Original Contribution

Transcatheter Pulmonary Valve Implantation in Patients With Right Ventricular Outflow Tract Dysfunction: Early and Mid-Term Results

El≈ºbieta Katarzyna Biernacka, MD, PhD1;  Witold Ru≈ºy≈Ç≈Ço, PhD2;  Marcin Demkow, PhD2;  Miros≈Çaw Kowalski, MD, PhD1; Mateusz ≈öpiewak, MD, PhD2,3;  Walerian Piotrowski, PhD4;  Mariusz Ku≈õmierczyk, MD, PhD5;  S≈Çawomir Bana≈õ, MD, PhD6;  Jacek R√≥≈ºanski, MD, PhD5;  Piotr Hoffman, PhD1

El≈ºbieta Katarzyna Biernacka, MD, PhD1;  Witold Ru≈ºy≈Ç≈Ço, PhD2;  Marcin Demkow, PhD2;  Miros≈Çaw Kowalski, MD, PhD1; Mateusz ≈öpiewak, MD, PhD2,3;  Walerian Piotrowski, PhD4;  Mariusz Ku≈õmierczyk, MD, PhD5;  S≈Çawomir Bana≈õ, MD, PhD6;  Jacek R√≥≈ºanski, MD, PhD5;  Piotr Hoffman, PhD1

Abstract: Objective. The aim of this study was to determine early and long-term results after transcatheter pulmonary valve implantation (TPVI) performed with the use of Medtronic Melody and Edwards Sapien valves in patients with full conduit or patched right ventricular outflow tract (RVOT) dysfunction. Methods and Results. The study comprised 40 consecutive patients (full conduit, n = 25; RVOT patch, n = 15) who underwent TPVI between December 2008 and April 2012. TPVI was successfully performed in 37 patients (92.5%). The gradient across RVOT decreased from 82.96 ± 37.90 mm Hg to 34.33 ± 22.2 mm Hg on the day following TPVI (P<.001) and remained low at follow-up of 20.4 ± 11.4 months. The competency of the pulmonary valve was restored and maintained during the follow-up. New York Heart Association class,  right ventricle end-diastolic volume, and right ventricular ejection fraction all improved as soon as 1 month after the procedure. Infective endocarditis was observed in 4 patients (1 died). Four patients underwent surgeries due to endocarditis, homograft rupture, stent migration, and early valve compression. Conclusion. TPVI may be performed safely and effectively in patients with right ventricle-pulmonary artery conduit and in selected patients with patched RVOT.

J INVASIVE CARDIOL 2015;27(6):E82-E89    

Key words: TPVI, pulmonary valve, patched right ventricular outflow tract (RVOT) dysfunction

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Transcatheter pulmonary valve implantation (TPVI) is a relatively new method for treating patients with right ventricular outflow tract (RVOT) dysfunction after surgical repair of congenital heart disease.1 The procedure has been shown to be feasible and safe in patients with full pulmonary conduit dysfunction.2-6 Indications for TPVI have been recently expanded for selected cases of patched RVOT.7-9 Low complication rate and a reduced number of open-chest reinterventions over a patient’s lifetime are among the main advantages of this procedure. The long-term follow-up results and valve durability are both unknown.     

The aim of this study was to examine early and long-term results after TPVI performed with use of the Medtronic Melody (MM) and Edwards Sapien (ES) valves in patients with full conduit and patients with patched RVOT dysfunction, and to find factors predictive of favorable prognosis that allow better patient selection for this procedure.

Methods 

Study population. The study population consisted of 40 consecutive patients (age range, 13 to 58 years; mean age, 25.4 ± 8.7 years; 22 males) who underwent TPVI at one center between December 2008 and April 2012. Patient characteristics are summarized in Table 1. The full right ventricle (RV) to pulmonary artery (PA) conduit was implanted in 25 patients (62.5%); 15 patients (37.5%) had the RVOT extended with the patch. The indications for the procedure arose from the surgical indications for the RVOT revision and the recommendations from the manufacturers (Table 2).10 The exclusion criteria were occlusion of central veins and comorbidities including an active infection and hypothyroidism. We selected patients on the basis of non-invasive screening, which included clinical assessment, transthoracic echocardiography, cardiovascular magnetic resonance (CMR) with contrast-enhanced angiography, or computed tomography. To determine the dimensions of the landing zone for the valve, some patients with borderline anatomy (especially those with patched RVOT) underwent cardiac catheterization with balloon sizing. The valve choice (18, 20, or 22 mm MM; 23 or 26 mm ES) depended on the RVOT size. The valves were slightly oversized in relation to minimal RVOT size in the landing zone; MM was selected for RVOT ≤21 mm, ES for RVOT ≥22 mm. All patients were pretreated with aspirin on the day before the procedure. Antiplatelet treatment was planned for 3 months. 

Procedure. All procedures were performed under general anesthesia with endotracheal intubation. The femoral or jugular vein (3 cases) was used for access. Cardiac catheterization with assessment of right heart, pulmonary, and aortic pressures preceded each procedure. Angiograms were performed in at least two orthogonal projections. Selected patients, based on their CMR findings, underwent coronary angiography with balloon inflation at the planned implantation site (2 patients were excluded due to possible coronary obstruction). Before valve implantation, all patients underwent routine prestenting of the target site with the IntraStent Max LD bare-metal stent (ev3 Endovascular). In 5 cases, prestenting and valve implantation were carried out separately. In these patients, there was no waist after prestenting the borderline-size outflow tract, and therefore it was decided to delay the valve implantation for 2 months in order to allow proper stent fixation as a result of tissue ingrowth. The Melody valve, which was mounted on a 18, 20, or 22 mm Ensemble delivery system (Medtronic, Inc), was introduced and deployed into the preimplanted stent.

The Retroflex3 delivery system (Edwards Lifesciences) was used for Edwards Sapien valve delivery. According to the chosen valve size (23 or 26 mm), a dedicated manual crimping device was used to install the valve onto the 30-mm long balloon of the Retroflex3. The entire system with the mounted valve was passed through the 24 Fr hydrophilic sheath over the guidewire, and advanced into the prestented RVOT (Figure 1). Hemodynamic and angiographic evaluations were repeated following valve deployment. A single Z-stitch was used for hemostasis at the venous access site, while manual compression was applied for arterial access site. Technical aspects of the procedures were discussed in previous publications.11,12

Study protocol. Preprocedural screening and postprocedural follow-up testing included clinical examination, 12-lead electrocardiogram, posteroanterior and lateral chest radiographs, transthoracic echocardiography (TTE), annual cardiopulmonary exercise test (CPET), and CMR (before procedure, 1 month after, and annually) . 

Patients were assigned New York Heart Association (NYHA) functional class I through IV. In most patients (unless contraindicated or impossible to perform), exercise capacity was measured by CPET. The TTEs were performed with the Vivid 7 echocardiographic system (GE Medical Systems). The maximal flow velocity across the RVOT was measured with the use of continuous Doppler, and the peak instantaneous RVOT gradient was calculated with the Bernoulli equation. Pulmonary regurgitation (PR) was graded as none (grade 0), trivial (grade 1), mild (grade 2), moderate (grade 3), or severe (grade 4) based on color-flow mapping of the RVOT and the branch pulmonary arteries. Greater than mild PR (as assessed by echocardiography) was defined as significant. 

CMR was performed in 36 patients before TPVI and in 32 patients during follow-up (3 patients were operated upon and 1 patient had a pacemaker implanted immediately after TPVI because of sinus bradycardia not related to the procedure) with a 1.5 T Avanto scanner (Siemens Medical). A stack of steady-state, free-precession, short-axis images was acquired and ventricular volumes were calculated with the use of the dedicated software (MASS, 6.2.1; Medis). RV end-diastolic volume (RVEDV) and left ventricular (LV) end-diastolic volume (LVEDV) were indexed for body surface area and expressed in mL/m2. Finally, RV and LV ejection fractions (RVEF and LVEF, respectively) were calculated. Pulmonary regurgitation fraction (PRF) was calculated as a percentage of backward flow over forward flow. All patients had posteroanterior and lateral chest radiographs performed to detect possible stent fractures. 

The results were analyzed the next day and at 1 and 6 months (all patients), as well as at 1, 2, and 3 years after the procedure (30, 20, and 9 patients, respectively). NYHA functional class, maximal volume of oxygen (VO2) consumption and RV functional improvements were compared according to leading RVOT dysfunction pattern: predominant pulmonary stenosis (PRF <25%, and maximally mild PR by TTE) and predominant PR (PRF ≥25% or significant PR by TTE). Baseline values of RVEDV, RVEF, PRF, and pulmonary gradient were analyzed as independent outcome predictors.

The valve implantation protocol was approved by local Ethics Committee. Informed consent for the procedure was obtained from all patients or their legal representatives.

Statistical analysis. All calculations were performed with SAS version 9.2. Collected data are reported as the mean ± standard deviation (SD). Time differences between the measurements were tested by Student’s t-test or, when dealing with non-normal distribution, the rank sign test. The differences between the groups for proportions were tested with the χ2 test. Univariate logistic regression analyses were also performed to examine the associations of  the increased values of RVEDV and NYHA at follow-up, and decreased values of RVEF and VO2 at follow-up. The receiver operating curve (ROC) was used to describe the predictive value of baseline parameters on positive vs negative transformation of  RVEDV, RVEF, and VO2 to categorical variables (0 vs 1). The cut-off values for the preprocedural measurements were found by applying the Youden index.

Two-sided P-value of <.05 was considered an indicator of statistical significance.

Results

Procedural results. We attempted MM valve implantation in 26 patients and ES valve in 14 patients. The mean duration of the procedure was 141.0 ± 43.4 minutes (range, 60-235 minutes) and the mean fluoroscopy time was 28.3 minutes (range, 12.3-60.1 minutes). 

TPVI was successfully performed in 37 patients (92.5%). The hospital stay was 77.2 ± 28.4 hours (range, 48 to 168 hours). A decrease of the peak Doppler gradient across the RVOT was observed from 61.65 ± 44.44 mm Hg at baseline to 32.41 ± 19.72 mm Hg at day 1 post TPVI (Figure 2A). In patients with significant PS (n = 27), there was a drop of the gradient across the RVOT from 82.96 ± 37.90 mm Hg at baseline to 34.33 ± 22.2 mm Hg at day 1 post TPVI (P<.001) (Figure 2B). After valve implantation, pulmonary valve competence was restored in almost all patients. Only trivial PR (PRF <10%) and mild PR (PRF 10%-15%) was observed in 5 and 2 patients, respectively (Figure 3). 

Procedural complications. Two major procedural complications occurred, both during the prestenting procedure:  rupture of the calcified aortic homograft11 and stent dislodgment. We also observed an early stent compression by the calcified aortic monocusp valve with the RV-PA gradient increase from 23 mm Hg to 120 mm Hg the day after successful MM implantation.13 All 3 patients underwent surgery without complications. None of the surgical revisions led to death.

Transient fever was observed in 21 patients during the first 2 days after TPVI: 19 patients (73%) after MM implantation and 2 patients (14%) after ES implantation. No signs or symptoms of infection were present. Fever resolved with no therapy. No significant vascular access-site complications were observed. 

Follow-up. The observation group comprised 37 patients who successfully went through the TPVI and the postprocedural period. Total follow-up time ranged from 6-42 months (mean, 20.4 ± 11.4 months; 33 patients completed 12 months, 22 patients completed 24 months, and 8 patients completed 36-42 months). During this period, 33/37 patients (89.2%) who were discharged from the hospital after the successful TPVI were free from reintervention or death. 

In 26 cases, NYHA functional class improved during the first month after the procedure (P<.001). Even patients who were classified as NYHA class I before TPVI felt significant improvement. NYHA class worsening was observed only in patients with infective endocarditis. 

We noticed insignificant improvement of the maximal VO2 consumption, from 20.1 ± 4.9 mL/kg/min at baseline to  21.9 ± 5.4 mL/kg/min (P=.09) as assessed by the CPET performed at 6-month or 12-month follow-up (30 patients). Significant improvement was observed (from 20.1 ± 4. 9 mL/kg/min at baseline to 27.35 ± 7.14 mL/kg/min in 20 patients at 2-year follow-up (P<.001) (Table 3). 

During the entire study follow-up period, no late stent fractures were observed on chest radiographs.  

At all follow-up times, the Doppler-measured mean peak systolic RVOT gradient remained low (Figures 1A and 1B). In 1 patient with a body mass index of 37 kg/m2 and severe pulmonary stenosis, the reduction of the RVOT gradient after the implantation of the MM initially expanded to 18 mm, and 2 months later to 20 mm, which was unsatisfactory. The patient was referred for surgery.

In all studied patients, the competence of the valves was well maintained during the entire follow-up; PR was trivial or none and it did not deteriorate in 2 patients with mild PR (Figure 3). 

Mean RVEDV decreased from 148.54 ± 45.93 mL/m2 at baseline to 127.87 ± 39.64 mL/m2 at 1 month post TPVI (P<.001). No further significant improvements were seen at the 12-month and 24-month follow-up exams (Figure 4A). The significant improvement of RVEF from 44.71 ± 10.11% at baseline to 49.31 ± 10.83% (P=.01) was observed as early as 1 month post procedure and remained stable for 2 years (Figure 4B). 

During the first month post procedure, significantly increased LVEDV from 92.63 ± 21.90 mL/m2 to 101.74 ± 24.99 mL/m2 (P<.001) was observed. We also noticed increased LVEF, from 55.56 ± 6.74% at baseline to 59.58 ± 5.41% at 1-month follow-up exam (P=.03). No further volume increase or improvement in LV function were seen at subsequent follow-up points (LVEDV, 102.97 ± 25.31 mL/m2 after 1 year and 113.58 ± 31.33 mL/m2 after 2 years [P>.05]; LVEF, 58.1 ± 6.71% after 1 year and 55 ± 4.57% after 2 years [P>.05]).

No correlation between sex, age, time since last surgery, NYHA functional class, type of RVOT reconstruction, and the clinical and hemodynamic results was found. Significant RVEF improvement was observed in patients with predominant PS (P<.001); RVEF was not significantly improved in patients with predominant PR (Table 4). The predictors of an increase in RVEF were: preprocedural RVEDV <177.22 mL (P=.03; odds ratio [OR], 0.983; 95% confidence interval,  0.967-0.999); pulmonary gradient >63.94 mm Hg (P=.02; OR, 1.034; 95% CI, 1.006-1.063); and PRF <10.99% (P=.02; OR, 0.943; 95% CI, 0.895-0.999). 

One of the patients gave birth to a healthy child 3 years after TPVI.

Late complications. Infective endocarditis was observed in 4 patients implanted with the MM valve. One patient died because of septic shock. Severe dysfunction of the valve was observed in 2 patients (Table 5). 

Discussion

Nowadays, transcatheter treatment of valvular heart disease is the most dynamically developing area of interventional cardiology. Experience with transcatheter aortic valve replacement is becoming more extensive due to the growing size of the elderly population with degenerative aortic stenosis. The evidence behind TPVI use for RVOT dysfunction is limited. However, TPVI does seem to provide good short-term results. There is little published on the long-term hemodynamic results, complications and valve durability.6,15,16 

This study showed that TPVI may be safely performed in patients with RV-PA conduit dysfunction and in selected cases of patched  RVOT. In the past, an RVOT patch was considered to be a contraindication to this procedure.17 In 2009, Momenah et al proposed TPVI use for patients with patched RVOT.9 The procedure was accomplished after intravascular deployment of a metal stent into the RVOT to create an artificial conduit. This method, which used the Melody valve, could be applied only to patients with relatively narrow RVOTs since the maximum available valve was 22 mm. Introduction of the Edwards Sapien valves (23 and 26 mm) for the pulmonary valve opening and the use of routine prestenting allowed percutaneous valve implantation in substantially more patients, including those with wider RVOTs and those needing patch correction. Our study group consisted of patients with several conduit types and patients with patched RVOT. To our knowledge, this is the largest studied group of patients undergoing TPVI into native RVOT.12 

Immediate results. TPVI was performed successfully in 92.5% of patients. With the exception of 1 case in which the valve was compressed during the first day after the implantation, excellent or good results were observed immediately after the procedure. The length of stay was relatively short. Patients were fit to work or go back to school immediately after discharge. The excellent early results of the RV-PA gradient reduction (about 60%) and the pulmonary valve competence restoration, both in the patients with the conduits and the native RVOT, were similar to those reported by other authors studying patients with conduits.2-5 It is noteworthy that the baseline mean pulmonary gradient was higher in this study (82.00 ± 39.03 mm Hg) than described in the other studies (37-58 mm Hg).4,5 The mildly increased pulmonary gradient at discharge was observed in only the case of the obese and tall patient, after Melody valve implantation. This may suggest that this kind of valve may be too small for some patients. 

It is particularly intriguing that in the majority of patients, the RV-PA gradient reduction was largest at 6-month follow-up exam rather than immediately after the procedure. Delayed hemodynamic improvement 3 months after TPVI was reported by Ródes-Cabau et al in 2008. This was explained by perivalvular edema and hematoma, and the development of inflammation before its delayed withdrawal.18,19 The effect of gradient reduction and pulmonary valve competence restoration remained stable at 2 and 3 years of follow-up in 20 patients and 9 patients, respectively. The NYHA class was significantly reduced after the TPVI procedure and remained unchanged during the study follow-up. These subjective results were not confirmed by CPET. We observed only a trend in peak oxygen uptake increase during the first year. Significant improvement of peak oxygen uptake was seen starting at 2 years after TPVI. In contrast to the results reported by Lurz et al, we didn’t observe significant differences in exercise tolerance in patients with a predominance of PS or PR.20 

Although CMR was only repeated in 30 patients, this study showed significant amelioration in RVEDV and RVEF. This was accompanied by the partial correction of the LVEDV and LVEF as early as 1 month after TPVI. These results were well maintained during 1 or 2 years of follow-up. This observation is similar to one by Lurz et al.20 We agree that the improvements in RVEDV and RVEF result from the repair of the PS or PR, and not from structural myocardial remodeling. The lack of continuous improvement beyond the first month is intriguing. This could be related to late performance of the intervention or suboptimal intervention with insufficient hemodynamic improvement. 

The predictors of functional and hemodynamic improvements after TPVI were in accordance with previous studies showing more improvement of submaximal exercise capacity and RV function in PS patients when compared with PR patients.20-22 We have found that TPVI leads to normalization or reduction of RV volume when the RVEDV is <177 mL/m2. In other studies,23-25 the cut-off value of RVEDV being predictive of hemodynamic improvement was reported to be in the range of 150-170 mL/m2. Furthermore, the patients with PR had greater NYHA class improvement. This allows us to conclude that patients with predominant regurgitation and higher RVEDV should not be disqualified from TPVI, as they may benefit from this procedure.   

Complications. The rate of serious complications was low. There were no periprocedural deaths. It is noteworthy that there were no complications related to coronary artery compression, which is one of the most dangerous events during TPVI.4 We examined all patients for possible coronary artery compression, as described above.

We did not observe any cases of late valve stent fracture, which was commonly reported in previous studies.26,27 As suggested earlier, the routine prestenting may be protective against this complication.11,28 However, the prestenting did not prevent the complication of valve compression in the patient with PS with severe non-centric calcification of the monocusp valve after the “réparation à l’étage ventriculaire” (REV) operation and surgical strategy was chosen, as the valve-in-valve procedure carried the risk of damage to the second valve.

In most of the study patients, prestenting and valve implantation were performed in a single-step procedure. We observed stent dislodgment during valve implantation in a patient with borderline-size outflow tract when valve implantation was performed in a single procedure with stent implantation. This convinced us that in patients with relatively wide RVOT without waist after prestenting, the valve implantation should be deferred by at least 2 months to allow proper fixation of the stent. Tissues growing into the stent provide a reliable landing zone for the new valve, minimizing the chance of stent migration during valve implantation.7 This two-step procedure, performed in 3 cases with the borderline-size outflow tract, was successful.

At a mean follow-up of 20.4 ± 11.4 months, 89.2% of patients who underwent successful TPVI were free from reoperation or death. These results are similar to those reported by other authors. The number of infectious complications (6.4% per patient/year) is concerning. It is a little higher than reported by the Hannover group in their 5-year follow-up study.15 Before TPVI, patients were examined for any possible dental, upper respiratory, urinary, or gynecological infections. We observed fever during the first 2 days after TPVI in patients who received the MM valve. The fever passed spontaneously, and was probably an immunological reaction. Endocarditis was observed later after TPVI. There was no evidence of relation between fever and endocarditis.  

Study limitations. We used the ES valves half as often as the MM valves. The follow-up period of the ES valves was much shorter.

Conclusion

This study showed that TPVI utilizing a routine prestenting strategy may be performed safely and effectively in a large percentage of patients with RV-PA conduit as well as in selected patients with patched RVOT. Patients with native pulmonary outflow tract may require the prestenting to be performed at least 2 months before the valve implantation. Early results are encouraging and well maintained during the follow-up period of 6-42 months (mean, 20.4 months). Predictors of RVEF improvement were RVEDV <177 mL/m2 and isolated PS. Infective endocarditis was the main cause of morbidity and reintervention.

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__________________________________________

From the 1Department of Congenital Heart Diseases; 2Department of Coronary Artery Disease and Structural Heart Diseases; 3Cardiac Magnetic Resonance Unit; 4Department of Epidemiology, Cardiovascular Disease Prevention and Health Promotion; 5Department of Cardiac Surgery and Transplantation; and 6Department of Anaesthesiology, Institute of Cardiology, Warsaw, Poland.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Demkow is a proctor for Medtronic. The remaining authors report no conflicts of interest regarding the contents herein.

Manuscript submitted October 28, 2013, provisional acceptance given January 10, 2014, final version accepted July 23, 2014.

Address for correspondence: Elżbieta Katarzyna Biernacka, MD, PhD, Professor, Department of Congenital Heart Diseases, Institute of Cardiology, Alpejska 42, 04-628 Warsaw, Poland. Email: k.biernacka@ikard.pl

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