Abstract:
An expandable elastic structure is introduced into the left ventricular chamber via intravascular catheter in a retrievable and safe manner, and having let anchors anchored to the layer of mid-myocardium of cardiac wall. The structure helps enhancing blood perfusion in the layer of both subendocardium and mid-myocardium and keeps the volume of both subendocardium and mid-myocardium in an expanded state, as such the expandable elastic structure helps restore cardiac muscular asynchronized contraction manner in a diseased heart of a patient. And eventually the expandable elastic structure prevents progressive remodeling process of a failing heart, and improves cardiac function.

Description:
NOTICE OF MATERIAL SUBJECT TO COPYRIGHT PROTECTION 
       [0001]    A portion of the disclosure of this patent document contains material which is subject to copyright protection under the copyright laws of the United States. The owner of the copyright rights has no objection to the facsimile reproduction by anyone of the patent document or the patent disclosure, as it appears in the United States Patent and Trademark Office patent file or records, but otherwise reserves all copyright rights whatsoever. 
       CROSS-REFERENCE TO RELATED APPLICATIONS 
       [0002]    Not Applicable 
         [0003]    STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH OR DEVELOPMENT 
         [0004]    Not Applicable 
         [0005]    THE NAMES OF THE PARTIES TO A JOINT RESEARCH AGREEMENT 
         [0006]    Not applicable 
         [0007]    REFERENCE OF MATERIAL SUBMITTED ON A COMPACT DISC 
         [0008]    Not Applicable 
       FIELD OF THE INVENTION 
       [0009]    The present invention pertains to the field of treating heart failure and other cardiac disorder, and more particularly to methods and devices for preventing progressive remodeling process of a failing heart by restoring cardiac muscular asynchronized contraction manner. 
       BACKGROUND OF THE INVENTION 
       [0010]    Heart Failure (HF) is a major and growing public health problem in the United States. Approximately 5 million patients in this country have HF, and over 550 000 patients are diagnosed with HF for the first time each year. In 2001, nearly 53 000 patients died of HF as a primary cause. The number of HF deaths has increased steadily despite advances in treatment. 
         [0011]    HF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood, and the majority of patients with HF show an impairment of left ventricle (LV) myocardial function. The impairment of LV myocardial function begins with some injury to, or stress on, the myocardium and is generally a progressive process, even in the absence of a new identifiable insult to the heart. The principal manifestation of such progression is a change in the geometry and structure of the LV, such that the chamber dilates and/or hypertrophies and becomes more spherical—a process referred to as cardiac remodeling. This change in chamber size and structure increases the hemodynamic stresses on the walls of the failing heart and depresses its mechanical performance. These effects, in turn, serve to sustain and exacerbate the remodeling process. Therefore, preventing the progressive remodeling process is seen as a major goal in the therapy of HF. 
         [0012]    According to the authoritative Guidelines of American College of Cardiology Foundation/American Heart Association, although some therapies such as drug therapy show promising in some patients with HF, there is no known therapy in prior art therapy which can prevent progressive remodeling process of HF except the therapy of heart transplantation, because, at least, it was largely unknown the mechanism of the progressive remodeling process of HF. Furthermore, heart transplantation procedures are very risky, extremely invasive and expensive and are performed on a small percentage of patients due to multiple limitations. Therefore, substantial efforts have been made to find a novel treatment for HF. 
         [0013]    Recent progress in the research of cardiac pumping mechanism provides an opportunity to develop a novel method to prevent the progressive remodeling process. Pathophysiology 17(2010)307 and The Thoracic &amp; Cardiovascular Surgeon 58(2010)1, report a new mechanism of cardiac muscular contraction manner. It is that the three parts of heart wall including subendocardium, mid-myocardium, and subepicardium differ in contraction/relaxation manner, such that it appears as asynchronized contraction manner. For example, during systole, the powerful contraction of the mid-myocardium and subendocardium contributes to blood ejection; however, the subepicardium remains relaxed and is not committed to contraction simultaneously. During diastole, the subepicardium is committed to contraction while both subendocardium and mid-myocardium remains relaxed. This theory provides an important protection mechanism for heart to avoid enlargement in which subepicardium plays a key important role, and to avoid ischemia which is caused by abnormal myocardial contraction manner other than caused by coronary artery diseases. 
         [0014]    On the other hand, alteration of cardiac muscular asynchronized contraction manner causes heart progressive remodeling process. First of all, it should be noticed that although subepicardium plays an important role in preventing excessive dilation of the heart during diastole, the subepicardium functions as such only when cardiac muscles contract in asynchronized manner. For example, subepicardium in simultaneous myocardial contraction manner does not counteract heart wall over expansion at the end of diastole and excessive dilation of the heart may occur in this case. Therefore, alteration of cardiac muscular asynchronized contraction manner may harm to this particular role of the subepicardium, and may cause ventricular dilation of the heart over time. Secondly, because cardiac muscular asynchronized contraction manner provides an important mechanism for blood perfusion in cardiac muscles, alteration of cardiac muscular asynchronized contraction manner is detrimental to blood perfusion in cardiac muscles and cause ischemia, the result of which, in turn, further deteriorate the capacity of cardiac muscular contraction for ejecting blood out of the heart. In summary, cardiac muscular asynchronized contraction manner plays an important role in maintaining heart function normally, and alteration of cardiac muscular asynchronized contraction manner causes progressive cardiac enlargement and cardiac pumping insufficiency. 
         [0015]    As such, restoring cardiac muscular asynchronized contraction manner in diseased heart may bring benefits to prevent progressive remodeling process and even cure heart diseases of this cause at early intervention. 
         [0016]    Therefore, there are substantial needs to develop methods and apparatus which may restore asynchronized contraction manner in a diseased heart of a patient, and which may be implantable in a retrievable and safe manner via intravascular catheter. 
       SUMMARY OF THE INVENTION 
       [0017]    It is therefore an object of the invention to provide methods and apparatus for treating HF and other heart disorder. 
         [0018]    It is a further object of the invention to provide methods and apparatus for restoring cardiac muscular asynchronized contraction manner in a diseased heart of a patient. 
         [0019]    It is also an object of the invention to provide methods and apparatus which are deliverable via an intravascular catheter in a retrievable and safe manner. 
         [0020]    In accord with these objects, which will be discussed in detail below, the novel system of the present invention includes a cardiac support device, a delivery device and an intravascular catheter. The system delivers an implantable expandable cardiac support device into the left ventricular chamber with a delivery device via an intravascular catheter. Cardiac support device has anchors anchored to the layer of mid-myocardium of cardiac wall of left ventricle in the expanded state of the cardiac support device, and anchors are configured to allow blood flow via anchors and enhance blood perfusion in the cardiac muscles. Anchors keep the volume of both subendocardium and mid-myocardium in an expanded state, and eventually restore cardiac muscular asynchronized contraction manner and improve cardiac function in a diseased heart. 
     
    
     
       BRIEF DESCRIPTION OF THE DRAWINGS 
         [0021]      FIG. 1  is a schematic view of a cardiac support device in a collapsed state coupled to a delivery device inside an intravascular catheter. 
           [0022]      FIG. 2  is a schematic view of a cardiac support device in an expanded state coupled to a delivery device inside an intravascular catheter. 
           [0023]      FIG. 3A  is a schematic view of a cardiac support device in a collapsed state. 
           [0024]      FIG. 3B  is a transverse cross sectional view of a cardiac support device in a collapsed state. 
           [0025]      FIG. 4  is a schematic view of a cardiac support device in an expanded state 
           [0026]      FIG. 5A  is a schematic front view of an anchor. 
           [0027]      FIG. 5B  is a transverse cross sectional view of a proximal binding site of an anchor of  FIG. 5A . 
           [0028]      FIG. 5C  is a transverse cross sectional view of an insertable part of an anchor of  FIG. 5A . 
           [0029]      FIG. 6A  is a schematic rear view of an anchor. 
           [0030]      FIG. 6B  is a transverse cross sectional view of a proximal binding site of an anchor of  FIG. 6A . 
           [0031]      FIG. 6C  is a transverse cross sectional view of an insertable part of an anchor of  FIG. 6A . 
           [0032]      FIG. 7A  is a schematic upper-side view of a left part of an anchor. 
           [0033]      FIG. 7B  is a transverse cross sectional view of a proximal binding site of an anchor of  FIG. 7A . 
           [0034]      FIG. 7C  is a transverse cross sectional view of an insertable part of an anchor of  FIG. 7A . 
           [0035]      FIG. 8A  is a schematic upper-side view of a right part of an anchor. 
           [0036]      FIG. 8B  is a transverse cross sectional view of a proximal binding site of an anchor of  FIG. 8A . 
           [0037]      FIG. 8C  is a transverse cross sectional view of an insertable part of an anchor of  FIG. 8A . 
           [0038]      FIG. 9  is a schematic view of a cardiac support device being inserted into a left ventricle by a delivery device via an intravascular catheter. 
           [0039]      FIG. 10  is a longitudinal cross sectional view of a cardiac support device anchored to a ventricular wall via anchors in an expanded state. 
           [0040]      FIG. 11  is a schematic view of a delivery device. 
       
    
    
     DETAILED DESCRIPTION OF THE INVENTION 
       [0041]    As mentioned above, the present invention includes devices and methods for restoring cardiac muscular asynchronized contraction manner in a diseased heart for treating dysfunctional left ventricle. 
         [0042]    Before the present invention is described in detail, it is to be understood that this invention is not limited to particular embodiments and applications described. It is also to be understood that the terminology used herein is for the purpose of describing particular embodiments only, and is not intended to be limiting, since the scope of the present invention will be limited only by the appended claims. Furthermore, the methods recited herein may be carried out in any order of the recited events which is logically possible, as well as in the recited order of events. Although any methods and materials similar or equivalent to those described herein can also be used in the practice or testing of the present invention, the preferred methods and materials are now described. 
         [0043]      FIG. 1  and  FIG. 2  illustrate a system for restoring cardiac asynchronized contraction manner which is used for the treatment of heart diseases which include but not limited to heart failure. The system includes a cardiac support device  10  and a delivery device  30  and an intravascular catheter  20 . 
         [0044]    As shown in  FIG. 3A  and  FIG. 3B  and  FIG. 4 , said cardiac support device  10  comprises a plurality of elastic arms  12 . Said elastic arms  12  are made of resilient materials including but not limited to Nitinol Alloys. The number of said elastic arms  12  can vary from three to more than ten, which depends on the nature of heart diseases and characteristics of resilient materials. Also, the length and width of said elastic arms  12  may vary based on the size of a ventricular chamber  100  and characteristics of resilient materials. In addition, the shape of said elastic arms  12  is not limited to cylindrical as shown in the embodiment of the present invention. The proximal end of said elastic arms  12  is joined together by a proximal circumferential band  15  extending therebetween, and said proximal circumferential band  15  is made of metal including but not limited to Titanium. The distal end of said elastic arms  12  is joined by a distal cover  13  which is made of metal including but not limited to Titanium , and there is a hole  14  in the center of said distal cover  13 . There are threads inside said hole  14 , in which a shaft  23  of a delivery device  30  is capable of connecting and locking to said distal cover  13  releasably through threads of said hole  14 , as such upon completion of inserting and installing said cardiac support device  10  inside a ventricular chamber  100 , said shaft  23  of said delivery device  30  is capable of being disconnected to said distal cover  13  and being removed from said ventricular chamber  100 . 
         [0045]    As shown in  FIG. 4 ,  FIG. 5A-C ,  FIG. 6A-C ,  FIG. 7A-C ,  FIG. 8A-C , each of said elastic arms  12  has an anchor  11  attached longitudinally. Said anchor  11  is made of non-resilient metal including but not limited to Titanium. Said anchor  11  comprises a proximal binding site  17  where said anchor  11  is attached to said elastic arms  12 , and a distal insertable part  18  which is inserted into the layer of mid-myocardium  90  of cardiac muscles as shown in  FIG. 10 . Said proximal binding site  17  of said anchor  11  is bound to the middle part of said elastic arms  12 . Each of said proximal binding sites  17  of said anchor  11  is permanently attached to each of said elastic arms  12  as shown in the embodiment of this patent document. Said proximal binding site  17  of said anchor  11  produces inward traction toward the center of ventricular chamber  100  in the expanded state of said cardiac support device  10 . This inward traction of said binding site  17  of said anchor  11  is produced by mechanical energy of said elastic arms  12  in an expanded state of said cardiac support device  10 , and transferred to both subendocardium and mid-myocardium via said insertable part  18  of said anchor  11  so that the volume of both subendocardium and mid-myocardium is kept in an expanded state during systole and diastole, in particular, during diastole. The extent of the expanded state of both subendocardium and mid-myocardium is predetermined by the length, diameter, elasticity, and number of said elastic arms  12 . 
         [0046]    Further, the midline of the projection surface of said distal insertable part  18  of said anchor  11  has a sharp edge  16 . Said sharp edge  16  is capable of having said anchor  11  inserted into the layer of mid-myocardium  90  of cardiac muscles, and also said sharp edge  16  prevents said insertable part  18  of said anchor  11  permanently binding to cardiac muscles so as to keep blood flow channel patency through said anchor  11 . Consequently, the expanded state of both subendocardium and mid-myocardium helps blood perfusion in the layer of subendocardium and mid-myocardium, and restores cardiac muscular asynchronized contraction manner in a diseased heart. 
         [0047]    Said cardiac support device  10  is delivered into said ventricular chamber  100  by said delivery device  30 . Said cardiac support device  10  is releasably coupled to said delivery device  30  through interlocking between said distal cover  13  and the distal end portion of said shaft  23 . As shown in  FIG. 11 , said delivery device  30  comprises said shaft  23  which is positioned into the center line of said cardiac support device  10  and having a distal end portion releasably coupled to said distal cover  13  of said cardiac support device  10  as described above, wherein said shaft  23  is made of metal including but not limited to Titanium, and wherein the proximal end portion of said shaft  23  is connected to the distal end of a resilient structure  24 ; a shaft releaser  22  having let said shaft  23  pass through the center line of said shaft releaser  22  and integrate together so that said shaft  23  can be screwed off and disconnected from said distal cover  13  of said cardiac support device  10  by rotating said shaft releaser  22 , wherein said shaft releaser  22  is made of metal or plastic; a shaft cover  21  extending from said shaft releaser  22  to said proximal circumferential band  15 , wherein said shaft cover  21  is made of metal including but not limited to Titanium, and wherein said shaft cover  21  is used for counteracting the traction of said shaft  23  for the purpose of expansion of said cardiac support device  10 ; a resilient structure  24  comprising metal coil springs which provide protection to heart tissue and said cardiac support device  10  when excessive traction is imposed on said shaft  23 ; a connecting element  25  which is made of nylon fiber and provides connection between the proximal end of said resilient structure  24  and a reel  27 ; said reel  27  which is made of metal or plastic and is capable of winding up said connecting element  25  on reel in order to expand said cardiac support device  10 ; a break  26  which is made of metal or plastic and is capable of keeping said elastic arms  12  expandable or collapsible in a desired extent by interacting with the teeth  28  of said reel  27 . 
         [0048]    An intravascular catheter  20  is made of polymer, and the size of said intravascular catheter  20  is in the same range as other percutaneous cardiac procedures, using sizes in the range of 18 Fr to 28 Fr. Said intravascular catheter  20  is deployed into left ventricular chamber  100  percutaneously through right carotid artery and aortic valve using a common guide wire (not shown), followed by the insertion of said cardiac support device  10  coupled to said delivery device  30  as shown in  FIG. 9 . In addition, said cardiac support device  10  can be retrieved from the anchored position by simply pulling back said cardiac support device  10  by a wire (not shown) via said intravascular catheter  20 .