TY - JOUR
AU1 - Conte,, Stefano
AU2 - Jashari,, Ramadan
AU3 - Eyskens,, Benedict
AU4 - Gewillig,, Marc
AU5 - Dumoulin,, Monique
AU6 - Daenen,, Willem
AB - Abstract Objective: Pulmonary regurgitation after valveless repair of right ventricular outflow tract obstruction (RVOTO) results in progressive right ventricular (RV) dilatation and dysfunction in an increasing number of patients. Since 1989, we have exclusively used cryopreserved homografts to restore pulmonary valve competence in these patients. Our 9-year-experience with pulmonary valve insertion (PVI) in such cases has been reviewed to evaluate the indications for this procedure and its benefits. Methods: From 1989 to 1998, 49 patients (original diagnosis: tetralogy of Fallot in 42 patients and pulmonary stenosis in seven) aged from 3 to 42 years (mean 18±9 years) underwent PVI with homografts late (mean 13±7 years) after valveless repair of RVOTO (transannular patch, n=38; pulmonary valvulotomy±infundibular patch, n=11). Preoperatively, all patients had severe pulmonary regurgitation, cardiomegaly, significant to severe RV dilatation and dysfunction, fatigue, reduced exercise tolerance, and were in NYHA class II (n=43) or III (n=6). Ten patients had ventricular arrhythmia. Results: There was one early death, due to air embolism, and one late death, due to ventricular arrhythmia. All survivors but one, who subsequently underwent heart transplant, had symptomatic improvement after homograft insertion. The mean RV end-diastolic diameter decreased from 38±9 to 26±8 mm (P<0.01), and cardiothoracic ratio decreased from 0.62±0.07 to 0.54±0.04 (P<0.01). Good late homograft function was the rule, with all the survivors being free of reoperation for valve failure. At a mean follow-up of 42±28 months, 41 patients (87% of the survivors) were in New York Heart Association (NYHA) class I and six in class II. Within this group three patients are still in treatment for RV failure and five for ventricular arrhythmias. In these patients, the average interval between RVOTO repair and PVI was significantly longer than in the others (18±7 vs. 12±6 years, P<0.01). Conclusion: Homograft PVI is safe and provides clinical improvement with a significant reduction in RV volume overload and excellent mid-term results in most patients with severe PR late after RVOTO repair. This procedure should be undertaken early in symptomatic patients, before severe RV failure and ventricular arrhythmias ensue. Reoperation, Congenital heart disease, Tetralogy of Fallot, Pulmonary valve, Homografts Introduction Pulmonary regurgitation (PR) is common after valveless repair (radical valvulotomy, valvulectomy, transannular patch) of right ventricular outflow tract obstruction (RVOTO) and it is generally well tolerated for many years [1],[2],[3]. Experimental and clinical studies failed to demonstrate adverse effects of isolated PR, at least on early to medium term [4],[5],[6]. However, in some patients severe long-term PR results in progressive right ventricular (RV) dilatation and failure [7],[8],[9],[10],[11],[12],[13], poor exercise tolerance [9],[14],[15],[16] and a highly increased risk for ventricular arrhythmias and sudden death [17],[18],[19]. In these patients pulmonary valve insertion (PVI) is usually recommended, but there is still no consensus as regards reliable criteria of indication [3],[6],[7],[8],[9],[10] and optimal conduits for PVI [6],[15],[19],[20],[21],[22],[23],[24],[25]. Since 1989, we have exclusively used cryopreserved homografts to restore pulmonary valve competence late after RVOTO repair. Our 9-year-experience with homograft PVI in such cases has been reviewed to evaluate the indications for this procedure and its benefits. Materials and Methods Patients Forty-nine consecutive patients with severe PR after previous valveless repair of RVOTO underwent PVI with homograft valved conduits at Gasthuisberg University Hospital, Leuven, Belgium, between September 1989 and March 1998. There were 33 boys and 16 girls ranging in age from 3 to 42 years (mean 18±9 years) at the time of PVI (Fig. 1 ), which was performed 1.5 to 32 years (mean 13±7 years) after initial RVOTO repair (1960–1995) (Fig. 2 ). This included transannular patch in 38 patients and pulmonary valvulotomy with or without right infundibular patch in 11. Initial diagnosis was tetralogy of Fallot (TOF) in 42 patients and pulmonary stenosis (PS) in seven. As the total amount of patients who underwent RVOTO repair in our centre has been 526 patients with TOF and 192 patients with PS, the rate of patients who underwent reoperation for PR was 8% in the TOF group and 4% in the PS group. Fourteen patients (29%) had received a systemic-to-pulmonary artery shunt (Blalock-Taussig shunt in 11 patients and Waterstone shunt in three) prior to initial repair. Before PVI, all patients had cardiomegaly, significant to severe RV dilatation and dysfunction, fatigue, reduced exercise tolerance, and were in New York Heart Association (NYHA) class II (n=43) or III (n=6). Moreover, ten patients had ventricular tachyarrhythmia, eight dyspnea, two cyanosis, and one chest pain. Mean RV end-diastolic diameter (RVEDD) by echocardiography was 38±9 mm, and mean cardiothoracic ratio by roentgenography was 0.62±0.07. Within the group of patients with ventricular arrhythmias (n=10) RV dilatation was significantly more severe than in the other patients (n=39) (mean RVEDD, 45.5±7 vs. 36±8 mm; P<0.01). Two patients with ventricular arrhythmias underwent unsuccessful radiofrequency ablation prior to PVI. Most patients had echocardiographic evidence of impaired RV contractility and some grade of tricuspid regurgitation in association with severe PR (Table 1 ). The severity of PR correlated significantly with the severity of RV dilatation and with the incidence of ventricular arrhythmias. Mean RVEDD in the 27 patients with PR grade 4 was significantly higher than in the 22 patients with PR grade 3 (41±8 vs. 34±8 mm, P<0.01). Among the 22 patients with PR grade 3, only 2 (9%) had ventricular arrhythmias; whereas, among the 27 patients with PR grade 4, the patients with ventricular arrhythmias were 8 (30%, P=0.02). Ten patients had also residual ventricular septal defect (VSD), two had atrial septal defect (ASD), one had partial anomalous pulmonary venous drainage (PAPVD), and four had branch pulmonary artery stenoses (with pressure gradients from 35 to 60 mmHg). Cardiac catheterization was performed on most patients before surgery mainly to delineate the pulmonary artery anatomy and to estimate the degree of RV dysfunction and the size of residual intracardiac shunts. Fig. 1 Open in new tabDownload slide Age distribution at pulmonary valve insertion. Fig. 1 Open in new tabDownload slide Age distribution at pulmonary valve insertion. Fig. 2 Open in new tabDownload slide Distribution of the interval between valveless repair of right ventricular outflow tract obstruction and pulmonary valve insertion. Fig. 2 Open in new tabDownload slide Distribution of the interval between valveless repair of right ventricular outflow tract obstruction and pulmonary valve insertion. Table 1 Open in new tabDownload slide Regurgitation grades of right heart valves Table 1 Open in new tabDownload slide Regurgitation grades of right heart valves Surgical technique Homograft PVI was performed following the major principles, previously described by our group [21]. Through a median re-sternotomy, the heart and the great vessels were dissected free from adhesions to obtain proper exposure. Cardiopulmonary bypass was established with aortic and bicaval cannulation. During moderate hypothermia (28–30°C), the heart was cross-clamped and myocardial protection was ensured by a single dose of cold cardioplegic infusion. A longitudinal incision was made through the RV outflow tract and extended into the main pulmonary artery. When present, the patch was excised in most patients, as any pulmonary valve remnant. By preference, a cryopreserved oversized pulmonary homograft was inserted between the main pulmonary artery and the right ventricle at the level of the crista supraventricularis. A xeno-pericardial patch was also inserted as a hood to cover the enlarged right ventriculotomy (Fig. 3 ). Three patients received an aortic homograft, since pulmonary homograft of appropriate size was not available. The diameter of the homografts inserted ranged between 19 and 29 mm (median 23 mm), with the large majority (n=41, 84%) ranging between 20 and 25 mm. All homograft valves were processed and delivered by the European Homograft Bank (Brussels Military Hospital, Belgium). Associated procedures included VSD closure (n=10), ASD closure (n=2), PAPVD repair (1), branch pulmonary arterioplasty (n=4), tricuspid valve plasty (n=2), aortic valve plasty (n=1), and pacemaker insertion (n=1). Aortic cross-clamp time ranged from 29 to 94 min (mean 49±15 min), and mean right ventricular/left ventricular systolic pressure ratio was 0.47±0.11 at the end of the procedure. Fig. 3 Open in new tabDownload slide Drawing illustrating the insertion of the homograft valved conduit between the right ventricular outflow tract and the main pulmonary artery. A xeno-pericardial patch is used as a hood to cover the enlarged ventriculotomy. Fig. 3 Open in new tabDownload slide Drawing illustrating the insertion of the homograft valved conduit between the right ventricular outflow tract and the main pulmonary artery. A xeno-pericardial patch is used as a hood to cover the enlarged ventriculotomy. Statistical methods Continuous data are presented as the mean±standard deviation. Comparisons were evaluated by Student's t-test or chi-square test. Significance was taken as P<0.05. Actuarial estimates were calculated with the Kaplan–Meier method. Results Early mortality was 2% (n=1). The one operative death was due to air embolism and occurred in a 16-year-old boy who underwent PVI and PAPVD repair 13.5 years after transannular patch repair of tetralogy of Fallot. The postoperative course in the other patients was generally uneventful. No complications related to PVI were observed in the early postoperative period. There was one late death, due to ventricular arrhythmia 4 years after PVI. This patient, who preoperatively was in congestive heart failure resistant to medical treatment with massive PR, severe tricuspid regurgitation and ventricular arrhythmia, had PVI 23 years after pulmonary valvulotomy and infundibular patch repair of RVOTO. All the other survivors have had hemodynamic improvement by elimination of PR. Echocardiography and roentgenography demonstrated significant reduction in RV dilatation. Compared with preoperative echocardiograms, there was in all patients a 32% reduction in mean RVEDD that decreased from 38±9 to 26±8 mm (P<0.01) (Fig. 4 ). Cardiothoracic ratio decreased from 0.62±0.07 to 0.54±0.04 (P<0.01) (Fig. 5 ). The 9-year actuarial survival rate was 93.5±5%. Progressive right ventricular failure has been halted in all survivors except one who did not achieve relief of symptoms after homograft insertion despite some hemodynamic improvement. This patient had massive PR, severe tricuspid regurgitation and atrial fibrillation at the time of PVI, which was performed 18.5 years after transannular patch repair of RVOTO. After PVI, he continued to be in NYHA class III despite full medical treatment. Heart transplant was performed 6 years after PVI, and the patient has done well subsequently. Five other patients had only mild symptomatic improvement after PVI and continue to receive medical treatment for RV failure (n=3) and/or for ventricular arrhythmias (n=5). All the other patients have had complete relief of symptoms with improved exercise tolerance and RV function. At a mean follow-up of 42±28 months, 41 patients (87% of the survivors) were in NYHA class I and six in class II (Fig. 6 ). On average, the seven patients who did not have major benefits from PVI (including the six patients who currently are in class II and the patient who died late) had been previously exposed to PR for a considerably longer time than the others (mean interval between RVOTO repair and PVI, 18±7 vs. 12±6 years, P<0.01) (Table 2 ). Moreover, the patients who underwent PVI more than 15 years after RVOTO repair (n=14) had only mild (22%) reduction in RV dilatation after PVI (mean RVEDD: from 41±6 to 32±9 mm, P=n.s). Within this group, among the eight patients who had severe RV failure and/or ventricular arrhythmias, five (62.5%) had minimal or no improvement after PVI and only three recovered from their symptoms. Even after PVI, the right ventricle continued to be significantly more dilated in the patients who preoperatively had ventricular arrhythmias (n=10) than in the others (n=38) (mean RVEDD, 34±10 vs. 25±6 mm; P<0.01). In fact, although patients with ventricular arrhythmias had a significant reduction (24%) in RV dilatation (mean RVEDD, from 45.5±7 to 34.5±10 mm; P<0.01) after PVI, this reduction was less important than in the others (31%) (mean RVEDD, from 36±8 to 25±6 mm; P<0.01). Good late homograft function was the rule, with all survivors being free of reoperation for valve failure. Six patients have mild PR and two have mild pulmonary stenosis, with no instances of calcification or degeneration of the homograft valve. Fig. 4 Open in new tabDownload slide Graphic showing the significant reduction of the right ventricular end-diastolic diameter (RVEDD; measured by echocardiography) after pulmonary valve insertion for severe pulmonary regurgitation (mean: thicker line). PRE-OP=Preoperative values; POST-OP=Postoperative values. Fig. 4 Open in new tabDownload slide Graphic showing the significant reduction of the right ventricular end-diastolic diameter (RVEDD; measured by echocardiography) after pulmonary valve insertion for severe pulmonary regurgitation (mean: thicker line). PRE-OP=Preoperative values; POST-OP=Postoperative values. Fig. 5 Open in new tabDownload slide Graphic showing the significant reduction of cardiothoracic ratio (CTR; measured on chest X-ray) after pulmonary valve insertion for severe pulmonary regurgitation (mean: thicker line). PRE-OP=Preoperative values; POST-OP=Postoperative values. Fig. 5 Open in new tabDownload slide Graphic showing the significant reduction of cardiothoracic ratio (CTR; measured on chest X-ray) after pulmonary valve insertion for severe pulmonary regurgitation (mean: thicker line). PRE-OP=Preoperative values; POST-OP=Postoperative values. Fig. 6 Open in new tabDownload slide Functional New York Heart Association (NYHA) class of patients before (PRE-OP) and after (POST-OP) pulmonary valve insertion. Fig. 6 Open in new tabDownload slide Functional New York Heart Association (NYHA) class of patients before (PRE-OP) and after (POST-OP) pulmonary valve insertion. Table 2 Open in new tabDownload slide Interval between RVOTO repair and PVI Table 2 Open in new tabDownload slide Interval between RVOTO repair and PVI Discussion The incidence of cardiomegaly from postoperative PR has been reported to be around 5% [12]. In several clinical studies PR, as isolated congenital lesion [5] or developing after surgical repair of RVOTO [1],[2],[3], has been reported to be well tolerated. However, in many of these studies such a conclusion was based primarily on the presence or absence of clinical symptoms of RV failure during a relatively short period of follow-up [11]. The benign nature of PR has not been sustained by objective data obtained during rest or exercise. Since symptoms from RV failure appear only when advanced and irreversible myocardial damage has occurred, early and more subtle adverse effects of PR may be easily missed if the evaluation depends on the clinical assessment alone [9],[10]. Experimental studies also have shown that, despite the lack of substantial RV failure [4], animals with experimentally induced PR had an increase in RVEDD and a decrease in cardiac output and ejection fraction [26]. Many authors have reported that severe long-term PR and related RV overload may result, despite the lack of symptoms, in progressive RV dilatation and dysfunction [7],[8],[9],[10],[11],[12],[13], and poor exercise tolerance [14],[15],[16]. The added effects of the abnormal right ventricle of patients with tetralogy of Fallot who underwent RVOTO repair (hypertrophy, conduction disturbances, and resection of muscle during repair) may contribute to RV dysfunction [9]. Of major concern is also the relation between long-term PR and the increased risk for ventricular arrhythmias and sudden death [17],[18],[19]. The data from this report support these findings. Despite the absence of evident symptoms, many of our patients had compromised exercise performance and abnormal RV hemodynamic and functional parameters, supporting the assumption that evaluation of symptoms alone does not reflect the functional RV derangement after valveless repair of RVOTO. Moreover, in our series the severity of PR correlated significantly, with the severity of RV dilatation and with the incidence of ventricular arrhythmias. Interestingly, RV dilatation was significantly more severe in patients with ventricular arrhythmias than in the others. In a recent study, Zahka et al. [17] also found a correlation in the long-term between the severity of PR and the diastolic RV area. Moreover, they identified PR as the best marker for ventricular arrhythmias. The deleterious effects of long-standing PR on RV function [7],[8],[9],[10],[11],[12],[13] influenced the surgical approach to repair of tetralogy of Fallot by avoiding transannular patches whenever possible and preserving the pulmonary valve and its annulus without leaving excessive pulmonary outflow obstruction [14],[15],[17]. It has been demonstrated that reduced RV compliance in these patients may protect against the detrimental effects of PR late after RVOTO repair [13]. So, as in most centres, our current policy for RVOTO repair in cases in which the use of a transannular patch is unavoidable is to insert a stiff and relatively small patch through a relatively short infundibulotomy. Appropriate and timely management of postoperative PR is essential for excellent long-term functional and hemodynamic results after RVOTO repair. After PVI, subjective clinical improvement has been reported in several studies [7],[8],[9],[10],[19],[20],[21],[22],[23],[24],[25]. Objective improvement in RV function following PVI has been also demonstrated. Some investigations have assessed the reduction in RV size after PVI because of PR [9],[10],[15]. Bove et al. [9] demonstrated, in a group of 11 patients, this change in RV size by significant reductions in roentgenographic assessments of cardiothoracic ratio and in echocardiographic ratio of right to left ventricular end diastolic dimension. Ilbawi et al. [10] showed a significant reduction of cardiothoracic index in 42 patients and a decrease in angiographic determinations of RV end systolic volume in 18. Warner et al. [15] reported a 30% reduction in echocardiographic RVEDD in 16 patients after PVI for PR. All these studies documented improvement in exercise tolerance after PVI. In our experience, restoration of pulmonary valve competence also resulted in a substantial reduction of RV cavitary size, as shown by the significant decrease in RVEDD (32%) and cardiothoracic ratio (13%). The favourable effect of this was evidenced in most patients by a major improvement in exercise performance and clinical symptoms. It has been hypothesized that improving RV function by PVI may decrease the chance of fatal arrhythmias [19]. In our experience, no patient developed new ventricular arrhythmias after PVI. On the other hand, patients who preoperatively had ventricular arrhythmias continued to have larger RV dimension than the others even after PVI, and only four out of ten recovered completely from their symptoms. The other six patients continued to be treated with amiodarone. This has been effective only in three patients. Among the remaining three, one died because of ventricular arrhythmia 4 years after PVI and two had automatic internal cardiac defibrillator (AICD) implanted. This was indicated because ventricular tachicardia was faster than preoperatively, probably because of the shortening of the conduction circuit after the reduction of RV dimension. When PR is associated with additional residual lesions that increase the RV preload, such as VSD or tricuspid regurgitation, or afterload, such as RVOT stenosis or peripheral pulmonary artery stenosis, progressive RV dilatation and dysfunction frequently occur [6],[7] and are poorly tolerated [1],[10],[16]. In patients with PR and additional residual lesions early PVI is essential to preserve normal RV function [10]. In the case of distal obstruction of the pulmonary artery or its branches PR is not tolerated, even if moderate [2]. This combination is a particularly ominous one due to the vicious circle that is established between PR and RV hypertension [8]. In recent years, the more frequent adoption of early repair of tetralogy of Fallot in infants allowed appropriate development of the pulmonary vascular tree by increasing the forward pulsatile pulmonary blood flow and eliminated pulmonary artery distortion from palliative shunts. This would decrease the incidence of residual pulmonary stenosis and minimize the deleterious effects of PR [10]. Through the mechanism of pulmonary hypertension and left-to-right shunting, a large VSD also adversely affects RV function. In case of VSD and PR, prompt reoperation for VSD closure and PVI is indicated. In fact, closure of VSD only can result in persistent RV failure and eventual death [6]. Tricuspid regurgitation may accelerate deterioration in functional status. A vicious circle between PR, RV dilatation and tricuspid regurgitation results with deterioration of RV function and rapid development of symptoms [7],[8]. The importance of a coexisting tricuspid regurgitation in creating excessive RV volume overload and as main indication for PVI has been emphasized [6],[8]. In contrast to these findings, in the majority of our patients PR produced severe RV volume overload even without concomitant surgical lesions. As regards tricuspid regurgitation, we think, as others [15], that it may be hazardous to delay PVI until after the onset of this additional lesion, since this may already represent an irreversible stage of RV failure. In our series only two patients had moderate to severe tricuspid regurgitation prior to PVI. As already documented by others [7], in our patients the reduction in RV size was accompanied by a regression of tricuspid regurgitation after PVI. In most reported series the indications for PVI have been primarily related to appearance of symptoms of ventricular failure [7],[8]. However, waiting for symptoms to appear may allow irreversible RV dysfunction to occur and result in minimal benefits from PVI [8],[10]. Ilbawi et al. [10] have reported complete recovery of RV function and work performance only in patients who had PVI within the first 2 years after tetralogy repair, while in all the other patients who had PVI at a later time (2–13 years after tetralogy repair), RV function remained abnormal and exercise tolerance did not improve significantly. They explained these findings with already existing irreversible myocardial damage before PVI. Therefore, they suggested early recognition of patients at risk of developing RV failure to proceed with PVI in time to have greater benefits and to prevent irreversible deterioration in RV function. Jonsson et al. [16] found that work capacity was inversely related to age at follow-up, RV systolic pressure at rest, and to presence of moderate or severe PR. From our experience it seems evident that the longer the time of exposure to postoperative PR, the smaller are the benefits after PVI. In fact, the seven patients who did not have major benefits from PVI had been previously exposed to PR for considerably longer time than the others, and the patients who underwent PVI more than 15 years after RVOTO repair had only mild reduction (P=n.s.) in RV dilatation after PVI with minimal or no recovery from severe symptoms. In patients with isolated significant PR serial exercise studies [14] and echocardiographic evaluation of RV size are strongly advised to detect early RV dysfunction. Evaluation of RV function with radionuclide ventriculography has also been proposed [9]. In agreement with other authors [5],[9],[10], we think that in these patients PVI should be performed as soon as the evidence of progressive RV dilatation and dysfunction is revealed, despite the absence of major symptoms. Timely PVI in these patients can determine substantial clinical and hemodynamic improvement with complete recovery of normal RV function and prevention from occurrence of ventricular arrhythmias. In symptomatic patients with long-standing PR early PVI is also indicated to arrest the progression of RV dilatation and dysfunction, despite it is not expected to result in a return of normal RV function. The difficult decision of balancing the risk of reoperation for repeated PVI against the risk of allowing cardiomegaly to progress is a decision likely to be faced more frequently in the years ahead, as many patients operated on in infancy for tetralogy of Fallot approach middle age or younger [19]. Since transannular patching has been popular in the past [3], it is probable that an increasing number of patients will present with severe PR and RV dysfunction [1]. In patients asymptomatic or without additional lesions PVI was not advised, due to the high failure rate of tissue valve in children because of early calcification [6],[7],[8]. However, more recent studies reported improved durability of both heterologous and homologous tissue valves when inserted in the pulmonary position [10],[19],[20],[21],[22],[23],[24],[25]. This improvement is probably a consequence of the lower pressures to which the valves are subjected in the right side of the heart [6],[10], to the preference for valves of larger size [15], and to the better biological characteristics of pulmonary homografts [21]. In fact, pulmonary homografts, introduced in 1987 [24], have less elastic tissue and a lower amount of calcium than aortic homografts [27]. From this experience and from a previous study by our group [21], none of the patients with a pulmonary homograft were reoperated for homograft dysfunction. On the contrary, in some instances aortic homograft had to be replaced due to dysfunction and calcification [21]. Furthermore, in our experience PVI has been associated with a very low operative risk (2%). Most authors reported similar results [7],[9],[10],[19],[20],[21],[22],[23],[24],[25]. In our experience, the use of aortic cross-clamping and cardioplegia during PVI was not associated with complications. Although this operation may also be done on beating heart, we feel that a motionless and clear operative field may improve the accuracy of the procedure. Comparative studies on results of xenograft and homograft conduits failed to demonstrate absolute superiority of one over the other [20],[22]. The ease and flexibility of implantation, the possibility of use conduits of larger size for a given patients, and the resistance to infection are certainly major advantages of homograft over xenograft conduits. Availability of a longer follow-up is, at the moment, the limiting factor to assess what is the most durable conduit in the pulmonary position. However, the excellent mid-term results (no case of conduit replacement) obtained after PVI with pulmonary homografts in this series compare favourably with those of a recent study showing optimal results after xenograft PVI [19]. Several investigators have shown excellent mid-term results with homografts placed in the pulmonary circulation [20],[21],[23],[24],[25]. The present report confirms these findings. Although no conduit replacement was required in their series, Warner et al. [15] reported persistent moderate PR in four of their 16 patients (25%) after a mean follow-up of 26 months from homograft PVI and related this recurrence to persistent peripheral pulmonary stenoses. They also reported various degrees of either valvar or conduit obstruction in six patients (37%). Our experience is rather different, with only six patients (13%) having mild PR and two (4%) mild pulmonary stenosis after a mean follow-up of 42 months from PVI. Nevertheless, we agree with these authors that all attempts to repair pulmonary artery stenosis, either by surgical augmentation or balloon dilatation, should be done at the time of PVI in order to prevent adverse effects on the homograft valve. We also agree that insertion of adult-size homograft may be in part responsible for the improved mid-term durability of these valved conduits observed in recent years. The preference for pulmonary homografts instead than aortic also played a major role in such an improvement. In summary, homograft PVI for PR late after RVOTO repair can be performed at low operative risk (2%) with excellent intermediate-term survival (93.5% at 9 years) and durability of the valve. This procedure provides considerable hemodynamic and clinical improvement with significant reduction of RV volume overload. We recommend to undertake this procedure early in symptomatic patients and in asymptomatic patients with progressive RV dilatation and reduced exercise tolerance. Better criteria for PVI timing needs to be defined to prevent irreversible RV failure, ventricular arrhythmias and sudden death. Longer follow-up is needed in order to determine if pulmonary homografts are the best valved conduits for PVI. References [1] Kirklin J.K. , Kirklin J.W. , Blackstone E.H. , Milano A. , Pacifico A.D. . 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TI - Homograft valve insertion for pulmonary regurgitation late after valveless repair of right ventricular outflow tract obstruction
JF - European Journal of Cardio-Thoracic Surgery
DO - 10.1016/S1010-7940(98)00306-6
DA - 1999-02-01
UR - https://www.deepdyve.com/lp/oxford-university-press/homograft-valve-insertion-for-pulmonary-regurgitation-late-after-DnPJO8DPEr
SP - 143
EP - 149
VL - 15
IS - 2
DP - DeepDyve
ER -