WO2014147605A2

WO2014147605A2 - A device and method for closure of apical muscular ventricular septal defects

Info

Publication number: WO2014147605A2
Application number: PCT/IB2014/062997
Authority: WO
Inventors: Amit Mishra
Original assignee: Amit Mishra
Priority date: 2013-10-29
Filing date: 2014-07-10
Publication date: 2014-09-25
Also published as: WO2014147605A3

Abstract

The present invention relates to device used for the closing of apical muscular ventricular septal defects of the heart which are present at distal end and difficult to identify and operate due to insufficient space available for operation.

Description

A device and method for closure of apical muscular ventricular septal defects Field of the invention

The present invention relates to device used for the closing of apical muscular ventricular septal defects of the heart.

Background of the invention

A ventricular septal defect (VSD) is an opening in the ventricular septum, or dividing wall between the two lower chambers of the heart known as the right and left ventricles. VSD is a congenital (present at birth) heart defect. It occurs because of non fusion of different parts of developing ventricular septum during fetal growth.

Normally, oxygen-poor (blue) blood returns to the right atrium from the body, travels to the right ventricle, then is pumped into the lungs where it receives oxygen. Oxygen-rich (red) blood returns to the left atrium from the lungs, passes into the left ventricle, and then is pumped out to the body through the aorta.

Basic types of VSD are explained below:

Perimembranous VSD - an opening in a particular area of the upper section of the ventricular septum (an area called the membranous septum), near the valves. This type of VSD is the most commonly operated upon since most perimembranous VSDs do not spontaneously close.

Apical muscular VSD - an opening in the apical muscular portion of the lower portion of the ventricular septum. This type of VSDs are very difficult because they are difficult to identify as well as difficult to operate and close due to insufficient space available for the operating or performing surgery when it is at distal ends and needed ventriculotomy is to be performed for closing these kind of VSDs. However left or right ventriculotomy has its own problems and complications like pseudoaneurysm formation, ventricular dysfunction and arrhythmias.

Atrioventricular canal type VSD - a VSD associated with atrioventricular canal defect. The VSD is located underneath the tricuspid and mitral valves. Conal septal VSD - the rarest of VSDs which occur in the ventricular septum just below the pulmonary valve.

Multiple VSDs- There may be existence of more than VSDs. It may be from any of the above.

Ventricular septal defects are the most commonly occurring type of congenital heart defect, accounting for 20 percent of congenital heart disease cases and from these 2% VSDs include apical muscular type.

The heart is forming during the first 8 weeks of fetal development. It begins as a hollow tube, then partitions within the tube develop that eventually become the septa (or walls) dividing the right side of the heart from the left. Ventricular septal defects occur when the partitioning process does not occur completely, leaving an opening in the ventricular septum.

Some congenital heart defects may have a genetic link, either occurring due to a defect in a gene, a chromosome abnormality, or environmental exposure, causing heart problems to occur more often in certain families. Most ventricular septal defects occur sporadically (by chance), with no clear reason for their development.

If not treated, this heart defect can cause lung disease. When blood passes through the VSD from the left ventricle to the right ventricle, a larger volume of blood than normal must be handled by the right side of the heart. Extra blood then passes through the pulmonary artery into the lungs, causing higher pressure than normal in the blood vessels in the lungs and causing pulmonary vascular disease and hypertension.

A small opening in the ventricular septum allows a small amount of blood to pass through from the left ventricle to the right ventricle. A large opening allows more blood to pass through and mix with the normal blood flow in the right heart.

The lungs are able to cope with this extra pressure for while, depending on exactly how high the pressure is. After a while, however, the blood vessels in the lungs become diseased by the extra pressure.

As pressure builds up in the lungs, the flow of blood from the left ventricle, through the VSD, into the right ventricle, and on to the lungs will diminish. This helps preserve the function of the lungs, but causes yet another problem. Blood flow within the heart goes from areas where the pressure is high to areas where the pressure is low. If a ventricular septal defect is not repaired, and lung disease begins to occur, pressure in the right side of the heart will eventually exceed pressure in the left. In this instance, it will be easier for oxygen-poor (blue) blood to flow from the right ventricle, through the VSD, into the left ventricle, and in to the body which is known as Eisenmenger complex. When this happens, the body does not receive enough oxygen in the bloodstream to meet its needs.

Because blood is pumped at high pressure by the left ventricle through the VSD, tissue damage may eventually occur in the right ventricle. Bacteria in the bloodstream can easily infect this injured area, causing a serious illness known as bacterial endocarditis.

Some ventricular septal defects are found in combination with other heart defects (such as in transposition of the great arteries) like Tetralogy of fallout, Multiple VSD, Atrial septal defects (ASD) and Patent ductus arteriousus (PDA).

The size of the ventricular septal opening will affect the type of symptoms noted, the severity of symptoms, and the age at which they first occur. A VSD permits extra blood to pass from the left ventricle through to the right side of the heart, and the right ventricle and lungs become overworked as a result. The larger the opening, the greater the amount of blood that passes through and overloads the right ventricle and lungs.

Symptoms of VSDs often occur in infancy and most common symptoms of VSD may include: fatigue, sweating, rapid breathing, rapid breathing, congested breathing, disinterest in feeding, or tiring while feeding and poor weight gain. However, each child may experience symptoms differently.

If the opening is small, it won't cause symptoms because the heart and lungs don't have to work harder. The only abnormal finding is a loud murmur (noise heard with a stethoscope). Small VSD may cause infarctus endocarditis.

If the opening is large, the child may breathe faster and harder than normal. Infants may have trouble feeding and growing at a normal rate. Symptoms may not occur until several weeks after birth. High pressure may occur in the blood vessels in the lungs because more blood than normal is being pumped there. Over time this may cause permanent damage to the lung blood vessels.

Ventricular septal defect is the commonest gross morphological congenital malformation of the heart after bicuspid aortic valve. Ever since the first successful VSD closure by Clarence Walton Lillehei, on control cross circulation, researches are on for developing techniques for closing multiple muscular VSD. Still depending on the condition of the patient the operation for multiple VSD including apical muscular VSD may be staged as pulmonary Artery (PA) banding as the first stage and finally the VSD closure.

In normal practice VSD closure is performed by surgical procedure known as ventriculotomy using Dacron patch, GORE-TEX patch, Pericardial patch by way of direct closure, Trans atrial closure, trans right ventricular apex and trans Left ventricular closure, Trans pulmonary artery closure, depending on the location of VSD, device closure using trans- vascular and perventricular route.

EP1595504 describes a defect patch device and method that patches a defect in the heart or other cardiovascular tissue. One aspect provides a PFO closure device and method that patches a PFO in the right atrium without the device extending through the PFO into the left atrium.

EP2082690 discloses a percutaneously implanted medical device suitable for treating heart failure such as congestive heart failure and diastolic dysfunction.

US6379368 describes an occlusion device for the closure of atrial or ventricular septal defects, for the closure of patent ductus arteriosus, patent foramen ovale, or other vascular defects. The occlusion device comprises a center section extending in an axial direction, with upper and lower straned wire fixation deice emanating from the center section.

US2007265641 describes a closure catheter for closing a tissue opening such as an atrial septal defect, patent foramen ovale or the left atrial appendage of the heart. The closure catheter carries a plurality of tissue anchors, which may be deployed into tissue surrounding the opening, and used to draw the opening closed. US2009171447 discloses a stent-valve associated methods and system for their delivery via minimally invasive surgery and guided wire compatible closure device for sealing access orifice are provided.

US2010131007 describes a self expanding medical occlusion device for treating heart defects in patients in particular closing abnormal opening in heart.

US20030139819 discloses septal defect occluders which can be used with a catheter deployment system to occlude septal defects. This occluder comprises a metal of frame structure that supports a biodegradable member. The frame strcutrure is made from a shape memory metal such as nitinol.

US20100305584 describes a septal defect having a suture like implantable treatment apparatus and device for delivering the implantable treatment apparatus and method for treating septal defect.

WO2008156464 discloses an intravascular device for treating certain medical condition and, more particularly relates to a low profile intravascular occlusion device for treating congenital defects including Atrial and Ventricular septal defects (ASD and VSD respectively), Patent Ductus Arteriosus (PDA) and Patent Foramen Ovale (PFO) as well as conditions that result from previous medical procedures such as Para- Valvular Leaks (PVL) following surgical valve repair or replacement.

Zhong-Dong Du et al described various device used for the closure of ventricular septal defect which are used by catheter guided device like Rashkind device, Amplatzer devices, Button device, Bard Clamshell umbrella and Gianturco coils.

References:

1) Kirklin JK, Castaneda AR, Keane MD, Fellows KE, Norwood Wl. Surgical management of ventricular septal defects. J Thorac Cardiovasc Surg. 1980;80:485-493.

2) Kitagawa T, Durham LA, Mosca RS, Bove EL. Techniques and results in the management of multiple ventricular septal defects. J Thorac Cardiovasc Surg. 1998;1 15:848-856. 3) Black MD, Shukla V, Rao V, Smallhorn JF, Freedom RM. Repair of isolated multiple muscular ventricular septal defects (the septal obliteration technique). Ann Thorac Surg. 2000;70:106-1 10.

4) Aaron BL, Lower ER. Muscular ventricular septal defect repair made easy. Ann Thorac Surg. 1975;19:568-570.

5) Hanna B, Bridges ND, Mayer JD, Castaneda AR. Clinical and myocardial status after left ventriculotomy for ventricular septal defects. J Am Coll Cardiol. 1991 ;17(Suppl):1 10A.

6) Seddio F, Reddy VM, McElhinney DB, et al. Multiple ventricular septal defects (how and when should they be repaired?). J Thorac Cardiovasc Surg. 1999;1 17:134-139.

7) Ootaki Y, Yamaguchi M, Yoshimura N, Oka S, Yoshida M, Hasegawa T. Surgical management of trabecular ventricular septal defects: the sandwich technique. J Thorac Cardiovasc Surg. 2003;125(3):508-12.

8) Chaturvedi RR, Shore DF, Yacoub M, Redington AN. Intraoperative apical ventricular septal defect closure using a modified Rashkind double umbrella. Heart. 1996;76:367-369.

9) Okubo M, Benson LN, Nykanen D, et al. Outcomes of intraoperative device closure of muscular ventricular septal defects. Ann Thorac Surg. 2001 ;72:416-423.

10) Evan M. Zahn, Neil Wilson, Warren Cutright and Larry A. Latson. Development and Testing of the Helex Septal Occluder, a New Expanded Polytetrafluoroethylene Atrial Septal Defect Occlusion System. Circulation..2001 ;104:71 1 -716.

So far no preferred device or method has been described for closing muscular VSD like difficult distal septal, apical and mid muscular and multiple muscular VSD, specially apical muscular VSD where it is difficult to close the defect because of difficulty in identification of defect, and to reach the defect and is almost impossible to close the defect because of unavailability of the sufficient space. Generally ventriculotomy is required to close such apical defects, which is responsible for post operative morbidity and mortality and ventricular dysfunction arrhythmia and aneurysm formation. Further ventriculotomy is lengthy surgical procedure with much more complication as it involves the cutting the ventricle parts of the heart for performing the surgery. Further ventriculotomy is also a costly surgery. Further transcathater closure of apical muscular VSDs is also not possible as there is no space at the apex for the device.

Thus there is a still need exists in the society to develop a device to close the apical muscular VSDs which are otherwise very difficult and complicated with risk to patients by simple, less time consuming and cost effective manner.

Inventors of the present invention have surprisingly prepared a device which can be useful to close apical muscular VSDs with easy and simple method in less time compared to ventriculotomy and does not involve much complications and additional risk to the patients with low coast compared to ventriculotomy.

Summary of the invention

One aspect of the invention is to provide a device for closing apical muscular ventricular septal defect comprising a disc comprising two layer of biocompatible material and a graft made up of biocompatible material wherein one end of graft is fixed to disc and one end is free.

Yet another aspect of the invention is to provide a device for closing apical muscular ventricular septal defect comprising a disc comprising one layer of polytetrafluoroethylene having thickness of 0.6 to 0.8 mm and another layer of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and a graft made up of expandable polytetrafluoroethylene having thickness 0.4 to 0.8 mm, wherein one end of graft is fixed to disc and one end is free.

Yet one more aspect of the invention is to provide a device for closing apical muscular ventricular septal defect comprising a disc comprising one layer of polytetrafluoroethylene having thickness of 0.6 to 0.8 mm and another layer of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and a graft made up of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and comprising at least two spikes over it and wherein one end of graft is fixed to disc and one end is free.

Yet another aspect of the present invention is to provide the method of fixing the device at apical muscular ventricular septal defects. Details description of the drawings

Fig. 1 is a side view of the apical muscular ventricular septal defect closing device.

Fig. 2 is a top view of the apical muscular ventricular septal defect closing device.

Fig. 3 is a side view of the apical muscular ventricular septal defect closing device with spikes over graft.

Fig. 4 is a side view of the apical muscular ventricular septal defect closing device with guided wire inserted in it.

Fig. 5A is a diagrammatic view of heart with apical VSD defect. Fig. 5B shows the process of fixing the device using forceps. Fig. 5C shows the final adjustment of device at the apical VSD.

Fig. 5D is a diagrammatic view of heart after placing device and closing of the apical VSD. Fig. 5E shows the checking of the position of device using the mirror.

Details description of the inventions

Main aspect of the invention is to provide a device for closing apical muscular ventricular septal defect comprising a disc comprising two layer of biocompatible material and a graft made up of biocompatible material wherein one end of graft is fixed to disc and one end is free. The device of present invention is described in details as below;

Fig. 1 is a side view of the apical muscular ventricular septal defect closing device which comprises a disc (1) comprising layer (2) and layer (3) of biocompatible material and a graft (4) of biocompatible material wherein the one end of graft is fixed to disc and one end remains free. Fig. 2 is a top view of the apical muscular ventricular septal defect closing device which comprises a disc (1) comprising layer (2) and layer (3) of biocompatible material and a graft (4) of biocompatible material wherein the one end of graft is fixed to disc and one end remains free.

Fig. 3 is a side view of the apical muscular ventricular septal defect closing device which comprises a disc (1) comprising layer (2) and layer (3) of biocompatible material and a graft (4) of biocompatible having spikes (5) over it of biocompatible material wherein the one end of graft is fixed to disc and one end remains free

Fig. 4 is a side view of the apical muscular ventricular septal defect closing device which comprises a disc (1) comprising layer (2) and layer (3) of biocompatible material and a graft (4) of biocompatible material wherein the one end of graft is fixed to disc and one end remains free with guided wire (6) inserted in it.

Fig. 5A to Fig.5E shows the step by step procedure of fixing the device at VSD.

The apical VSD can be alone or in combination of any other type of VSDs.

The term "apical muscular ventricular septal defects" as used herein means the septal defects which are difficult to close the defect because of difficulty in identification of defects and to reach the defect and is almost impossible to close the defect surgically without ventriculotomy because of unavailability of the sufficient space without risk to patients.

The term "biocompatible material" as used herein means a material, synthetic or natural and which remain in intimate contact with living tissue and which does not threaten, impede, or adversely affect living tissue.

The biocompatible material for preparing layer (2), layer (3), graft (4) and spikes(5) is to be selected from the group consisting of poly(ethylene oxide) (PEO), polytetrafluoroethylene (PTFE), expandable polytetrafluoroethylene (ePTFE), polyethylene terephthalate (PET), polyvinyl alcohol, acrylate polymers, silicone and derivatives thereof. Preferably the polytetrafluoroethylene (PTFE, available under the trade mark Teflon), expandable polytetrafluoroethylene (ePTFE available under the trade mark GORE-TEX) are to be used for the preparation of layer (2), layer (3), graft (4) and spikes (5). Preferably the biocompatible material to be used for the preparation of layer (2), layer (3), graft (4) and spikes (5) should be of specific thickness. The preferred thickness of polytetrafluoroethylene (PTFE) should be in the range of 0.6 to 1 mm and that is of expandable polytetrafluoroethylene (ePTFE) should be in the range of 0.4 to 0.8 mm.

The material used for preparing layer (2), layer (3), graft (4) and spikes (5) may be same or different. Preferably the material of choice for the preparation of layer (2), graft (4) and spikes (5) are same and that is expandable polytetrafluoroethylene (ePTFE) while the material of choice for the preparation of layer (3) is polytetrafluoroethylene (PTFE).

One more embodiment of the present invention is to provide a device for closing apical muscular ventricular septal defect comprising a disc comprising one layer of polytetrafluoroethylene having thickness of 0.6 to 0.8 mm and another layer of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and a graft made up of expandable polytetrafluoroethylene having thickness 0.4 to 0.8 mm, wherein one end of graft is fixed to disc and one end is free.

The size of the disc (1 ) can be varied as per the size of defects in patients. Similarly the size or diameter of the graft is also can be varied as per the size of the defects in the patients.

The device for closing apical muscular ventricular septal defects can be prepared by cutting the biocompatible material for layer (2) and layer (3) of the same size. Fixing layer (2) and (3) by any suitable means like by suturing or by biocompatible adhesive material which can provide strong bonding between layer (2) and layer (3). Further the graft (4) is prepared by the cutting biocompatible material of required size and rolling it to prepare a hollow tube and fixed by any suitable means like by suturing or by biocompatible adhesive material which can provide strong bonding or alternatively readymade hollow tube can be selected. Thus prepared graft is further fixed with disc in center as described in Fig. 1 , Fig. 2, Fig. 3 and Fig. 4 by any suitable means like suturing or by biocompatible adhesive material which can provide strong bonding.

Another embodiment of the invention is to provide a device for closing apical muscular ventricular septal defect comprising a disc comprising one layer of polytetrafluoroethylene having thickness of 0.6 to 0.8 mm and another layer of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and a graft made up of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and comprising at least two spikes over it and wherein one end of graft is fixed to disc and one end is free.

In one embodiment the graft is prepared as described above and further at least two or more spikes (5) prepared form the biocompatible material are fixed over the graft as described in Fig. 3. These spikes are fixed to the graft so that in worst situation it keeps device at its place without any possibility of movement and leakage from the whole. The number of spikes can be increased or decreased but at least two spikes are to be required to serve the purpose of fixing the spikes.

In yet another embodiment, the device can be prepared according to the Fig. 4 where in the guided wire is inserted inside the graft and which passes along with the disc in the center which is used to direct the device at appropriate location in the heart and one it is fixed at septal defects, the guided wire is removed and the device gets fixed at the septal defects and close it.

One more embodiment of the present invention is such wherein the graft is prepared with some spongy material which swells after the fixation in VSD to make the fixing tight and avoid any possibility of leakage through little space between VSD and graft of device. In this case either the whole graft is prepared from same spongy material or only the upper part of graft which comes in contact with VSD can be prepared with spongy material and rest can be of biocompatible material as described herein.

These are the few methods and models which can be prepared and used for the closing of apical muscular ventricular septal defects as described herein, however a person skilled in the art can easily do the little and obvious modification in the device model.

The device for closing apical muscular ventricular septal defects of the present invention can be fixed as per the procedure outline below;

Using two dimensional echo cardiography and Trans Esophageal Ecocardiography TEE, pre operatively the size and the number of the defect is to be identified. It is very important to identify the defect in relation to moderator band whether it is anterior or posterior and its opening on the left side of the septum or not and whether it is single or multiple. Under cardioplegic arrest right atrial is opened and the VSD can be identified with the help of suction cannula. Inter arterial septum is cut opened vertically and the right angle forceps is to be passed through the VSD and the device is to be caught hold with the right angle force and pulled through the septum with gentle force, the graft is further pulled in a zig zag fashion to secure the firm fixation of device at the left ventricular side of the septum. The graft can be fixed on the right ventricular side with the help of pledegeted prolene suture. The position of the device can be checked with the help of dental mirror through mitral valve. After coming off bypass blood samples were drawn in the operating room from right atrium and pulmonary artery to look for any significant residual shunt/graft.

More specifically the procedure can be performed as per the below steps;

a) identifying the size and number of apical muscular vascular septal defects using echo cardiography;

b) preparing device according to size identified;

c) cutting and opening atrial septum vertically and passing forceps at right angle through the VSD and pulling through the septum with gentle force and

d) fixing the graft on the right ventricle side with the help of suture

Further the procedure can be easily understood by the diagrammatic view provided in the figure 5A to figure 5E.

The device of the present invention and the method of using this device for closing of apical muscular VSDs is very simple, less time consuming and also do not pose any complication or additional risk to patient. Further the said device and procedure is less costly compared to known ventriculotomy.

Example

Seventeen patients with isolated or multiple apical muscular ventricular septal defects with or without associated heart diseases were operated. The apical VSD was closed using the device of the present invention. Details are provided in below table.

muscular VSD, Severe closure.

PAH.

9 4.5 TGA PM VSD, MM VSD, ASO with nil Died after 45 days months apical 5x5mm VSD, Multiple VSD secondary to

Severe PAH. closure. severe PAH and sepsis.

3 years 10 Multiple VSD, 4x4 mm Multiple VSD 1.60% Doing wel on outlet muscular VSD, closure with follow up.

apical VSD 6x6mm & large PA debanding

PM VSD, Severe PAH S/P and PA plasty.

PA Banding PDA ligation.

2 years 6 Multiple VSD, 5x5mm, Multiple VSD 2.60% Doing wel on apical VSD, 4mm MM VSD closure with follow up.

and S/P CO-A repair with PA debanding

PA banding. and PA plasty.

1.5 6 SI, DC, cor triatrium, large Excision of LA 3.8% Doing wel on years PM VSD, 4x4mm apical membrane follow up.

VSD, ASD, Severe PAH. with ASD and

multiple VSD

closure.

7 years 15 TOF with absent LPA, 8x8 ICR with apical 2.6% Doing wel on mm size apical VSD. VSD closure. follow up.

3 2.9 Multiple VSD,4x4 PM VSD multiple VSD 3.3% Had LV months with multiple apical (largest closure with dysfunction in

4x4mm) and small PDA, PDA ligation. immediate post severe PAH. operative period.

Doing wel on follow up.

6 4.2 Multiple VSD, large inlet VSD closure 2.60% Doing wel on months VSD, with 5x5mm apical with PDA follow up.

VSD with small PDA, ligation.

severe PAH.

5 3.2 Large PM VSD, 4x4mm multiple VSD 4.20% Doing wel on months MM VSD, 5x5mm apical closure. follow up.

VSD, severe PAH.

4 years 13 Multiple VSD, inlet 8x8mm, multiple VSD 8.20% Had RV

6x6 mm apical VSD , S/P closure, PA dysfunction in post

Co-A repair and PA debanding and op period, post op banding. PA plasty. echo showed multiple tiny VSDs.

Doing wel on follow up.

4 3.4 Obstructed cardiac TAPVC TAPVC repair nil Doing wel .

months with 5x5 mm size apical with VSD

VSD, Severe PAH. closure.

6 years 10 Large apical (16x8mm) PDA ligation 3% Doing wel .

VSD, MM VSD (6x6 mm) with multiple

with PDA bidirectional VSD closure.

shunt, severe PAH. Apical VSD

closed using

two disk

devices.

2 years 7 TGA, VSD, PS. with 6x6 Rastalli with nil Doing wel on mm size apical muscular apical VSD follow up.

VSD. closure.

9 4.2 Multiple VSD (PM, inlet, Multiple VSD 3.2% Need to go back months post muscular), apical 5x5 closure with after on bypass for mm, secundum ASD, PDA, ASD closure closing closing

Severe PAH. with PDA posterior undiagnosed post ligation. muscular muscular VSD.

VSD

15 7 4 Supra mitral membrane Multiple VSD 2.80% Doing well. months with multiple apical VSD closure with

(largest 4x4mm), PDA, supra metal

Severe PAH. membrane

excision with

PDA ligation.

16 10 years 22 TOF with 8x8 mm size ICR with 4.9% Had severe apical VSD and 4x4mm multiple VSD biventricular size MM VSD. closure. dysfunction and needed tracheostomy for ventilatory weaning. Doing well on follow up.

17 1.1 5.5 Multiple VSD, large PM Multiple VSD 2.80% Doing well on years VSD and apical 4x4mm closure. follow up.

with absent LPA, Severe

PAH.

PDA-Patent ductus arteriosus, DORV-Double outlet right ventricle, TGA-Transposition of Great arteries, RA-Right atrium, PA-Pulmonary artery, PAH-Pulmonary arterial hypertension, PM-Perimembranous, MM-Mid muscular, TOF-Tetralogy of fallot, TAPVC-total anomalous pulmonary venous connection, VSD-ventricular septal defect, ASD-atrial septal defect, LPA- Left pulmonary artery, Si-Situs inversus, DC-dextrocardia, ASO-arterial switch operation, ICR-intracardiac repair, S/P- status post, Step up- difference of Sp02 between RA and PA.

Results

Seventeen patients were operated of ages ranging from 3 months to 7 years. One of these 8 month old patients with transposition of great arteries with multiple ventricular septal defects died after 35 days due to severe pulmonary artery hypertension and sepsis. Another newborn with intracardiac total anomalous pulmonary venous connection with a 4mm apical ventricular septal defect also died after three days since this ventricular septal defect could not be identified. All other patients are doing well on follow up.

Conclusion From the details of above study, we can conclude that the device of the present invention is cost-effective easy to prepare and effective in closing apical muscular ventricular septal defect

Claims

1 . A device for closing apical muscular ventricular septal defect comprising a disc comprising two layer of biocompatible material and a graft made up of biocompatible material wherein one end of graft is fixed to disc and one end is free.

2. The device for closing apical muscular ventricular septal defect of claim 1 , wherein the biocompatible material is selected from the group consisting of poly(ethylene oxide) (PEO), polytetrafluoroethylene (PTFE), expandable polytetrafluoroethylene (ePTFE), polyethylene terephthalate (PET), polyvinyl alcohol, acrylate polymers, silicone and derivatives thereof.

3. The device for closing apical muscular ventricular septal defect according to claim 1 , wherein the disc comprising two different layers of biocompatible materials one is of polytetrafluoroethylene and other is expandable polytetrafluoroethylene and graft is made up of expandable polytetrafluoroethylene.

4. The device for closing apical muscular ventricular septal defect according to claim 3, wherein the polytetrafluoroethylene is having thickness of 0.6 to 1 mm and expandable polytetrafluoroethylene is having thickness of 0.4 to 0.8 mm.

5. A device for closing apical muscular ventricular septal defect comprising a disc comprising one layer of polytetrafluoroethylene having thickness of 0.6 to 1 mm and another layer of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and a graft made up of expandable polytetrafluoroethylene having thickness 0.4 to 0.8 mm, wherein one end of graft is fixed to disc and one end is free.

6. A device for closing apical muscular ventricular septal defect comprising a disc comprising one layer of polytetrafluoroethylene having thickness of 0.6 to 1 mm and another layer of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and a graft made up of expandable polytetrafluoroethylene having thickness of 0.4 to 0.8 mm and comprising at least two spikes over it and wherein one end of graft is fixed to disc and one end is free.

7. A method of fixing the device of claim 1 , 5 and 6, comprising the steps of

a) identifying the size and number of muscular vascular septal defects using echo cardiography; b) preparing device according to size identified;

c) cutting and opening atrial septum vertically and passing forceps at right angle through the VSD and pulling through the septum with gentle force and d) fixing the graft on the right ventricle side with the help of suture.