of ventricular tachycardia who died suddenly 2 years after pulmonary valve insertion. Postoperative echocardiographic measurements were available in 34 patients at a mean follow-up of 5 years. There was a 30% reduction in right ventricular end-diastolic diameter indexed to body surface area after surgery (30.1 +/- 10.2 to 18.6 +/- 6.0 mm/m(2), p < 0.0001). Two patients required conduit replacements at 1 and 9 years postoperatively. CONCLUSIONS: Timely insertion of a competent pulmonary valve in children, adolescents, and young adults with significant PR after tetralogy of Fallot repair results in subjective and objective improvement in exercise capacity and is associated with reduction in right ventricle size.     

Pulmonary valve insertion during reoperation for tetralogy of Fallot

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.     

Homograft replacement of the mitral valve: eight-year results

OBJECTIVE: The objective of this study was to assess whether the mitral homograft represents a valuable alternative for complete or partial mitral valve replacement. METHODS: Since 1993, 104 patients underwent mitral homograft replacement surgery. The mean age was 38 +/- 15 years. The causes of mitral valve disease were rheumatic disease (n = 76), infective endocarditis (n = 24), and others (n = 4). Sixty-five of these procedures were total homografts, and 39 were partial homografts. RESULTS: The mean follow-up was 52 +/- 35 months (maximum, 117 months). Overall hospital mortality was 4 (3.8%) of 104 patients and 2.5% versus 8.7% for patients without endocarditis and with endocarditis, respectively (P <.19). There were 9 late deaths (cardiac, 4; noncardiac, 5). There have been 5 early (<3 months) and 10 late reoperations. Of the remaining 77 patients, New York Heart Association class was I in 61, II in 14, and III in 2. Four patients had endocarditis, and 5 had an ischemic or hemorrhagic event. Freedom from major cardiac events was 71% +/- 6% at 8 years (partial at 81% vs total at 63%, P <.19). Among patients with a total homograft, freedom from major cardiac events was 61% +/- 9% and 85% +/- 8% at 6 years in patients younger than and older than 40 years, respectively (P =.09). CONCLUSION: The risk of early dysfunction related to a mismatch between the mitral homograft and the patient's valve is the main pitfall of the technique. Beyond that stage, the results were comparable with those of bioprostheses in a cohort of young patients.     

Pulmonary valve insertion late after repair of Fallot's tetralogy.

OBJECTIVES: To analyze the results of pulmonary valve insertion late after initial repair of Fallot's tetralogy. Pulmonary insufficiency (PI) after correction of Fallot's tetralogy is usually well tolerated in the short term, but is associated with symptomatic right ventricular dilatation and an increased risk of ventricular arrhythmias over longer periods of time. METHODS: From 1993 to July 2000, 51 patients were reoperated for PI at a mean age of 25.7+/-11.9 years. The mean age at initial repair was 6.4+/-7.2 years. Patients with a conduit inserted at initial operation, with absent pulmonary valve syndrome or with a more than moderate ventricular septal defect at reoperation were excluded from the study. A cryopreserved pulmonary (96%) or aortic (4%) homograft was implanted in the orthotopic position with the use of cardiopulmonary bypass 19.3+/-9.1 years (2.7-40.3 years) after initial correction. Preoperative symptoms (New York Heart Association, NYHA class), degree of PI (echo-Doppler, MRI), right ventricular dimensions (MRI) and QRS duration were compared to findings at last follow-up. RESULTS: Follow-up is complete and had a mean duration of 1.7+/-1.4 years. Hospital mortality was 2%. No serious morbidity occurred. Severe PI was present preoperatively in all patients. At last follow-up echo-Doppler studies showed PI to be absent or trivial in 96% and mild in 4% of patients. In 13 patients MRI studies were performed both pre- and postoperatively: in this group PI was reduced from a mean of 48 to 4%. After 6 months NYHA capacity class had improved significantly from 2.3+/-0.6 to 1.4+/-0.5. After 1 year end-diastolic and end-systolic right ventricular volumes were reduced significantly. Right ventricular ejection fraction and QRS duration remained unchanged. CONCLUSIONS: PI late after correction of Fallot's tetralogy may lead to serious symptomatic right ventricle dilatation. After pulmonary homograft insertion right ventricular dimensions decrease rapidly and functional improvement is observed in almost all patients.     

Medtronic Freestyle valve for right ventricular reconstruction in pediatric Ross operations

BACKGROUND: The use of homograft conduits to reconstruct right ventricle (RV) to pulmonary artery (PA) connections is an essential component of the Ross operation. Homograft availability and cost may be problematic when considering the Ross operation. We elected in January 1998 to utilize commercially available xenografts as an alternative to homografts for RV/PA reconstruction in the pediatric Ross operation. Our early results using the Medtronic Freestyle valve (Medtronic, Minneapolis, MN) for RV/PA reconstruction are presented. METHODS: We reviewed our database for all Ross operations performed on children since January 1998. A total of 16 patients were identified. Eleven children received a Medtronic Freestyle valve, 2 children received a homograft, and 3 children received another type of xenograft. Echocardiographic evaluation of all children who received the Medtronic Freestyle valve was performed at hospital discharge and at two subsequent outpatient evaluations. RESULTS: The median peak instantaneous pressure gradient across the xenograft was 16 +/- 9 mm Hg (immediately after surgery before hospital discharge); 22 +/- 20 mm Hg at 23 +/- 11 months (first postdischarge follow-up); and 27 +/- 20 mm Hg at 35 +/- 9 months (second postdischarge follow-up). Linear regression analysis revealed an increasing pressure gradient with time (R(2)-adjusted = 0.44, p < 0.0001). At the same three observation points, the xenograft annulus diameter decreased: 25 +/- 1.2 mm; 19 +/- 4.3 mm; and 20 +/- 1.8 mm. Linear regression analysis revealed a decreasing annulus diameter with time (R(2)-adjusted = 0.41, p < 0.0001). CONCLUSIONS: The Medtronic Freestyle valve provides a possible alternative to homografts for the reconstruction of the RV/PA connection in the pediatric Ross operation. Long-term follow-up is necessary to evaluate this xenograft as an alternative to the homograft.     

A study of isolated tricuspid valve surgery late after left heart valve operation

Management of severe tricuspid regurgitation late after left heart valve operation is controversial. There has been reluctance to the operation due to the high risk of repeat operation, coexistent right ventricular dysfunction and pulmonary hypertension. We investigated 6 cases of isolated tricuspid valve surgery (tricuspid valve replacement: 2, tricuspid valve plasty: 4) late after left heart valve operation. Before operation, these patients showed poor general condition (4 cases were NYHA III or IV) but good left ventricular function [mean ejection fraction (EF) 66 +/- 9.6%]. Hospital mortality was 0% and the mean mid-term actual event-free survival over 2 +/- 1.8 years was 80%. Most of patients demonstrated NYHA I and improvement of hepatomegaly after operation. There were many complications in 2 cases that had been performed previous operation more than 20 years before. In summary, the patient who complained symptoms due to right heart ventricular failure and showed good left ventricular function after left heart valve surgery should be considered to undergo tricuspid valve operation before the occurrence of other complications.     

Improved right ventricular function following late pulmonary valve replacement for residual pulmonary insufficiency or stenosis

Residual severe pulmonary insufficiency or stenosis may result in significant myocardial dysfunction late after repair of tetralogy of Fallot. Although pulmonary valve replacement has been advocated for selected patients, objective improvement in right ventricular function has been difficult to demonstrate. We undertook pulmonary valve replacement in 11 patients to treat residual insufficiency (n = 8) or stenosis (n = 3) and evaluated them before and after operation by radionuclide ventriculography and M-mode echocardiography. Patients' age at the original repair was 6.6 +/- 0.6 years (range 2 to 8 years) and at subsequent valve replacement was 14.6 +/- 1.5 years (range 5 to 20 years). Indications for pulmonary valve replacement were conduit stenosis indicated by a gradient greater than or equal to 75 mm Hg (n = 3), symptoms (n = 2), progressive cardiomegaly (n = 3), and new onset of tricuspid insufficiency (n = 3). Prior to pulmonary valve replacement, right ventricular ejection fraction was 0.29 +/- 0.12 (range 0.12 to 0.48) and rose to 0.35 +/- 0.10 (range 0.19 to 0.48) at a mean of 10.5 +/- 2.3 months after operation (p less than 0.05). Improvement (defined as an increase in ejection fraction greater than 0.05) was noted in seven patients whereas four demonstrated no change. Left ventricular ejection fraction before operation (0.55 +/- 0.12) was unchanged after pulmonary valve replacement (0.54 +/- 0.06). M-mode echocardiography demonstrated significant reduction in right ventricular dilatation. Right ventricular/left ventricular end-diastolic dimension fell from 1.03 +/- 0.30 to 0.73 +/- 0.13 after operation (p less than 0.01). Cardiothoracic ratio fell from 0.59 +/- 0.02 to 0.55 +/- 0.02 at a mean of 12 months after pulmonary valve replacement (p less than 0.01). Subjective improvement in exercise tolerance was noted in all seven patients who showed an increase in right ventricular ejection fraction. Of the remaining four patients, two had no improvement, one felt symptomatically improved, and one was too young for evaluation. These data demonstrate objective improvement in right ventricular function following pulmonary valve replacement and confirm the usefulness of this procedure in patients with significant right ventricular dysfunction secondary to residual pulmonary insufficiency and stenosis.     

Ross procedure in rheumatic aortic valve disease.

OBJECTIVE: To assess the results of aortic valve replacement with the pulmonary autograft in patients with rheumatic heart disease. METHODS: From October 1993 through September 2003, 81 rheumatic patients with aortic valve disease, mean age 29.5+/-11.9 years (11-56 years) underwent, the Ross procedure with root replacement technique. Forty patients were 30 years of age or below (young rheumatics). Associated procedures included mitral valve repair (n=19), open mitral commissurotomy (n=15), tricuspid valve repair (n=2), and homograft mitral valve replacement (n=2). RESULTS: Early mortality was 7.4% (six patients). Mean follow-up was 92.3+/-40.9 months (7-132 months, median 109 months). Sixty of the 73 patients whose follow-up was available (82%) had no significant aortic regurgitation. Re-operation was required in seven (8.4%) patients for autograft dysfunction with failed mitral valve repair (n=3), autograft dysfunction alone (n=2) and failed mitral valve repair alone (n=2). No re-operations were required for the pulmonary homograft. There were six (7.5%) late deaths. Actuarial survival and re-operation-free survival at 109 months were 84.5+/-4.1% and 90.5+/-3.7%, respectively. Freedom from significant aortic stenosis or regurgitation was 78.4+/-5.2% and event-free survival was 64.6+/-5.8%. When compared to rheumatics above 30 years of age, the relative risk of autograft dysfunction was high in the young rheumatics. CONCLUSION: The Ross procedure is not suitable for young patients with rheumatic heart disease. However, it provides acceptable mid-term results in carefully selected older (>30 years) patients with isolated rheumatic aortic valve disease.     

Compared fate of small-diameter Contegras and homografts in the pulmonary position.

OBJECTIVE: This study analyzes whether small-diameter Contegras behave in the same way as small-diameter homografts, when implanted for the first time in pulmonary position. METHODS: Small-diameter conduits include 12 and 14 mm Contegras and 8-14 mm homografts. Graft dysfunction is defined as right ventricular outflow tract obstruction with peak echo-Doppler gradient>40 mmHg, or grade III/IV graft regurgitation. Graft failure is defined as need for conduit replacement or need for catheter or surgical reintervention. Thirty-eight patients who received small Contegras (n=25) and small homografts (n=13) from October 2002 to end December 2006 were studied. The most frequent indication was pulmonary atresia and ventricular septal defect (n=20; 10 associated with major aorto-pulmonary collateral arteries), followed by truncus arteriosus (n=12). Most patients' characteristics were comparable except that recipients of homografts were smaller (p for body area=0.014). Survival, freedom from graft dysfunction, failure and explantation were estimated by the Kaplan-Meier method. The log-rank test was used to compare outcomes. RESULTS: There were three early and four late deaths. No death was graft related. Survival was 80+/-8.2% for patients with Contegras and 77+/-11.7% for those with allografts: p=0.82. Mean follow-up duration is 22+/-16 months. Freedom from dysfunction for Contegras conduits decreased in the first 6 months and stabilized at 58+/-11% from month 14. For homografts it decreased only 1 year after implantation, down to 35+/-19.7% from month 31: p=0.61. Freedom from Contegras failure diminished the first 16 months to level out at 57+/-13%. No homograft failed the first 2 years. With a p-value of 0.14, homografts tended to fail less frequently. Five grafts were explanted. Freedom from explantation was similar (p=0.98): 90+/-6.7% for Contegras and 75+/-21.6% for homografts at year 3. CONCLUSION: In the first 4 years after pulmonary implantation of small-diameter Contegras and homografts, the fate of both conduits was statistically similar, in spite of different behavior. As Contegras is 'off-the-shelf' available, it constitutes a sound alternative to homograft for right ventricular outflow tract reconstruction in neonates and infants.