A device for sealing defects in the tissues of a patient's internal organs.

Abstract

The present invention relates to an apparatus for sealing a defect 9 in a patient's visceral tissue, having a scaffold with longitudinally elastic supports arranged radially in a manner similar to an inverted umbrella structure. [Solution] The device comprises a delivery guide wire 3 and a control guide wire 4, and the support 1 is a loop having a peak inflection point, connected to the delivery guide wire 3 at its distal end and to the control guide wire 4 at its proximal end, and an elastic membrane is stretched on the outer surface of the support 1 into the shape of an inverted umbrella cap.

Description

Technical Field

[0001] The subject of the present invention is a device for sealing a tissue defect of a patient's internal organs, having a scaffold comprising a longitudinal elastic support in a radial arrangement similar to an inverted umbrella structure. The present invention is particularly suitable for temporarily or permanently sealing a defect in the wall of the left ventricle and maintaining this seal during the time required for healing of the defect, but is not limited to this application.

Background Art

[0002] Left ventricular free wall rupture (FWR) or ventricular septal rupture (VSR) are rare but are associated with a very high risk of death and mechanical complications of myocardial infarction (MI). These situations can also occur independently of MI, for example as a result of trauma. Before the era of fibrinolytic reperfusion, VSR occurred in 1 - 3% of MI patients and FWR occurred in 2 - 6% of MI patients. The in - hospital mortality rate of VSR patients was 45% without shock symptoms and 90% with these symptoms, while it was approximately 50% in FWR patients treated in the hospital. In the era of fibrinolytic reperfusion, the incidence of VSR and FWR decreased significantly to 0.2 - 0.3%. In the era of mechanical reperfusion by primary coronary angioplasty, the incidence of these complications is even lower. The peak incidence of FWR and VSR in the era without reperfusion occurred 5 - 7 days after the onset of MI. The muscle adjacent to the rupture site is usually thin and brittle. In patients treated with thrombolytic therapy, the median time from the onset of chest pain to FWR or VSR was 24 - 30 hours in the GUSTO - I trial and 16 - 24 hours in the SHOCK trial.

[0003] VSRs vary in size from a few millimeters to several centimeters. Morphologically, VSRs are classified as simple or complex. Simple perforations have separate channels at the same level on both sides of the perforation. Complex ruptures, on the other hand, are characterized by a large intramural hematoma and irregularly shaped channels penetrating necrotic tissue. Septal perforations in patients with anterior wall infarction are usually located near the apex and are generally simple. However, in patients with inferior wall myocardial infarction, VSRs are often complex and involve the base of the inferior posterior part of the septum. VSRs may be accompanied by free wall rupture or papillary muscle rupture. Septal perforation causes a shunt from the left ventricle to the right ventricle, accompanied by right ventricular volumetric overload, increased pulmonary blood flow, and secondary left atrium and left ventricle volumetric overload. As left ventricular systolic function is reduced and systemic output decreases, compensatory contraction of the systemic vascular bed occurs along with increased systemic vascular resistance, which in turn further increases the size of the shunt between the left and right ventricles. Shunt size depends on perforation size, pulmonary vascular resistance, systemic vascular resistance, and left-to-right ventricular function. As left ventricular function begins to deteriorate and systolic pressure decreases, the left-to-right shunt and its proportion decrease.

[0004] Next, FWRs typically result in pericardial tamponade, electromechanical dissection, and sudden death. In some cases, a thrombus adjacent to the rupture site can occlude leakage in the pericardium, leading to the formation of a pseudoaneurysm. Based on pathological criteria, FWRs can be classified into type I, with a sudden rupture of the myocardial tear; type II, with an erosive site in the infarct zone showing progressive deterioration of the tear; and type III, associated with early left ventricular aneurysm formation. Clinically, depending on the size of the FWR and the dynamics of pericardial hemorrhage, FWRs can be classified into exudative and spurting types.

[0005] Surgical closure of VSR and FWR after infarction is the treatment of choice (Class I recommendation, evidence level C). Without this therapy, 90% of VSR patients and 100% of FWR patients die within two months. In both cases, cardiac surgery may be considered with protection of intra-aortic retrograde pulsation and / or left ventricular support using an extracorporeal membrane oxygenation (ECMO) device. Despite significant advances in surgical techniques, mortality rates for both complications remain very high, ranging from 10–90% for VSR and 30–40% for FWR, depending on the initial clinical state.

[0006] Koh et al. presented the treatment outcomes of 25 patients with periinfarct VSR between 1997 and 2008. The overall in-hospital mortality rate in the study group was 44%, which was significantly higher in the group receiving conservative treatment compared to surgery. Mortality was higher in patients with subbasal VSR than in patients with anterior apical VSR.

[0007] To date, there is no clear established timing for surgery following MI onset. There is debate about immediate surgical closure of the VSR, regardless of the patient's hemodynamic status, in order to avoid further deterioration of shock symptoms. The debate over early VSR closure stems from the fact that the septal bifurcation of the coronary artery, subjected to shear forces from flowing blood, and the boundary process of necrotic changes, are favorable to VSR dilation, which can lead to hemodynamic decompensation. On the other hand, many surgeons believe that surgery should be delayed for 3-4 weeks, or even 6 weeks, until scar formation in the surrounding tissue of the VSR is complete. This allows for more secure suturing of the defect margins and prevents tearing. However, it should be noted that for patients characterized by significant bilateral leakage, a 3-6 week period is a highly destructive and dangerous challenge. Therefore, in selected patients, the use of minimally invasive percutaneous methods may be considered to eliminate the VSR, and thus the right ventricular shunt, or at least partially reduce its size.

[0008] In most cases, acute FWR is associated with sudden death. The dynamic nature of the symptoms makes it difficult to effectively treat even acute FWR diagnosed in a hospital. Subacute rupture may be successfully treated if diagnosed and immediately transported to a center involved in cardiac surgery. The gold standard in the treatment of FWR is cardiac surgery to decompress cardiac tamponade and repair the rupture. If symptoms worsen rapidly, the procedure should be accompanied by pericardiocentesis. The largest meta-analysis to date by Matteucci et al. included 363 surgically treated FWR patients. The authors demonstrated a 50% lower surgical risk in patients with effusion rupture compared to spurting rupture. The mortality risk in FWR patients repaired with sutureless techniques was 40% lower compared to those with sutures. Sutureless surgical sealing of FWR can be performed using a collagen sponge or pericardial patch fixed to the epicardium with adhesive to cover the MI area. In contrast, suturing techniques are defined as repairing FWRs by using sutures to close myocardial tears or to secure epicardial patches. Exudative perforations can be sutured, patched, or closed with tissue adhesive. In surgical survivors, sutured FWRs should be monitored for early detection of leakage or aneurysm formation.

[0009] Endovascular VSR procedures are typically performed under general anesthesia, and the device is delivered through a long sheath inserted via arterial and venous femoral access. Most systems for VSR closure operate in a similar manner. They typically consist of the same basic components, such as a balloon for measuring the size of the perforation, the implant itself, and the system used to deliver it. The implant consists of two foldable discs or umbrellas of different sizes made of polyester, stretched over a metal mesh and separated by a narrow waist or straight, with its width varying depending on the indication. The delivery system consists of a percutaneously inserted sheath, a guidewire, and polyurethane catheters of various lengths, sizes, and curvatures to optimize the procedure. In the first stage, a diagnostic catheter is positioned in the left ventricle, and then the guidewire is passed through the VSR to the pulmonary artery, where it is captured and externalized into the femoral vein, forming a continuous arteriovenous loop. The size of the perforation is measured by transesophageal echocardiography and fluoroscopy with a calibration balloon, and its location is determined by echocardiography. Contraindications for percutaneous VSR closure include perforation size greater than 35 mm, VSR location near the apex of the heart, lack of sufficient margin to allow occluder placement, and location near the mitral, tricuspid, and / or aortic valves. The closure device, screwed onto a guidewire, is introduced through an arteriovenous loop created within the region of interest of the interventricular septum, where the device is implanted.

[0010] Small residual leaks may be observed immediately after implantation, but these usually resolve within the following weeks or months. After the occluder is implanted, the patient is treated with anticoagulants, usually aspirin, for about six months while the occluder heals. Over time, the endocardial and scar tissue fuse with the implant, permanently fixing its position and often eliminating any residual leaks. To date, the optimal timing for periinfarct VSR closure has not been established. Currently, various devices, including ASD Amplatzer, VSD Amplatzer, or CardioSEAL, are used for periinfarct VSR closure.

[0011] Percutaneous intrapericardial FWR therapy using fibrin glue injection is an alternative to FWR surgery, particularly in cases of exudative FWR. Hattori et al. showed that fibrin glue introduced into the pericardium forms a stable fibrin layer within 1 day, but the glue degrades within 1 week. Next, Murata et al. found no inflammatory adhesion of the epicardium to the pericardium in an autopsy study after fibrin glue injection. Both studies demonstrate that fibrin glue is biocompatible and biodegradable.

[0012] There are several significant limitations to the available endovascular techniques used for VSR closure. The rigid sets used to deliver the occluder to the septum can cause detachment of necrotic tissue fragments, leading to an increase in the size of the defect. Implanted occluders, fixed to fragile septal tissue, are not uncommonly displaced into the right ventricle, and in most cases require cardiac surgery. Furthermore, the available sizes of occluders may not be sufficient to close large defects, and residual left-to-right leakage after this type of treatment is one of the most common problems. Thiele et al. presented the results of treating periinfarct VSR with Amplatzer occluders for atrial or ventricular septal defects. Between 2003 and 2009, 29 patients underwent this procedure, 16 of whom had symptoms of cardiogenic shock. Occluder implantation failure in two patients with shock resulted in death by day 30 of follow-up. Subsequently, despite successful procedures, 12 of the remaining 14 patients (86%) died within one month. On the contrary, in the group of patients without symptoms of shock, treatment failed in two cases, and of the 11 patients who were successfully treated, four died during the 30-day observation period.

[0013] Minimally invasive endovascular techniques hold great promise for improving treatment outcomes for periinfarct VSR and FWR. Firstly, they can help in the early stabilization of VSR patients during the course of MI, particularly those with symptoms of cardiogenic shock, and can prevent organ hypoperfusion outcomes. Left ventricular support systems such as ECMO, Impella, or TandemHeart, which have not been tested in controlled studies in patients with mechanical complications of MI, are becoming more commonly adopted and are yielding increasingly favorable outcomes in the treatment of cardiogenic shock. Single case reports or serial cases indicate that, in some clinical situations, they can be valuable adjuncts to surgical treatment. However, their use is associated with the risk of exacerbating left ventricular injury in the case of Impella or TandemHeart pumps, or the risk of vascular complications in the case of ECMO.

[0014] In patients with mechanical complications of MI such as VSR or FWR, the concept of individualized treatment is compelling, which requires understanding the disease specificity of each individual patient, recognizing the complexity of the clinical state within the full range of associated circumstances, and finally selecting the most effective possible treatment. Currently, the specificity of each patient with shock during VSR or FWR is determined based on laboratory tests, echocardiography, and hemodynamic measurements. It is clear that currently available treatment technologies do not meet the expectations directed towards them, and therefore, there is a need to develop new treatments for the rare mechanical complications of MI.

[0015] Rupture and bleeding from the genitals, including the vagina or uterus, affects women of reproductive age and most frequently affects them during pregnancy. Less frequently, rupture of these organs occurs as a result of trauma. Risk factors for vaginal rupture and bleeding include first sexual intercourse, obstetric and / or gynecological history, or stressful positions during intercourse, but vaginal rupture always requires gynecological intervention.

[0016] Uterine rupture is a rare, life-threatening obstetric condition involving a laceration of the uterine wall, including the serosal membrane. Hospital incidence of uterine rupture ranges from 1 in 100–500 births in developing countries to 1 in 3000–5000 births in developed countries. Uterine scarring is the most commonly reported cause of uterine rupture in any third trimester of pregnancy, followed by placenta accreta, multiple births, post-cesarean section conditions, and irrational administration of oxytocin and prostaglandins. In developed countries, the rate of post-cesarean section uterine rupture has further decreased from a global average of 1 in 100 to 1 in 2000. Uterine rupture without scarring is extremely rare, estimated at 1 in 8000 to 1 in 15000 births. Uterine rupture may be associated with the use of misoprostol for mid-pregnancy abortions. Next, the risk of rupture is less than 0.35% in a scarred uterus and 0.04% in a non-scarred uterus. Multiple pregnancies are another predisposing factor for uterine rupture, as repeated pregnancies lead to thinning of the uterine muscle. The maternal mortality rate from uterine rupture is 0.2% in developed countries, but can reach up to 30% in poorer countries, mainly due to a lack of adequate care. The risk of uterine rupture leading to hysterectomy ranges from 14 to 33%. Uterine rupture in early or mid-pregnancy is extremely rare and can be difficult to diagnose clinically due to the variety of clinical symptoms and course. However, regardless of the stage of pregnancy, uterine rupture should always be considered before considering any other non-gynecological cause in any pregnant woman experiencing severe abdominal discomfort. Other common symptoms of uterine rupture include vaginal bleeding, maternal tachycardia, uterine hypotonicity and / or flaccidity, and abdominal tenderness.

[0017] While genitourinary injuries occur in approximately 10% of all abdominal and pelvic injuries, bladder ruptures account for only 1.6% of these cases. Due to the structural protection provided by the pelvic bones, bladder injuries are rare and are usually associated with high-intensity trauma. Bladder ruptures can be classified as extraperitoneal or intraperitoneal. Retroperitoneal ruptures are more common and are usually the result of a strong blow to the anterior bladder. Ruptures are usually due to intravesical pressure following a blow to the abdominal-pelvic region, causing a rupture in one of the weaker areas of the bladder, such as the apex. Clinical symptoms in patients with bladder injuries can vary depending on the severity of the injury, but most patients report suprapubic pain, gross hematuria, and dysuria. Pelvic fractures are very common in patients with bladder injuries. Pelvic fractures have been found to be associated with increased morbidity and mortality in patients with bladder injury, and the identification of a pelvic fracture should always raise clinical suspicion to assess genitourinary injury. Bladder rupture is rare but is associated with a significant patient morbidity and approximately 22% mortality. The Japanese Urological Association's clinical guidelines recommend cystography in stable patients with hematuria and / or pelvic fracture, or in any other patient with signs and symptoms suggestive of bladder injury. The guidelines state that bladder drainage is standard care for both extraperitoneal and intraperitoneal bladder rupture. Furthermore, the guidelines also recommend surgical repair of all bladder ruptures to prevent peritonitis following intraperitoneal leakage of bladder contents.

[0018] Polish Patent Application No. 433283 discloses a device for closing a peristometrial perforation of the interventricular septum of the heart, in the form of a scaffold having an open working support structure for a device for closing a peristometrial perforation of the interventricular septum of the heart, made of biocompatible, hematocompatible, and non-toxic materials, and reflecting the shape and size of the interior of the left ventricle of the heart, taking into account the papillary muscles and valves. The sealing material is placed on a scaffold having an open working support structure that covers the tissue defect in the interventricular septum of the heart with considerable clearance, thereby preventing blood flow from the left ventricle to the right ventricle. The main objective of this device is to reduce mortality and improve the prognosis, including the directly life-threatening mechanical complications of MI. Furthermore, the device can be used in clinical situations where existing methods are ineffective or even contraindicated. The concept of the device is based on the elastic interaction of the interventricular septum where the peristometrial perforation is located, and the scaffold is covered with a dressing material stretched in the area adjacent to the site of the rupture, introduced via transaortic access. The device is intended to stop uncontrolled shunting from the left ventricle to the right ventricle of the heart, further deoxygenation of arterial blood, and ultimately deterioration of left ventricular contractility. Covering the left ventricular endocardium, this VSR closure device is fixed to the left ventricular outflow tract and elastically deforms along with the contracting and relaxing left ventricle.

[0019] The above-described apparatus solves the problems of the prior art, but has drawbacks that are eliminated by the subject matter of the present invention. [Prior art documents] [Patent Documents]

[0020] [Patent Document 1] Polish Patent Application No. 433283 [Non-patent literature]

[0021] [Non-Patent Document 1] Koh et al. [Non-Patent Document 2] Matteucci et al. [Non-Patent Document 3] Hattori et al.

Non-Patent Document 4

Non-Patent Document 5

Summary of the Invention

[0022] The present invention relates to an apparatus for sealing a tissue defect of a patient's internal organs, having a scaffold with a longitudinal elastic support in a radial arrangement similar to an inverted umbrella structure. The apparatus includes a delivery guide wire and a control guide wire, and the support is a loop having a peak inflection point, connected to the delivery guide wire at their distal ends and to the control guide wire at their proximal ends, and an elastic membrane is stretched on the outer surface of the support in the shape of an inverted umbrella cap.

[0023] Preferably, the support has a flat outer shape, more preferably a tape or a flat wire.

[0024] Preferably, the supports are arranged at a constant circumferential interval around the guide wire.

[0025] Preferably, the apparatus includes at least four supports.

[0026] Preferably, the support is made of a shape memory material having a width of about 0.8 mm and a thickness of about 0.15 mm, more preferably a NiTi alloy.

[0027] Preferably, the membrane is reinforced with flexible struts made of a shape memory material extending along the entire circumference of the membrane.

[0028] More preferably, the struts have a sine wave course having a number of periods preferably corresponding to the number of supports and an amplitude of about 10 - 50% of the length of the support, the minimum point of the sine wave is near the center of the course and located at the contact point between the strut and the support, and the maximum point of the sine wave is slightly below its peak inflection point and located at the center of the distance between the supports.

[0029] More preferably, the strut is integrated with the membrane.

[0030] Preferably, the membrane is made of PCL.

[0031] More preferably, the strut is made from a NiTi alloy.

[0032] Preferably, the delivery guide wire and the control guide wire are slidably connected by a proximal guide sleeve, the guide sleeve is fixedly attached to the control guide wire and slidably surrounds the delivery guide wire, and the proximal end of the support is fixedly connected to the control guide wire via the guide sleeve.

[0033] Preferably, the distal end of the support is connected to the delivery guidewire by a distal fixation sleeve.

[0034] Preferably, the delivery guide wire and control guide wire are made of NiTi alloy and more preferably include circular wires having a diameter of about 0.5 mm.

[0035] More preferably, the guide sleeve and fixing sleeve are made of silver, surgical steel, or titanium.

[0036] Preferably, the device has spikes arranged circumferentially at the distal end of the device on the outer surface of the membrane in the portion surrounding the connection point of the support.

[0037] Preferably, the device has 3 to 5 spikes, more preferably 2 to 3 mm in height.

[0038] Preferably, the membrane is non-permanently attached to the support by more preferably reabsorbable surgical sutures, allowing the membrane to remain in the patient's body and the rest of the device to be removed.

[0039] More preferably, the membrane is covered with a cell proliferation-promoting layer, and the support is covered with an antithrombotic layer.

[0040] Preferably, at least one support is provided with a radiation marker. The subject matter of the present invention is described in the embodiments shown in the drawings. [Brief explanation of the drawing]

[0041] [Figure 1] A schematic diagram of the structure of the apparatus according to the present invention in an embodiment is shown. [Figure 2] This illustrates the principles of device placement and positioning in the organs of patients with wall defects. [Figure 3] The possible methods for delivering the device to an organ are shown, including the device in a folded state for intracatheter placement before insertion into the catheter (3a), and in an unfolded state after release (3b), and the function of the device after placement in the patient's organ, in this case the ventricle, during diastole (c) and systole (d). [Figure 4] The arrangement of guide wires and the method of connecting them in an exemplary embodiment are shown in more detail. [Modes for carrying out the invention]

[0042] The figure shows that a device for sealing a defect 9 in the tissue of a patient's internal organs has a scaffold comprising a longitudinal elastic support 1 arranged radially in a manner similar to an inverted umbrella structure, the device comprising a delivery guidewire 3 and a control guidewire 4, the support 1 being a loop, the distal end of the loop being connected to the delivery guidewire 3, the proximal end of the support being connected to the control guidewire 4, having a peak inflection point, and an elastic membrane 2 stretched on the outer surface of the support 1 in the shape of an inverted umbrella cap.

[0043] Due to its structure, namely the fact that the support 1 and membrane 2 are flexible, the device can be folded and arranged together with the delivery guidewire 3 and control guidewire 4 of the delivery catheter 11.

[0044] Naturally, for the purpose of the device, all elements of the device are made of biocompatible, hemocompatible, and non-toxic materials that have mechanical properties that allow them to conform to the inner surface of the patient's viscera where the existing defect 9 is to be sealed. When using a device to seal a ventricular defect 9, the supports 1 must have mechanical properties related to high elasticity, preferably shape memory, so that they remain in constant contact with the endocardial surface during both ventricular systole and diastole. At the same time, the elements must be flexible enough that resistance against the contracting ventricle does not impair their mechanical work and contractile capacity, taking into account the weakening of myocardial strength in the affected area due to pathological changes that may cause the defect 9. An important factor in the usefulness of the material is its resistance to repeated compression, so that the structure can remain in the ventricle for the time necessary for the healing of the defect 9 without causing mechanical damage to the load-bearing elements of the structure. The expected time required for the healing of the ventricular wall 10 is typically 3 to 6 weeks, which corresponds to 1.8 million to 6 million ventricular cycles.

[0045] When used in the ventricle, the spatial shape of the device design assumes that its apex fits the apex of the left ventricle. When the patient is in a vertical position, this point is the lower end of the device, to which all support 1 is connected. From this point, support 1 extends upward from the delivery guidewire 3 toward the base of the heart along the surface of the ventricular wall 10. The length of the device support 1 (arm) extended in the ventricle is selected to allow coverage of the defect 9 without causing a risk of blocking or damaging the internal structures of the ventricle responsible for its proper function. First, the device support 1 bypasses the papillary muscle and ends below the pathway of the chordae tendineae, which are involved in the sealing of the mitral valve. The device support 1 connects to the delivery guidewire 3 at its distal end, and at a height below the attachment of the chordae tendineae to the papillary muscle, it is bent toward the center of the ventricle and reconnected to the control guidewire 4. Both guidewires 3, 4 are led to the outside of the ventricle. The delivery guidewire 3 is used to introduce the device to the target site, namely the periapical region of the left ventricle in this example, via the delivery catheter 11 (Figure 3a). The control guidewire 4 allows the operator to change the spatial shape of the device from the moment of insertion into the catheter 11 when the device is assembled until the moment the device achieves its final working shape within the ventricle, adapts to its target position, and stabilizes.

[0046] The structure becomes longer but significantly narrower when folded with catheter 11 (Figure 3a). Figure 3c shows that, thanks to the shape memory effect stored in the material, when the device is unfolded inside the ventricle, it takes the appropriate shape of an inverted umbrella that conforms to the apex of the ventricle, while the support 1 is positioned along the ventricular wall in its long axis and rests on it up to the point of bending. The movement of the control guidewire 4 when the position of the delivery guidewire 3 is locked allows for an increase or decrease in the distance between the base and top of the device, resulting in an increase or decrease in the degree of spread of the support 1 of the structure and an increase or decrease in the tension of the stretched membrane 2 in the support, respectively. The optional possibility of locking the position of the control guidewire 4 relative to the delivery guidewire 3 fixes the distribution and degree of tension of the structural support in an optimal arrangement for the size of the ventricle and its contractile force.

[0047] The elastic membrane 2 is positioned on the support 1 of the device along the length of contact with the surface of the organ, which is intended to fulfill the functional assumptions of the device, namely, to stop the outflow of blood or other bodily fluids through the defect outside the cavity of the patient's organ (see Figure 2, where Figure 2a shows a healthy organ, Figure 2b shows an organ with a defect 9, and further schematically shows a cross-section of an organ with a defect 9 that will be closed by the device according to the present invention). Precisely positioning the support structure of the device inside the organ ensures that the membrane 2 adheres tightly to its inner surface, while the internal pressure system of the organ provides further stabilization and compression effects. When the device is positioned inside the ventricle, during diastole and while the mitral valve is open, the pressure of blood flowing into the left ventricle gently presses the membrane 2 against the endocardial surface, ensuring its tight fit and seal. During ventricular contraction, the increase in blood pressure constitutes an additional element of compression of the membrane 2, while the decreasing ventricular volume while pumping blood into the aorta maintains pressure, thereby maintaining the force pressing the membrane 2 against the endocardial surface. Compared to the prior art, the membrane 2 is tightly fitted around its entire circumference, meaning that the device can effectively close the defect 9 at any position, provided the defect 9 is located beneath the membrane. With the prior art mesh dressing, the device needs to be positioned quite precisely so that the dressing is placed in the defect. This significantly complicates and prolongs the procedure and further limits its effectiveness. Furthermore, during research, it has been found difficult to find a way to introduce and, above all, properly deploy a mesh structure. The use of a balloon (similar to a stent) would probably be necessary, but in that case, it would be problematic to make the device foldable for removal. This is certainly impossible using percutaneous methods. The present invention also solves this problem. The prior art mesh generates a large contact area between the structure and the interior of the organ wall 10, and over a large area, a portion of the structural mesh may come into contact without the dressing, leading to internal growth of the structure, which should be avoided. In the present invention, the support is isolated from the organ wall by a membrane along its entire circumference and therefore does not come into contact with the interior of the organ wall 10 at all.Furthermore, proper cooperation between the mesh and the organ is more difficult to achieve compared to the operation of the device according to the present invention, and especially when used in the ventricle, during systole the support is compressed against the compression wall and the mesh tends to undulate, while during diastole the support follows the expanding ventricular wall and the mesh that undulated during systole may not be able to keep up.

[0048] The material of membrane 2, like the materials of the remaining elements of the device, is biocompatible, hemocompatible, and non-toxic. From the standpoint of mechanical properties, it is made of a material with high elasticity, thereby allowing it to conform to the geometric shape of the inside of the organ and the supporting structure (support 1) of the device, and its airtightness ensures effective blocking of fluid flow through tissue defects in the organ wall 10. The preferred material for membrane 2 is PCL.

[0049] A key aspect of the device is also the cross-sectional profile of the support 1, which ensures proper operation within the organ (in the case of the ventricle, toward the inside of the ventricle during systole and toward the outside during diastole) without causing lateral deflection that could destabilize the device's position and alter the spatial arrangement of the structure. The optimal choice appears to be a flat profile of the support 1 (tape, flat wire) with a wider surface area oriented toward the organ wall 10, which prevents the aforementioned lateral deflection; however, the shape of the support 1 is not limited to this, and any other shape that provides practical advantages in a given application can be used. The best material for the support 1 is NiTi alloy (nitinol). When used inside the ventricle, the optimal dimensions are approximately 0.8 mm in width and 0.15 mm in thickness (taking into account manufacturing variations).

[0050] In a preferred embodiment, the supports 1 are arranged at regular circumferential intervals around the guidewires 3, 4, and it is best if there are at least four of them. This example is preferred for use in the ventricle. However, in a particular embodiment, the supports may be arranged irregularly, and their number may vary; for example, there may be three supports 1 in a smaller organ. In principle, however, it is a matter of balancing the number of supports 4 that provide sufficient support without becoming too large at the same time, and the pressure to fix the defect 9 in the organ (the more supports 1 there are, the larger the volume of the composite device becomes, requiring the use of a larger, and therefore thicker, catheter 11 to introduce the device into the organ, which becomes a problem at some point because there are limits to the volume of the blood vessel). The supports can also be arranged irregularly to accommodate organs with less regular shapes.

[0051] In the preferred embodiments shown in Figures 1 and 2, the film 2 is reinforced with elastic struts 5 made of a shape memory material (preferably NiTi alloy, i.e., nitinol) extending along the entire circumference of the film 2. Preferably, the struts 5 have a sinusoidal course with a number of periods corresponding to the number of supports 1 and an amplitude of about 10 to 50% of the length of the supports 1, the minimum point of the sinusoidal wave located near the center of its course at the point of contact between the struts 5 and the supports 1, and the maximum point of the sinusoidal wave located slightly below its peak inflection point at the center of the distance between the supports 1.

[0052] The purpose of strut 5 is to improve the pressure of membrane 2 against the inner surface of the organ and to prevent fluid from entering between membrane 2 and the inner surface of the organ. The sinusoidal shape of strut 5 provides flexibility that allows the entire device (support structure including support 1 together with the installed membrane 2) to fold and fit into the delivery catheter 11. Furthermore, it also allows for a reduction in the circumference of strut 5, for example, during ventricular contraction, preventing the generation of excessive resistance that could lead to impaired ventricular contractile function. Shape memory allows strut 5 to unfold and take the appropriate shape when the device is withdrawn from the delivery catheter 11 in the ventricle, and also allows it to follow the heart wall 10 during diastole to improve the pressure of membrane 2 against the endocardium. It is optimal when strut 5 is an integral part of membrane 2 and can be hidden between its layers for a more complete integration. Thus, strut 5 is intended to be only an auxiliary element of membrane 2 and not an element of the load-bearing structure, and is attached to support 1 together with membrane 2, but not independently of membrane 2.

[0053] In the embodiment shown in the figure, the delivery guide wire 3 and the control guide wire 4 are slidably connected by a proximal guide sleeve 6, which is fixedly attached to the control guide wire 4 and slidably surrounds the delivery guide wire 3, and the proximal end of the support 1 is fixedly connected to the control guide wire 4 via the guide sleeve 6. It is advantageous if the guide sleeve 6 is a clamp sleeve and the distal end of the support 1 is connected to the delivery guide wire 3 by a distal fixing sleeve 7. Those skilled in the art will understand that the guide wires do not need to be connected to each other, but their connection improves the stability of the device, the simplicity of inserting the device into an organ, stabilizes the longitudinal movement of the control guide wire 4 relative to the delivery guide wire 3, and prevents lateral or rotational movement. In a preferred embodiment, the delivery guide wire 3 and the control guide wire 4 are made of NiTi alloy, preferably having a circular cross-section and a diameter of about 0.5 mm (within manufacturing tolerance). The guide sleeve 6 and the fixing sleeve 7 may be made of, for example, silver, surgical steel, or titanium, and the inner surface of the guide sleeve 6 may be covered with a material that facilitates sliding on the delivery guide wire 3, preferably graphite, Teflon®, or another material having similar properties.

[0054] In the embodiments shown in Figures 1 and 2, the device has spikes 8 arranged circumferentially at the distal end of the device on the outside of the membrane 2 in the portion surrounding the connection point of the support 1. The spikes 8 directed toward the organ wall 10 are an additional element that stabilizes the position of the device in the organ. It is preferable to have 3 to 5 spikes 8, preferably with a height of 2 to 3 mm.

[0055] In a preferred embodiment, the membrane 2 is preferably attached non-permanently to the support 1 by reabsorbable surgical sutures, allowing the membrane 2 to remain in the patient's body and the rest of the device to be removed. In this example, it is preferable that the membrane 2 is covered with a cell proliferation-promoting layer and the support 1 is covered with an antithrombotic layer.

[0056] In this embodiment, at least one support 1 is provided with a radiation marker to enable visualization of the device.

[0057] As described in relation to the above embodiment, the method of installing the membrane 2 on the support 1 of the device envisions a variation of the design with three possible functional modifications (permanent or non-permanent connection of the membrane 2 to the support 1).

[0058] 1. Permanent placement using non-absorbable materials resistant to the patient's internal conditions allows the device to remain intact during the healing period of the tissue in the defect area, and then the device as a whole (membrane and support) is removed during a second procedure aimed at final closure of the defect, either using cardiac surgical techniques (suturing) or percutaneously (using an occluder). In this situation, the support and membrane must be covered with an anticoagulant layer to prevent coagulation and infiltration of the membrane into the healing tissue.

[0059] 2. Permanent placement using non-absorbable materials resistant to the conditions of the left ventricle of the heart; the membrane is coated with a substance that promotes tissue integration with the endocardium, and the entire structure remains permanently in the heart.

[0060] 3. Non-permanent placement using absorbable materials allows for tissue integration between the membrane and organ by stimulating endogenous mechanisms, while simultaneously freeing the membrane from the support structure of the device. Subsequently, after the removal of the support structure, the membrane remains integrated with the wall and is retained in the organ. In this situation, only the support needs to be covered with an anticoagulant layer to prevent coagulation, while the membrane should be covered with a layer that promotes cell proliferation.

[0061] In this embodiment, three possible methods for introducing the device into the left ventricle of the heart are envisioned. i. A more invasive surgical approach using a small-access right transverse thoracotomy, in which a closure device is implanted via a transaortic approach using cardiopulmonary bypass. ii. Minimally invasive percutaneous methods via transarterial or transvenous routes.

[0062] The surgical procedure envisions an intubated patient, under general anesthesia and mechanical ventilation, with central venous lines, arterial lines, and an electrocardiogram connected, in which case the heart is exposed via a right thoracotomy. An appropriate cannula is inserted into the right atrium via the ascending aorta and right jugular vein. Once cardiopulmonary bypass is connected and full blood flow is complete, the ascending aorta is clamped to induce cardiac arrest. Under visual guidance, a system with a perforation closure device is delivered to the left ventricle via the ascending aorta and then the aortic valve. Under endoscopic guidance, the device is introduced into the left ventricular cavity, and the endocardial surface is covered with the device's scaffold from the apex to the base of the papillary muscle. Depending on the patient's clinical condition, during the first 4-6 weeks of the recovery period, under general anesthesia and with cardiopulmonary support, the occluder is removed via a prethoracotomy through a right ventricular approach, and the perforation is sutured or closed with the occluder.

[0063] The percutaneous method envisions that, in intubated patients breathing from a ventilator with an introduced central venous line, arterial line, and electrocardiogram, under general anesthesia, arterial access is made (from the femoral artery, ulnar cephalic vein, or carotid artery), through which the device is introduced into the left ventricle via the ascending aorta and aortic valve using a delivery catheter, under the control of fluoroscopy and transesophageal or intracardiac echocardiography. After deploying and stabilizing the device inside the ventricle, it is further secured by suturing a guidewire with external access. This means that after a recovery period, the device can be removed in the same way it was inserted, without requiring invasive surgical procedures. Further procedures involve placing a membrane over the device structure. In the case of permanent placement, after the device is removed, the cardiac occluder can be used as a continuation of non-invasive treatment to permanently close the tissue defect. In the case of non-permanent placement, removal of the supporting structure and confirmation of successful closure of the perforation with the endodontic membrane are the final steps of the interventional therapy.

[0064] The design of the device and the selection of the membrane placement method, and therefore the treatment procedures used, depend on the patient's overall condition and the size of the defect. Thus, both variations of the device become available for medical treatment, and the safest and most effective treatment method is assumed to be at the physician's discretion.

[0065] The third method used is also percutaneous, but utilizes venous access. In intubated patients, breathing from a ventilator with a central venous line, arterial line, and electrocardiogram, venous access (from the jugular vein) is made under general anesthesia to the entrance to the right atrium of the heart. Using a transseptal needle, puncture is made into the atrial septum, allowing access to the left ventricle through the left atrium and mitral valve of the heart. Through this access, a device is introduced into the left ventricle using a delivery catheter, under the control of fluoroscopy and transesophageal or intracardiac echocardiography. After deploying and securing the device within the ventricle, it is further secured by suturing a guidewire via external access. The remaining procedure is identical to that of arterial access. The advantages of this solution are: i. the larger diameter of the venous vessel compared to the arterial vessel, which allows for the safe use of larger delivery catheters; and ii. longer-term patient safety due to a lower risk of occlusion of the venous lumen compared to arteries, through coagulation on the guidewire of the device extending inside the vessel.

[0066] The device can also be used in organs other than the heart, provided that it has internal space and possible application routes, with certain modifications to its size and shape. Examples of additional applications of the device may include: i. sealing bladder tissue defects applied through the urethra to allow urine to flow into the peritoneal cavity; ii. sealing uterine perforations applied through the vagina; and iii. sealing perforations in specific compartments of the digestive tract that allow food to flow into the peritoneal cavity, applied through the esophagus (in the case of the proximal compartment) or the anus (in the case of the distal compartment).

[0067] Naturally, the present invention is not limited to the examples of embodiments described above, and the features set forth in the claims can be combined in any combination suitable for a particular application of the solution.

Claims

1. A device for sealing a defect (9) in the tissue of a patient's internal organs, comprising a scaffold having longitudinal elastic support (1) arranged radially in a manner similar to an inverted umbrella structure, wherein the device comprises a delivery guidewire (3) and a control guidewire (4), the support (1) being a loop having a peak inflection point and connected to the delivery guidewire (3) at its distal end and to the control guidewire (4) at its proximal end, and an elastic membrane (2) stretched on the outer surface of the support (1) into the shape of an inverted umbrella cap.

2. The apparatus according to claim 1, characterized in that the support (1) has a flat outer shape, preferably a tape or a flat wire.

3. The apparatus according to claim 1 or 2, characterized in that the support (1) is arranged around the guide wires (3, 4) at a constant circumferential interval.

4. The apparatus according to any one of claims 1 to 3, characterized by comprising at least four support bodies (1).

5. The apparatus according to any one of claims 1 to 4, characterized in that the support is made of a shape memory material, preferably a NiTi alloy, having a width of about 0.8 mm and a thickness of about 0.15 mm.

6. The apparatus according to any one of claims 1 to 5, characterized in that the membrane (2) is reinforced by a flexible strut (5) made of a shape memory material that extends along the entire circumference of the membrane (2).

7. The apparatus according to claim 6, wherein the strut (5) preferably has a sinusoidal course having a number of periods corresponding to the number of supports (1) and an amplitude of about 10 to 50% of the length of the supports (1), the minimum point of the sinusoidal course being located near the center of the course at the point of contact between the strut (5) and the supports (1), and the maximum point of the sinusoidal course being located slightly below the peak inflection point at the center of the distance between the supports (1).

8. The apparatus according to claim 6 or 7, characterized in that the strut (5) is integral with the membrane (2).

9. The apparatus according to any one of claims 1 to 8, characterized in that the aforementioned membrane (2) is made of PCL.

10. The apparatus according to any one of claims 6 to 9, characterized in that the strut (5) is made of a NiTi alloy.

11. The apparatus according to any one of claims 1 to 10, characterized in that the delivery guide wire (3) and the control guide wire (4) are slidably connected by a proximal guide sleeve (6), the guide sleeve (6) is fixedly attached to the control guide wire (4) and slidably surrounds the delivery guide wire (3), and the proximal end of the support (1) is fixedly connected to the control guide wire (4) by the guide sleeve (6).

12. The apparatus according to any one of claims 1 to 11, characterized in that the distal end of the support (1) is connected to the delivery guide wire (3) by a distal fixing sleeve (7).

13. The apparatus according to any one of claims 1 to 11, characterized in that the delivery guide wire (3) and the control guide wire (4) are made of a NiTi alloy and preferably include a circular wire with a diameter of about 0.5 mm.

14. The apparatus according to any one of claims 11 to 13, characterized in that the guide sleeve (6) and the fixing sleeve (7) are made of silver, surgical steel or titanium, and the inner surface of the guide sleeve (6) is coated with a material that facilitates the sliding of the guide sleeve (6) on the delivery guide wire (3), preferably graphite, Teflon®, or another material having similar properties.

15. The apparatus according to any one of claims 1 to 14, characterized in that, in the portion of the support (1) surrounding the connection point, the outer surface of the membrane (2) has spikes (8) arranged circumferentially at the distal end of the apparatus.

16. The apparatus according to claim 15, characterized in that it has 3 to 5 spikes (8) which are preferably 2 to 3 mm in height.

17. The apparatus according to any one of claims 1 to 16, characterized in that the membrane (2) is preferably attached non-permanently to the support (1) using reabsorbable surgical sutures, leaving the membrane (2) in the patient's body and allowing the remaining part of the apparatus to be removed.

18. The apparatus according to claim 17, characterized in that the membrane (2) is covered with a cell proliferation promoting layer and the support (1) is covered with an antithrombotic layer.

19. The apparatus according to any one of claims 1 to 18, characterized in that a radiation marker is provided on at least one support (1).

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