Original Contribution

Clinical Manifestations of Heart Failure Abate With Transcatheter Aortic Paravalvular Leak Closure Using Amplatzer Vascular Plug II and III Devices

Grzegorz Smolka, MD1, Piotr Pysz, MD2, Wojciech Wojakowski, MD1, Andrzej Ocha≈Ça, MD1, Ewa Peszek-Przyby≈Ça, MD1, Tomasz Roleder, MD2, Marek Jasinski, MD3, Zbigniew Gasior, MD2

Grzegorz Smolka, MD1, Piotr Pysz, MD2, Wojciech Wojakowski, MD1, Andrzej Ocha≈Ça, MD1, Ewa Peszek-Przyby≈Ça, MD1, Tomasz Roleder, MD2, Marek Jasinski, MD3, Zbigniew Gasior, MD2

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Abstract: Objectives. To evaluate the transcatheter paravalvular leak closure (TPVLC) aptitude to reduce manifestations of heart failure caused by aortic paravalvular leak (PVL). Background. TPVLC is a valuable alternative to reoperation. While technical feasibility of the method is well established, data on long-term clinical outcome are less abundant. Methods. We launched a prospective registry of patients with clinically significant aortic PVL. They were scheduled for TPVLC with Amplatzer vascular plug (AVP) II and III devices serving as occluders. The efficacy and safety were monitored at 6-month follow-up exam. Results. The occluder deployment reached a success rate of nearly 90%. Following the procedure, we recorded significant improvement both in terms of patient functional capacity and echocardiographic determinants of left ventricular performance. Simultaneously, NT-proBNP plasma concentration and hemolysis markers decreased. Only local complications related to puncture site occurred. Conclusions. Heart failure caused by aortic PVL can be safely and efficiently treated with TPVLC using AVP II and III devices as occluders.

J INVASIVE CARDIOL 2013;25(5):226-231

Key words: heart failure, aortic PVL, TPVLC, AVP II, AVP III


Paravalvular leak (PVL) is usually related to disruption of prosthetic valve sewing ring sutures. Sometimes it may also result from fistula formation in close vicinity of prosthesis. Technical challenges during surgical valve replacement, such as bulky calcification of the annulus or annular fibrosis, are the most frequent culprits. Infectious endocarditis (IE) complicated by abscess formation is another typical cofactor. As a result of incomplete apposition of the prosthesis structure against the native annulus, a single or multiple regurgitant jets located externally to the sewing ring appear. In most cases, paravalvular flow is present immediately after valve implantation, but is mild and asymptomatic.1-3

Depending on individual pathomorphology, paravalvular flow may not only compromise hemodynamics but also prompt hemolysis and present clinically as heart failure (HF) and/or anemia. The potential influence on IE occurrence is unknown. 

Hemodynamically significant aortic PVLs result in left ventricle (LV) volume overload and HF symptoms.4 They can either be treated surgically or with transcatheter deployment of occluding devices.5 Reoperation is necessary when a PVL is accompanied by prosthetic valve dysfunction or instability (“rocking valve”), need for coronary bypass surgery or IE. In many patients, however, the operative risk is prohibitive whereas long-term follow-up may often be complicated by recurrent leak and increased mortality. Recently, transcatheter PVL closure (TPVLC) has emerged as a new treatment strategy that can be offered to patients with an isolated PVL or to those with a very high risk of repeat surgery. The well-established feasibility of this approach, along with the safety superior to this approach compared to reoperation,6 might be a rationale for lowering the threshold of referral for interventional treatment. Our aim was to investigate TPVLC aptitude to reduce PVL-triggered HF manifestations. We launched a prospective registry of patients with significant aortic PVL referred for TPVLC with Amplatzer vascular plug (AVP) II and III devices (St Jude Medical). The procedure’s influence on HF symptoms and left ventricle (LV) remodeling was assessed at 6-month follow-up.


Patients. This study was designed as a prospective registry of adults (>18 years old) after surgical aortic valve replacement (AVR) complicated by hemodynamically significant PVL. All patients were disqualified from surgical PVL correction on grounds of prohibitive perioperative risk as assessed by EuroSCORE II and STS grading. Additionally, we also considered individual features including number of previous open chest surgeries, quality of surrounding tissue met during last valve replacement, or risk of patent bypass graft damage. A Heart Team comprised of cardiac surgeon, invasive cardiologist, and imaging specialist jointly made the ultimate choice for TPVLC. The hemodynamic significance was defined by presence of aortic PVL and either HF symptoms (New York Heart Association [NYHA] class III or IV) with no other identifiable cause for them or following echocardiography findings, regardless of symptoms: (1) holodiastolic flow reversal in the proximal part of the descending aorta; (2) lack of LV size reduction after AVR or recurrent and progressive LV dilation in follow-up; and (3) forward transprosthetic flow velocity higher than expected with given prosthesis type and size, provided normal function of prosthetic leaflets. The ratio of regurgitant jet to left ventricular outflow tract (LVOT) width was not taken into account because of usually strongly eccentric PVL backflow direction. The exact dimensions of the PVL channel were only used to optimize the choice of occluding devices type, number, and size and not to grade the regurgitation itself. Other inclusion criteria included the persistence of PVL for at least 6 months following the diagnosis along with anatomy considered suitable for transcatheter treatment. The exclusion criteria comprised of active IE, prosthesis dysfunction (other than PVL) or instability, and acute coronary or aortic syndromes. Pregnant women and patients unable to express informed consent were also excluded. 

Study design. Medical history, physical examination, and echocardiography were assessed initially and then 3, 30, and 180 days after procedure. Blood samples were collected according to the same timeline. Transthoracic echocardiography (TTE) was performed with Vivid 7Pro and Philips iE33 machines. In case of non-diagnostic TTE images due to poor acoustic window or PVL site shadowing by prosthetic valve, transesophageal echocardiography (TEE) was applied with real-time three-dimensional imaging if required (Philips iE33 system). Additionally, whenever TTE and TEE failed to satisfyingly describe PVL channel morphology, electrocardiography (ECG)-gated multi-detector computed tomography (MDCT) was also performed. This modality was found particularly useful for TPVLC feasibility evaluation. Patients with multiple small channels or a PVL directly beside coronary ostium were considered unsuitable for TPVLC. Blood samples were collected from the antecubital vein after 30 minutes rest in the horizontal position. Laboratory tests included N-terminal pro-B type natriuretic peptide (NT-proBNP), complete blood count, reticulocytosis, total and unconjugated bilirubin, and lactate dehydrogenase (LDH). In all patients, inflammatory markers (sedimentation rate [SR] and c-reactive protein [CRP]) were initially sampled. Additionally, in selected individuals, blood cultures were taken to exclude active IE. The intervention was considered successful after achieving complete obliteration of the PVL or reducing the backflow to merely a trivial residual leak. The latter was defined by presence of a trace of paravalvular regurgitation in color Doppler flow mapping accompanied by total resolution of originally recorded indirect indicators of significant PVL (absence of holodiastolic flow reversal in descending aorta, normalization of forward transprosthetic gradient). The primary endpoints were changes of left ventricular end-diastolic volume (LVEDV) and NT-proBNP plasma concentration following TPVLC. The parameters monitored for safety comprised cardiac-related death, myocardial infarction (MI), LV wall perforation, stroke, major bleeding (loss of hemoglobin >2 g/dL), conversion to heart surgery, and hematoma or fistula in the access site necessitating vascular surgery. 

Transcatheter PVL closure. Technical details of transcatheter PVL closure have been described previously.7Generally, the procedure was carried out under local anesthesia with additional conscious analgosedation with fentanyl and diazepam. The guidance was based on fluoroscopy and TEE. All leaks were approached in a retrograde manner via transfemoral (preferably) or transbrachial access. Unfractionated heparin was administered intravenously with regard to body mass to achieve the activated coagulation time (ACT) of 300 to 350 seconds. Standard procedure was initiated with a telescopic set of 6 Fr 100 cm guiding catheter and 5 Fr 125 cm JR diagnostic catheter. The choice of guiding catheter shape was driven by the PVL site. We used an AL for left coronary sinus and an MP or JR for other locations. The crossing was performed with different guidewires: coronary 0.014˝ or 0.018˝ and in some cases 0.036˝ hydrophilic wire, depending on specific PVL features. The diagnostic guidewire was then replaced with a stiff one (0.032˝), the tip of which was carefully preshaped before placing it in the LV apex. The telescopic set was now replaced with a long, 7-9 Fr (depending on number and size of planned occluders) sheath (90-110 cm). AVPs, which are pliable structures that nicely adapt to the generally irregular PVL channel, were used as occluders in all cases (Figure 1).

After initial experience with the round-shaped AVP II, we switched to the oval-shaped AVP III, which we found better suited this procedure, particularly

for crescent and oblong PVLs. Moreover, the smaller middle module of the AVP III results in less elongation during deployment as compared to the AVP II, which reduces distal module overhanging and in our opinion may promote future endothelialization of the device. Occluder size was decided according to TEE and in some cases also MDCT measurements. After quantifying the cross-section dimensions of the PVL channel, the plug was chosen with approximately 30% oversizing of the middle module. In the majority of cases, the use of multiple (usually two) smaller plugs was preferred to a single larger plug.

Such approach was intended not only to achieve more condensed filling of the channel but also to reduce the risk of the plug’s excessive elongation in an irregularly shaped channel. After positioning the plugs in the channel, we carefully analyzed the efficacy of sealing, the stability of the plugs, the function of the prosthesis leaflets, and the relation between the edges of the occluders and coronary ostia. If any of these were found unsatisfying, the plugs were removed and repositioned or replaced with ones of different size to achieve the procedural success as defined previously. After removing the sheath, the access site was compressed in the first 3 patients and closed with Perclose ProGlide device (Abbott) in all others (if use of a sheath larger than 8 Fr was expected, a presuture was initially placed). In case of multiple PVLs, after successful closure of the first one (which was originally considered the largest), the remaining ones were reassessed echocardiographically and, if needed, the next stage of transcatheter treatment was scheduled. The patients were included in our follow-up only after accomplishing all required stages. Intravenous antibiotic prophylaxis was administered periprocedurally in all patients. Oral anticoagulation therapy was resumed within 24 hours of procedure completion, provided a lack of complications either on echocardiography or concerning the access site. Unless otherwise stated, data are presented as mean values with 95% confidence interval (CI). The Student’s t-test was applied with normal distribution and the Wilcoxon test in other cases.


A total of 20 patients with diagnosis of aortic PVL were referred to our hospital for TPVLC throughout 11 consecutive months (November 2010 to October 2011). After initial assessment of PVL morphology, TPLVC was considered unfeasible in 3 individuals who had multiple small leaks resulting in significant regurgitant volume. Under such circumstances, the unlikelihood of achieving total PVL occlusion along with high probability of persisting hemolysis prompted disqualification from the procedure. Demographic and medical data of 17 patients in whom TPVLC was finally attempted are presented in Table 1. Four subjects had history of IE managed either with single AVR (n = 1), redo AVR (n = 2) or conservatively (n = 1) in a case with IE of prosthetic AV and prohibitive risk of reoperation (16 months before TPVLC). The procedural data are presented in Table 2. Two patients were diagnosed with 2 separate significant PVLs; thus, 19 total TPVLC attempts were made. TPVLC failed in 2 individuals: 1 with a very tortuous channel in the left coronary sinus and 1 with a channel too wide for stable anchoring of the occluders. In the 15 remaining patients, a total of 17 PVLs were successfully treated. Two AVP III plugs were simultaneously deployed into a single PVL in 8 cases (47.1% of treated PVLs). The occluders were sized 4-12 mm (median, 8 mm; interquartile range [IQR], 6-8 mm). We initially implanted 7 AVP II plugs (in the first 6 procedures), after which we decided to modify the technique and switched to AVP III, 17 of which were subsequently used. The procedural success was 88.2% per patient and 89.5% per PVL. Figure 2 illustrates the registry flow design.

The mean procedure time reached 65 minutes (median, 57.5 minutes; IQR, 45-120 minutes) with a mean dose of 80 mL (median, 80 mL; IQR, 50-115 mL) of Omnipaque contrast agent. 

The influence of successful TPVLC on NYHA class, LV size, and hemolytic markers is presented in Table 2 and Figure 3. Patients in NYHA class I or II represented only 26.7% (4/15) of the population prior to intervention, then 86.7% after 3 months and 93.3% (13/15) after 6 months (P<.05). No patient deteriorated in terms of functional capacity.

TTE performed during 30-day and 6-month follow-up visits revealed significant decreases in both LV end-diastolic diamter (LVEDD) and LV end-systolic diameter (LVESD), as well as LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV). Moreover, LVEDD, LVESD, and LVEDV reduction already reached the level of statistical significance on the day 3 post TPVLC (Table 2). Despite successful TPVLC, 1 patient with severe ischemic LV dysfunction did not manifest any clinical or echocardiographic improvement. Interestingly, even though his LVEDV remained roughly unaffected, we did record NT-proBNP reduction. This, however, may at least partially be attributed to intensified loop diuretic treatment in follow-up.

Mean LV ejection fraction (LVEF) remained unaltered throughout the study (61.3% initially vs 60.9% at 6 months). 

TPVLC effectiveness was also verified by quantifying NT-proBNP plasma concentrations. A significant reduction of these was noted soon after the procedure and remained stable at 6-month follow-up exam (Table 2 and Figure 4). 

In 7 patients, diuretic dose was reduced following TPVLC. One patient was reverted to the initial dose based on clinical assessment after 30 days. In the other patients, diuretics were continued in unaltered manner after TPVLC.

Generally, statistically significant reduction of hemolysis was noted with marked increase of hemoglobin concentration after 6 months, from mean values of 11.4 g/dL to 13.7 g/dL (Table 2). Nevertheless, in 2 patients, hemolysis seemed to increase following TPVLC. Their initial LDH plasma concentrations of 1100 IU/mL and 1188 IU/mL, although transiently decreased to 828 IU/mL and 334 IU/mL on day 3, then rose again to 1429 IU/mL and 1229 IU/mL, respectively. Both patients had initially elevated unconjugated bilirubin levels (0.64 mg% and 0.60 mg%). After 6 months, it decreased to 0.39 mg% in 1 patient, and remained raised in the other (0.73 mg%). Throughout the study, both patients had moderately reduced hemoglobin concentration without need of transfusion.

No death, MI, LV wall perforation, stroke, major bleeding, or need for heart surgery occurred. 

Three patients (20%) suffered from local puncture-site complications, with need for vascular surgery in 1 patient (6.7%). In 2 cases, these were late (on day 3, after achieving therapeutic INR with oral anticoagulation) pseudoaneurysms of the femoral artery. While 1 was effectively obliterated percutaneously with thrombin injection, the other required surgical revision with intraoperative transfusion of 2 units of red blood cells (hemoglobin loss of 1.8 g/dL). Brachial hematoma was the third complication and occurred in a patient with type III aortic arch. The initial attempt via the transfemoral approach proved unfeasible and the occluder was finally successfully deployed via right brachial artery (such access, in settings of severe angulation of ascending aorta, enabled more straightforward crossing of the PVL). No puncture site complications occurred in patients in whom vascular closure devises were used.

In 1 patient with a large PVL located on the verge of right- and non-coronary sinuses, a transient widening of QRS complexes (from 110 ms to 140 ms with left bundle branch block morphology) was noted promptly after implantation of 2 AVP III devices (size 8 mm). It resolved completely within 48 hours of the procedure after a single intravenous dose of steroid. At 6-month follow-up exam, no other conduction disturbances or new onsets of arrhythmias were observed.

No patients were lost to follow-up.


Even though clinically more benign then mitral PVL,8 aortic PVL, besides significant hemolysis, forms an established indication for reoperation. The occurrence of PVL in patients who have undergone AVR for severe aortic regurgitation can compromise the regression of LV dilation.9 Early mortality in redo AVR reaches 3.5%-6%.10,11 Additionally, the reoperation usually does not eliminate primary reasons for PVL formation such as impaired tissue quality.12 Transcatheter treatment, having been constantly developing during last 20 years,13 poses a noteworthy alternative. Feasibility and safety of the method has been reported in large groups of patients.6,14

NYHA. We registered a significant improvement of functional capacity in patients after TPVLC. This remains in concordance with what had been recorded following surgical correction of severe AR.15

LV remodeling. LV dilation is one of the aortic regurgitation (AR) consequences. Its regression after AVR has been well documented.16 To our best knowledge, we are the first to report an analogous phenomenon following percutaneous elimination of paravalvular AR. As with AVR,17 marked reduction of LV size was recorded shortly after the procedure and was maintained at 6-month follow-up. The lack of improvement in 1 patient was probably attributable to severe ischemic LV dysfunction.

NT-proBNP. Successful TPVLC resulted in significant reduction of NT-proBNP concentration. Cardiomyocytes are known to excrete this hormone if stretched18 and its plasma concentration in heart failure patients has been proven to correlate with the disease stage.19 Nevertheless, the exact role of NT-proBNP assessment in patients with valvular heart disease is yet to be fully determined.20 Its postulated role might be to identify those individuals from the low-symptomatic cohort who might benefit from early AR elimination.21

Complications. Since PVLs themselves are prone to cause hemolysis,22 their incomplete closure, with a high-velocity jet through even a smaller channel left, might actually exacerbate it.23 Two of our patients experienced a moderate aggravation of hemolysis after TPVLC. On periprocedural TEE following device deployment, both patients had a trivial residual leak with no technical chance of another plug implantation in the operator’s opinion. Other treated patients, as previously stated, seem to have also benefitted from TPVLC in terms of hemolysis reduction.

Our study, designed to assess the reduction of LV size after TPVLC, did not enroll a sufficient number of patients to analyze their survival. Still, a beneficial effect in this aspect might be expected, considering previously gathered data on improved survival after AVR due to AR.19

TPVLC was initially performed with devices dedicated for vascular fistulas,24 atrial septal defects, ventricular septal defects,25 or patent ductus arteriosus.26 Considering the devices currently available on the market, the AVP III seems to be best suited for the usually more or less oval-shape of PVLs.27 Except for incidental reports, we have few data on the endothelialization of implanted devices and lack of it even months following deployment seems possible.28 In our opinion, a strategy aimed at avoiding the protrusion of the device’s distal modules beyond the plane of the prosthesis ring might promote endothelialization. Deployment of two or more smaller devices instead of a single larger device lessens the impact of occluder elongation caused by compression of the middle module within the channel. As a result, extensive overhanging is prevented, which may enhance endothelialization of the plugs. 

In summary, TPVLC is capable of improving exercise tolerance and reversing LV remodeling in patients with hemodynamically significant aortic PVLs. In the majority of cases, implantation of multiple devices is required to achieve complete PVL closure. The procedure’s performance may be further enhanced in the future with development of dedicated devices offering more thorough sealing along with a better chance of endothelialization. The influence of the procedure on survival remains yet to be determined. 


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From the 13rd Division of Cardiology, Medical University of Silesia, Katowice, Poland, 2Division of Cardiology, Medical University of Silesia, Katowice, Poland and 32nd Division of Cardiac Surgery, Katowice, Poland.

Funding: The study was supported with the grant of the Ministry of Science and Higher Education of the Republic of Poland (grant #N N402 526839). The authors report no financial relationships or conflicts of interest regarding the content herein.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted November 26, 2012, provisional acceptance given December 4, 2012, final version accepted December 28, 2012.

Address for correspondence: Grzegorz Smolka, MD, 3rd Division of Cardiology, ul.Ziolowa 47, 40-635 Katowice, Poland. Email: gsmolka@me.com