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Eur J Cardiothorac Surg 2006;30:4-9
© 2006 Elsevier Science NL

Is device closure for direct access valved stent implantation safe?

Malgorzata Pawelec-Wojtalik a , * , Jerzy Nozynski b , Michal Wojtalik c , Maciej Piaszczynski c , Rafal Surmacz a , Dorota Bukowska d , Wojciech Mrówczynski c

a Department of Pediatric Radiology, University of Medical Sciences, Poznan, Poland
b Department of Histology and Embriology, Silesian Medical University, Zabrze, Poland and Department of Histopathology, Silesian Centre for Heart Diseases, Zabrze, Poland
c Department of Pediatric Cardiac Surgery, University of Medical Sciences, Poznan, Poland
d Department of Veterinary Medicine, University of Agriculture, Poznan, Poland

Received 17 October 2005; received in revised form 30 March 2006; accepted 31 March 2006.

* Corresponding author. Tel.: +48 61 8491 480; fax: +48 61 8669 130. (Email: mpwojt{at}poczta.onet.pl).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Objective: Despite the progress made in the development of valved stents for trans-apical valve replacement, a reliable closure of the access orifice remains a major issue. The present study was designed to evaluate if device closure of the ventricular wall is safe. Materials and methods: Transventricular access for pulmonary valve replacement was simulated with a 26F sheath and the resulting orifice was closed with an Amplatzer Muscular VSD Occluder (AMuscVSDO) in chronic sheep experiments (body weight 45–48 kg). Mean procedure time, blood loss, and standard hemo-dynamics were recorded. The animals were sacrificed electively and the histopathological changes in and around AMuscVSDO in the right ventricular wall were systematically studied by semi-quantitative analysis of collagenisation, inflammatory response and ‘resorptive’ process. Results: Mean procedure time was 31 ± 10.7 min, blood loss was 22.5 ± 8.7 ml, heart rate was 123 ± 22.6 bits/min before and 128 ± 28.7 bits/min after, mean arterial blood pressure was 88 ± 16.7 mmHg before and 82.6 ± 18.3 mmHg after the procedure. Mean survival was 5.3 weeks. The collagen and scar formation studies revealed three different periods: (1) initial fibrosis (0–3 weeks); (2) so-called ‘capsulation’ (3–9 weeks after the implantation of the Occluder); and (3) final remodelling and differentiation (9 weeks). The fabric inside the Occluder played the role of a collagenisation promoter, active from the 3rd week till it vanishes. Inflammation plays a role as a temporary reaction (0–3 weeks) during the healing process, with no signs of any active, focal or circumscribed, myocardial damage. Conclusions: (1) The closure of the free ventricular wall perforation with AMuscVSDO is safe due to the scar tissue resulting from the healing process around and in the device. (2) The myocardial healing around and inside an implanted AMuscVSDO represents two processes: extensive fibrosis ensues around metallic wires with the progression towards the inside of the myocardium, whereas inside AMuscVSDO the loose connective tissue fills the myocardial lesion. During cicatrisation, the fabric elements of AMuscVSDO act as the ground for collagen formation and fibroblast proliferation. (3) The cicatrisation processes after ventricular AMuscVSDO implantation show remodelling, with rearrangement of collagen fibres architecture and distribution.

Key Words: Valved stents • Closure device • Amplatzer device • Pathology • Hybrid procedures


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Interventional cardiology is developing rapidly. Recently, many authors have informed about stented valve implantations into pulmonary artery, aorta and mitral place with the use of 23F–24F sheath [1,2]. These procedures are performed via the exposure of the femoral vein, artery, or directly the heart wall. Yet, a small size of femoral arteries or thrombosis is a limitation. Our new idea included puncturing the heart directly percutaneously and next, implanting the stented valve into the heart and closing the hole in the free wall with Amplatzer Muscular VSD Occluder (AMuscVSDO). Also, approximately 95,000 Amplatzer Occluders have been used between two blood filled chambers. Nothing is known about their use for sealing a hole in a ventricle against outer world. In recent studies we have proven that it is possible to use the AMuscVSDO to close the perforation made in the free wall of right and left ventricles as a preparation for stented valve implantation [3,4]. However, nothing is known about the healing process and the histology that take place after the implantation of Amplatzer Occluder into the free wall of the heart.

The aim of this study was to determine histologically if the device closure of the free wall perforation of the heart after direct access stented valve implantation is safe.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 5. Conclusions
 References
 
In compliance with the European convention on Animal Care and on permission of the Ethic Committee of University of Medical Sciences in Poznan, the experiment was performed on six sheep weighing 45–48 kg. Under general anaesthesia, they were intubated and mechanically ventilated. In each case, a catheter was placed in the jugular vein to gain access for the delivery of medication and blood sampling. Before the procedure, a 50 J/kg dose of heparin was administrated intravenously. Activated clotting time (ACT) was checked before and after the procedure using the DRG device. The aim was to keep ACT between 180 and 200 s.

Four extremity ECG leads were placed to record heart rate and rhythm disturbances. An arterial caniula was inserted in right jugular artery to provide direct blood pressure monitoring and blood sampling.

The heart was exposed through right IV intercostal space lateral thoracotomy. The right ventricular wall was punctured with a needle and a guide wire, under direct observation, away from the major coronary vessels. 14F and next 26F sheaths were introduced into the right ventricle (RV). The location of the sheath was checked by transthoracic echocardiography through left parasternal view using an ECHOSON apparatus with 3, 5 MHz sector transducer. After the placement of the sheath in the right ventricular cavity, the AMuscVSDO was introduced. We used a typical Amplatzer introduction set 10F for that purpose. First, distal disc was opened inside right ventricle and, after the withdrawal of the external disc, outside the heart, causing the closure of the RV opening. One animal was examined postmortem directly after the procedure, and specimens of the implanted Amplatzer with the adjacent cardiac wall were obtained. Next, the animals were electively sacrificed at 3 (two animals) and 9 weeks (three animals) after Occluder implantation and late myocardial specimens were obtained. Then, the full thickness ventricular tissue was immersed in 95% alcohol. The specimens were sent to Cardio-Vascular Surgery, CHUV Vaudois in Lausanne, Switzerland. They were later routinely processed and embedded in resin (MMA). After polymerisation, the plastic blocs were cut using grinding microtome. The slides contained endocardial, epicardial and myocardial tissue with metallic elements of the Occluder. After this step, the slides were stained routinely with Elastica kit (Merck), according to van Gieson.

Semi-quantitative assessment was done using the ranks from 0 to 4+ for the intensities of the following parameters: myocardial inflammatory infiltrations, myocardial collagenisation (especially scar formation), textile inflammatory infiltrations, textile resorptive infiltrations (resorptive multinucleated cells), textile fibroblast in-growth, and textile collagenisation—collagen production by ingrown fibroblasts.

In the 0 week group, 20 fields under magnification 250x were examined, whereas in the subsequent groups 21 fields were assessed.

All rank results were analysed using nonparametric methods, including descriptive statistics, intergroup comparisons by Mann–Whitney test, and correlation of median ranks with the time of observation with Spearman rank correlation.

The Statistica 5.5 software was used.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 5. Conclusions
 References
 
All procedures were performed successfully. The time of main procedure was 31 ± 10.7 min. Blood loss through and around AMuscVSDO was 22.5 ± 8.7 ml during the first few minutes after opening of AMuscVSDO at the cardiac wound. Heart rate before implantation of AMuscVSDO was 123 ± 22.6 bits/min and just after the procedure 128 ± 28.7 bits/min. Mean arterial pressure before and after the procedure was 88 ± 16.7 and 82.6 ± 18.3 mmHg, respectively.

3.1 Cicatrix and collagen formation
There was no evidence of collagenisation or cicatrisation of myocardial tissue in the 0 week sample. Only few thin collagen fibres were visible in interstitium, perivascular space and subendocardial layer. The metallic elements of Amplatzer Occluder were anchored in cardiac structures, like endocardium and underlying tissues.

The beginning of morphological maturation of the scar was observed at 3rd week; there were fewer collagen fibres, concentrated predominantly at the periphery, surrounding the wires. This arrangement seemed a fibrous capsule rather than a collagenised scar. The metal wires were surrounded by compact and thick bundles of collagen, and from these points thin collagen fibres spread into the myocardium and in lesser degree to the connective tissue inside the cicatrix. The inner part of the cicatrix became more vascularised than previously, practically still without collagen fibres.

From the 9th week on, the differences between the endocardium and epicardium became evident. Epicardial surface represented laminar fibrosis of subepicardial layer and the collagenisation around the wires, whereas the subendocardium presented more compact and dense collagen bundles around the wires, forming a thick fibrous layer (Fig. 1 ). In parallel, the vascularisation was in progress, more intensely on the epicardial surface. Right ventricular subendocardial layer contained mainly large lacunar thin-walled vessels with irregular shapes, whereas in epicardium the arterioles with differentiated vascular walls and rounded lumens were visible.


Figure 1
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  		Fig. 1. Sheep myocardial specimen, 9th week after AMuscVSDO implantation. Dense red collagen bundles form the subendocardial scar. No reactive inflammatory infiltrations. Van Gieson stain, magnification 40-fold.

 
In semi-quantitative analysis of myocardial collagenisation, significant increase was seen between the 3rd and 9th week. Contrary to inflammation, collagen production correlated significantly and positively with the time of Occluder implantation (Table 1 ). Textile collagenisation showed significant increase from the 3rd to the 9th week (Table 2 ).


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  		Table 1. Semi-quantitative assessment of selected myocardial histological changes after the AMuscVSDO implantation
 

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  		Table 2. Semi-quantitative assessment of textile histology after its myocardial implantation with an AMuscVSDO
 
3.1.1 Fabric, its ‘biodegradation’ and resorptive processes
The fabric fragments were visible already in the 0 week samples as interstitial fragments with increased fuchsinophilia, soaked by plasma and tissue fluid, demonstrating slight birefringence of the fibres.

In the 3rd week, the fabric was infiltrated by numerous mononuclear cells. Single fabric fibres with increased birefringence were easily visible in the slides. Besides, numerous thin collagen fibres were visible as red fibres closely related to the birefringent fabric fibres. Thus, collagenisation took place inside the fabric, when the fabric fibres may act as a stimulating factor or promoter.

In the 9th week, the ingrown cells were predominant in the fabric architecture, whereas fabric fibres were scarce and arranged by collagen. This hybrid tissue became vascularised by a few capillary vessels, clearly visible. The resorptive and inflammatory cells were still present, yet in a smaller amount than previously.

The semi-quantitative analysis of resorptive cells in textile sheet showed a significant raising presence tendency till the 9th week of observation. This change showed the strongest correlation with the time elapsed since implantation. Fibroblasts in-growth into textile intestacies showed significant increase from the 3rd to the 9th week. This change like the presence of resorptive cells was strongly correlated with time (Table 2).

3.1.2 Inflammatory infiltrations—inflammatory response
As it has already been pointed out, the inflammatory infiltrations were present from the 3rd week after Occluder implantation and were related with the presence of the fabric and its biodegradation. Initially, in the 3rd week the inflammatory infiltration was dense, composed mostly of lymphocytes, histiocytes/macrophages. The inflammatory infiltrations were visible on the border of the fabric, surrounding single adjacent wires. In the 9th week the resorptive processes with giant cells was more intense.

The semi-quantitative estimation of myocardial inflammatory infiltrations showed rapid increase of median rank in the 3rd week with the subsequent significant decrease at the 9th week (Table 1). Textile inflammatory infiltrations correlated weakly but significantly with the time after implantation (Table 2) (Fig. 2 ).


Figure 2
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  		Fig. 2. Fabric structure, 9th week after AMuscVSDO implantation. The connective tissue grows into the fabric. Few round shaped arterioles thick-walled, and lacunar thin-walled capillaries. Dark red collagen fibres are formed progressively around some birefringent fabric fibres by elongated fibroblasts. Small number of inflammatory cells and dark resorptive giant cells. Van Gieson stain, magnification 250-fold.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
5. Conclusions
 References
 
So far, 95,000 Amplatzer devices have been implanted into the heart to close the ASD and VSD [5]. We show that device closure of the hole in the heart wall after direct access stented valve implantation is safe. All sheep were in good condition after the procedure in farm and they were terminated according to schedule (at 0, 3 and 9 weeks after the implantation of AMuscVSDO).

The use of plastic tissue embedding and refining technique of slides preparation allowed us to study not only the place after the Occluder extraction, like in several works, but also pathological changes related with the presence of all elements of the AMuscVSDO (such as metal elements or fabric) with reference to the time elapsed from its implantation. These changes concerned time sequences of collagen and cicatrix formation, resorptive or inflammatory reaction, and finally scar remodelling.

The tissues around the Occluder did not show any leakage, suggesting complete healing and closure of experimentally produced myocardial lesion. This location may be beneficial, resulting in complete healing, whereas interatrial implantation leads in small percentage to erosion, probably as a result of deficient aortic rim and disturbed elasticity and motility of the septum [6]. In our material, no signs of contact toxicity of alloy with myocardial tissue were visible. The observations of Capek et al. [7] suggested that this kind of metallic alloy initiates local fibrin deposition from the blood, followed by the proliferation of fibrovascular tissue and the formation of fibrovascular capsule. The accumulation of the fibrin derived from plasma took place within hours following the Occluder implantation and was visible mainly in fabric elements, as textile fibres had soaked with amorphous and protein-rich tissue fluid. Later, this phenomenon was clearly visible in our series just 3 weeks after AMuscVSDO implantation, and in the later period the remodelling of the capsule was joined with vascularisation and rearrangement of collagen fibres. Comparable results were described by Hirshorn et al. [8,9], in intracardiac electrode tips studies, where titanium produced fibrous reaction practically without inflammatory resorptive infiltration, similar to platinum.

The collagen distribution visible in the 9th week differed microscopically from any scars, where the role of collagen is to join unchanged tissue by bands and fibres, allowing the restitution of its continuity. These collagen bands and fibres were placed in parallel, or cross, without any precise network [10,11]. The classic work of Lodge-Path [12] indicates that collagen fibres are visible in infarcted myocardium on the 9th day; later, the amount increases and fibre rearrangement starts in about the 4th week. At this time, the collagen fibres are arranged parallel to the adjacent muscle and pericardium. On the other hand, collagen production in myocardial infarction (MI) scar starts as early as on the 4th day after myocardial infarction and an accumulation of fibrillar collagen is seen a few days later [13]. This process increases during the first 10 days after MI, then stabilises, and after several months returns to the normal state. Our observations suggest that collagen arrangement depends also on the presence of mechanical support, i.e. implanted metal wires. Moreover, the support enhances the morphological remodelling of the scar. The role of progenitor cells, both bone marrow-derived and perivascular myofibroblasts should also be emphasised, as a source of cellular basis for cardiac rebuilding and as a collagen producer [14]. Operative cardiac wounds are yet another type of myocardial lesion. The literature concerning this problem is rather scarce. In an article prepared by Tamura et al. [15], healing process of operative cardiac wound was studied pathologically in 14 patients. In this study, myocardial wounds at 18th day after left ventricular venting showed fibrosis in the surrounding cardiac muscle and granulation tissue. A typical collagen scar appeared from 1 month after the operation. The findings are similar to our observations revealing that, in the 3rd week, an early collagen capsule was formed rather than a typical scar.

Another part of the Occluder (important for collagen formation) was the fabric or fabric element. In our observations, fabric fibres play a role as a support for connective tissue cells, mainly fibroblasts coming from the surrounding tissue, and promoting collagen production. Collagen fibres form along or around these fibres. It starts quite early, in the 3rd week, and subsequently increases. Thus, Ti–Al alloy and polyester fabric works simultaneously as a skeleton and an inducer of collagen synthesis, providing soft tissue network or scar in the place of AMuscVSDO implantation. The role of the fabric is not overestimated in our observations. The observations made by Pearl et al. [16] and later by Tweden et al. [17] concerning the use of fabrics showed that the fabric implanted in cardiac tissue serves as the basis or the foundation to connective tissue cells and during approximately 6 weeks the fabric gets seeded with fibroblasts. Similar results were obtained by Maurer and Bernhard [18], using PTFE sutures for the replacement of the chordae tendinae in a 52-year-old man.

The sum of healing processes and lack of necrotic or infected elements resulted in infiltrations of the cellular composition. Those cells represented mainly macrophage and lymphocyte line. It differed significantly from all typical infiltrations observed in myocardial scars [13,15]. The number of tissue macrophages does not reflect the intensity of the tissue damage. Only in acute damage, when the main pathophysiological process is inflammatory cells migration, the number of macrophages may express a degree of tissue injury or, more precisely, the number of macrophages with the expression of osteopontin, glycoprotein implicated in cell adhesion and migration [19]. In experimental myocardial damage by freeze–thawing, the activation of macrophages characterised as osteopontin-positive cells takes place mainly on days 1 and 2, whereas in the following days and weeks till the 4th week, this marker diminishes rapidly independently of the abundance of macrophages. Thus, the presence of both mononuclear and multinucleated macrophages reflects rather resorption and/or rebuilding.

As it has already been mentioned, the studies of AMuscVSDO and surrounding tissues are rather scarce. With hindsight, a few papers should be commented on in spite of our observations. The experimental studies with the closure of ASD in lamb model with double umbrella Occluder pointed out only the endothelisation of the devices [20]. A more precise morphological study of ASD Clamshell Septal Occluder in dogs was published by Kuhn et al. [21]. After 1 month, neointima was seen with connective tissue in-growth, some macrophages and foreign body giant cells. At this time, the formation of connective tissue capsule was seen, just like in our experiment. In these studies, the metallic elements of Occluder were cut off; thus, the observations did not show the collagen–metal interaction. Apart from that, the results are comparable with ours.

In yet another animal experiment, ASD was occluded with ASDOS device [22]. The pathomorphological changes referred to by authors as chronic changes, appeared in pigs after 3 and 6 months following the implantation. The formation of collagen capsule was also reported, but inflammatory infiltrations were scarce, because of the use of polyurethane as a part of the Occluder. Like in the previously cited work, the lack of metallic (nitinol) elements made the observation of collagen–metal relation impossible.

A similar study was made by Amin et al. [23], using AMuscVSD Occluder. The authors pointed out that 3 months after the operation the metallic elements of the Occluder were covered with endocardial surface with focal fibrosis. In light of our results, the site of implantation of the Occluder has no influence on the healing process.

In the study by Zahn et al. [24], the in-growth of connective tissue into PTFE interstices was emphasised; the results probably inspired the authors of another work [25] to construct and perform an experiment with the use of an Occluder with autologous-cell-seed and collagen-coated Dacron in Starflex device. A thick layer of granulation tissue was achieved as early as in the 4th week.

The term ‘biodegradation’ represents only microscopic feature of the implanted textile element. In fact, the textile is made of nondegradable compounds, and it persists in implantation site, but the in-growth of fibroblasts, collagen and matrix production by these cells in textile ‘interstices’ gives a distention of textile interstitium with relative decrease of density of textile elements. These changes should be considered as focal and reparative connective tissue hyperplasia inside distended pseudoatrophic architecture of textile.


   5. Conclusions
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
References
 

1. The closure of the free ventricular wall perforation with AMuscVSDO is safe due to the scar tissue resulting from the healing process around and in the device.
2. The myocardial healing around and inside an implanted AMuscVSDO represents two separate processes: extensive fibrosis ensues around metallic wires with the progression towards the inside of the myocardium, whereas inside AMuscVSDO the loose connective tissue fills the myocardial lesion. During cicatrisation the fabric elements of AMuscVSDO play a special role, acting as the ground for collagen formation and fibroblast proliferation.
3. The cicatrisation processes after ventricular AMuscVSDO implantation show remodelling, with rearrangement of collagen fibres architecture and distribution.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 

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