U.S. patent application number 10/192402 was filed with the patent office on 2003-03-20 for anti-arrhythmia devices and methods of use.
This patent application is currently assigned to TriCardia, LLC. Invention is credited to Holmes, David R. JR., Schwartz, Robert S., Tassel, Robert A. Van.
Application Number | 20030055491 10/192402 |
Document ID | / |
Family ID | 23172707 |
Filed Date | 2003-03-20 |
United States Patent
Application |
20030055491 |
Kind Code |
A1 |
Schwartz, Robert S. ; et
al. |
March 20, 2003 |
Anti-arrhythmia devices and methods of use
Abstract
An apparatus and method of use are disclosed for treating,
preventing and terminating arrhythmias. In particular, the
apparatus is implantable within or on various tissues and
structures and is used to prevent or block conduction of aberrant
impulses. A variety of methods of the present invention may be used
to attack arrhythmias by short-circuiting impulses, inducing
fibrosis, ablating tissue or inducing inflammation. In addition,
the device and methods may also be used to treat aneurysms. The
device may also be used to treat hypertension, and to function as a
blood pressure regulator.
Inventors: |
Schwartz, Robert S.;
(Rochester, MN) ; Tassel, Robert A. Van;
(Excelsior, MN) ; Holmes, David R. JR.;
(Rochester, MN) |
Correspondence
Address: |
OPPENHEIMER WOLFF & DONNELLY LLP
840 NEWPORT CENTER DRIVE
SUITE 700
NEWPORT BEACH
CA
92660
US
|
Assignee: |
TriCardia, LLC
|
Family ID: |
23172707 |
Appl. No.: |
10/192402 |
Filed: |
July 8, 2002 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
60303573 |
Jul 6, 2001 |
|
|
|
Current U.S.
Class: |
623/1.21 |
Current CPC
Class: |
A61F 2/24 20130101; A61F
2/82 20130101; A61F 2/07 20130101; A61F 2/848 20130101; A61M 29/02
20130101; A61M 29/00 20130101; A61F 2/2481 20130101; A61F 2/90
20130101; A61F 2002/8483 20130101; A61F 2/2487 20130101; A61F
2002/821 20130101; A61F 2220/0016 20130101 |
Class at
Publication: |
623/1.21 |
International
Class: |
A61F 002/06 |
Claims
What is claimed is:
1. A method of treating cardiac arrhythmias comprising: delivering
a treatment device to a target site; manipulating said device to
conform a shape of said device to a shape of said target site;
modifying a tissue makeup at the target site; allowing said
modification of tissue makeup to proceed so as to induce a response
that results in electrically decoupling said tissue; and leaving
said treatment device implanted at said target site.
2. A method as set forth in claim 1, wherein delivering a treatment
device to a target site includes delivering said device to a body
cavity.
3. A method as set forth in claim 2, wherein delivering a treatment
device to a target site includes delivering said device to a
pulmonary vein.
4. A method as set forth in claim 3, wherein delivering a treatment
device to a target site includes delivering a stent to said
pulmonary vein.
5. A method as set forth in claim 2, wherein delivering a treatment
device to a target site includes delivering said device to an
ostium of a pulmonary vein.
6. A method as set forth in claim 5, wherein delivering a treatment
device to a target site includes delivering a stent to said ostium
of said pulmonary vein.
7. A method as set forth in claim 6, wherein manipulating said
device further conforms said target site to said shape of said
device, bringing said ostium into a lumen of said device.
8. A method as set forth in claim 2, wherein delivering a treatment
device to a target site includes delivering said device to a left
atrium.
9. A method as set forth in claim 8, wherein delivering a treatment
device to a target site includes delivering a stent to said left
atrium.
10. A method as set forth in claim 1, wherein modifying the tissue
makeup is performed by stretching said tissue.
11. A method as set forth in claim 10, wherein stretching said
tissue does not produce tissue laceration.
12. A method as set forth in claim 10, wherein stretching said
tissue induces tissue laceration.
13. A method as set forth in claim 10, wherein stretching said
tissue induces organ ischemia.
14. A method as set forth in claim 10 wherein stretching said
tissue induces fibrosis.
15. A method as set forth in claim 1, wherein modifying the tissue
makeup includes mechanically impairing at least a portion of said
tissue.
16. A method as set forth in claim 15, wherein mechanically
impairing said tissue includes penetrating said tissue with pointed
structures fixed on said treatment device.
17. A method as set forth in claim 1, wherein modifying the tissue
makeup includes mechanically changing at least a portion of said
tissue.
18. A method as set forth in claim 17, wherein mechanically
changing at least a portion of said tissue includes distorting a
geometry of an ostium such that atrial cells at an ostial site are
repositioned within a lumen of said device.
19. A method as set forth in claim 1, wherein disrupting the tissue
make-up includes introducing a bioactive agent to said target
site.
20. A method as set forth in claim 19, wherein said bioactive agent
comprises a metallic coating.
21. A method as set forth in claim 1, wherein more than one
treatment device is delivered to more than one target site.
22. A method as set forth in claim 21, wherein said target site is
selected from the group consisting of right pulmonary venous
ostium, left pulmonary venous ostium, right pulmonary arterial
ostium, left pulmonary arterial ostium, right pulmonary vein, left
pulmonary vein, right pulmonary artery, left pulmonary artery,
coronary sinus, atrial tissue and any combination thereof.
23. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes inducing inflammation.
24. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes inducing fibrosis.
25. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes inducing elastance caused by
elastin synthesis.
26. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes inducing calcification of said
tissue.
27. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes inducing cell proliferation.
28. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes inducing collagen formation.
29. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes inducing extra-cellular
changes.
30. A method as set forth in claim 1, wherein modifying said tissue
makeup at the target site includes introducing a therapeutic
drug.
31. A device for modifying conduction, electrical connection and
propagation properties in a tissue comprising: a structural
platform made of a biocompatible material; said platform
conformable to a shape of a target tissue site; said platform
having a treatment component sized and shaped to induce a fibrotic
response in said target tissue; and, said treatment component being
configured to cause sufficient fibrotic response so as to
substantially eliminate said cardiac arrhythmias.
32. A device according to claim 31, wherein said platform presses
against said target tissue to leave at most a minimal gap.
33. A device according to claim 31, wherein said structural
platform is an implantable pulmonary vein support structure.
34. A device according to claim 33, wherein said treatment
component includes pointed structures fixed on an external surface
of said pulmonary vein support structure.
35. A device according to claim 33, wherein said structural
platform is a pulmonary vein stent.
36. A device according to claim 33, wherein said structural
platform is a coronary sinus stent.
37. A device according to claim 33, wherein said structural
platform is a cardiac vein stent.
38. A device according to claim 33, wherein said structural
platform is an arterial tissue stent.
39. A device according to claim 33, wherein said structural
platform is a pulmonary artery stent.
40. A device according to claim 31, wherein said structural
platform is an implantable coronary sinus support structure.
41. A device according to claim 31, wherein said structural
platform is an implantable cardiac vein support structure.
42. A device according to claim 31, wherein said structural
platform is an implantable arterial tissue support structure.
43. A device according to claim 31, wherein said structural
platform is an implantable pulmonary artery support structure.
44. A device according to claim 31, wherein said structural
platform is conformable to substantially an internal shape of a
pulmonary vein.
45. A device according to claim 31, wherein said treatment
component includes a therapeutic substance.
46. A device according to claim 45, wherein said treatment
component includes a plurality of pointed structures.
47. A device for modifying tissue at a target tissue site of an
organ comprising: at least one deployment platform; said deployment
platform including a treatment component configured to induce a
material tissue response at said target tissue site; and said
treatment component configured to induce a material tissue response
sufficient to modify local physiologic properties of said organ so
as to achieve a desired therapeutic goal for said organ.
48. A device according to claim 47, wherein said organ includes a
heart and associated cardiopulmonary vessels.
49. A device according to claim 48, wherein said tissue site
includes tissue associated with a pulmonary vein.
50. A device according to claim 49, wherein said tissue includes
tissue comprising a pulmonary ostium.
51. A device according to claim 48, wherein said therapeutic goal
is the electrical decoupling of said target tissue.
52. A device according to claim 47, wherein said organ includes an
abdominal aorta.
53. A device according to claim 52, wherein said therapeutic goal
comprises an increase in structural integrity of said organ at an
aneurysm site.
54. A device according to claim 53, wherein said material tissue
response is a fibrotic response.
55. A device according to claim 52, wherein said therapeutic goal
is to increase elasticity of said tissue at said target tissue
site.
56. A device according to claim 47, wherein said deployment
platform is a body lumen support structure.
57. A device according to claim 56, wherein said body lumen support
structure is a stent like structure.
58. A device according to claim 48, wherein said body lumen support
structure is sized and shaped for placement into a pulmonary
vein.
59. A device according to claim 47, wherein said body lumen support
structure is sized and shaped for placement in an abdominal
aorta.
60. A device according to claim 47, wherein said deployment
platform is sized and shaped for placement on an external surface
of a body organ.
61. A device according to claim 60, wherein said deployment
platform is sized and shaped for placement on an external surface
of a pulmonary vein.
62. A device according to claim 57, wherein said treatment
component includes mechanical barbs.
63. A device according to claim 57, wherein said treatment
component includes a chemical coating on said stent-like
structure.
64. A method of inducing a material tissue response at a target
site comprising: delivering a treatment device to said target site;
ensuring contact of a treatment component of said treatment device
with tissue at said target site; inducing said material tissue
response at said target site as a result of ensuring contact of
said treatment component with said tissue; allowing said material
tissue response to continue at said target site at least until a
therapeutic goal is substantially achieved.
65. A method according to claim 64, wherein a therapeutic goal of
electrical decoupling of said tissue is achieved.
66. A method according to claim 65, wherein an electrical
decoupling resulting in the elimination of cardiac arrhythmias is
achieved.
67. A method according to claim 66, wherein delivering a treatment
device to a target site includes delivery to a region that at least
includes a pulmonary ostium.
68. A method according to claim 67, wherein delivering said
treatment device includes delivery to a region that further
includes a pulmonary vein.
69. A method according to claim 64, wherein inducing the material
tissue response includes inducing fibrosis.
70. A method according to claim 64, wherein inducing the material
tissue response includes inducing elastance.
71. A method according to claim 64, wherein a therapeutic goal of
increasing structural integrity of said tissue is achieved.
72. A method according to claim 71, wherein increasing structural
integrity includes reinforcing tissue of an abdominal aorta in a
region of an aneurysm.
73. A method according to claim 64, wherein ensuring contact of a
treatment component with said tissue includes ensuring contact of a
drug with said tissue.
74. A method according to claim 64, wherein ensuring contact of a
treatment component includes urging mechanical barbs of said
treatment device into said tissue.
Description
CROSS REFERENCE TO RELATED APPLICATIONS
[0001] The present application claims priority to U.S. Provisional
Patent Application No. 60/303,573, filed Jul. 6, 2001, whose
contents are fully incorporated herein by reference.
BACKGROUND OF THE INVENTION
[0002] Cardiac arrhythmia affects millions of people worldwide and
is broadly defined as an abnormal or irregular heartbeat that may
involve changes in heart rhythm, producing an uneven heartbeat, or
heart rates, causing a very slow or very fast heartbeat. Common
types of arrhythmias, explained in further detail below, include
bradyarrhythmias and tachyarrhythmias, both being typically
ventricular or supraventricular in origin.
[0003] Bradyarrhythmias are slow heart rhythms (e.g., less than 60
beats per minute) that may result from a diseased or failing
sinoatrial (SA) node, atrioventricular (AV) node, HIS-Purkinje, or
bundle branch system, as explained in further detail below.
Ventricular arrhythmias are arrhythmias that begin in the lower
chambers of the heart. In contrast, supraventricular arrhythmias
are arrhythmias that originate above the ventricles of the heart,
such as the upper chambers (i.e., atria) or the middle region
(e.g., AV node or the beginning of the HIS-Purkinje system).
Ventricular and supraventricular arrhythmias are generally
characterized by accelerated rates (e.g., more than 100 beats per
minute) that exceed what is considered normal heartbeat rhythms
(e.g., between 60 and 100 beats per minute).
[0004] The most common type of supraventricular arrhythmia is
atrial fibrillation, with incidence of more than a quarter-million
cases each year in the U.S. alone, and a prevalence of nearly 2.0
per 1000 US patient-years. To better understand the mechanism and
characteristics of atrial fibrillation, a general understanding of
the mechanical and electrical activity of the heart is helpful. For
this purpose, attention is directed to FIG. 1.
[0005] FIG. 1 depicts a cross-sectional diagram of a normal,
healthy heart 10. The heart 10 is a four-chamber, double-sided pump
made of muscle tissue that contracts when subjected to electrical
stimulation. The electrical stimulation that produces a heartbeat
originates in the SA node 12, located at the junction of the
superior vena cava 14 with the right atrium 16, and spreads
radially through the atria causing the muscle of the heart's upper
chambers to contract and pump blood to the ventricles. From the
atria, the electrical signal then converges on the AV node 18,
located in the right posterior portion of the interatrial septum.
The impulse from the AV node 18 then passes to the bundle of HIS
20, which branches at the top of the interventricular septum 22 and
runs subendocardially down either side of the septum, and travels
through the bundle branches 24. The signal then passes to the
Purkinje system 26 and finally to the ventricular muscle causing
the lower chambers of the heart to contract and pump blood to the
lungs and the rest of the body. After contraction of the lower
chambers, the sinus node initiates the next rhythm or heart beat
and the entire cycle is repeated. In general, it is rate of
discharge from the SA node 12 (also referred to as the normal
cardiac pacemaker) that determines the rate at which the heart 10
beats.
[0006] This synchrony of contraction between the atria and
ventricles produces a normal heartbeat. In its broadest sense,
atrial fibrillation (AF) represents a loss of synchrony whereby the
atria quiver (beating at a rate of about 600 beats per minute)
instead of beating or contracting effectively. The loss of atrial
contraction and conduction of electrical signals from the atria to
the ventricles often cause blood to pool and clot in the atria, and
especially in the atrial appendages. If the clot becomes dislodged
from the atrium, it can travel through the bloodstream and create a
blockage in a vessel that supplies blood to the brain, resulting in
stroke. It is estimated that fifteen percent of all strokes occur
in people with AF, which translates to about 90,000 strokes each
year in the United States alone.
[0007] Conventional therapy or treatment options for AF include
medication, AF suppression and surgery. Medication or drug therapy
is generally the first treatment option employed to control the
rate at which the upper and lower chambers of the heart beat.
Conventional medications used to treat AF include beta-blockers,
such as metoprolol or propanolol, and calcium-channel blockers,
such as verapamil or diltiazem, which depress conduction and
prolong refractoriness in the AV node. Other medications such as
amiodarone, ibutilide, dofetilide, propafenone, flecainide,
procainamide, quinidine and sotalol are used to affect the
electrophysiology of the heart to maintain normal sinus rhythm and
can thereby terminate or, in some cases, prevent AF. Although
anticoagulants or blood-thinners such as warfarin or aspirin are
not designed to treat AF, these medications are often used to
reduce the risk of clot formation and stroke which, as previously
discussed, often occur in patient's suffering from AF.
[0008] AF suppression, frequently a second treatment option for
patients with AF, may be accomplished using an implanted pacemaker
to stimulate the heart in a way that preempts any irregular
rhythms. In general, the pacemaker stimulates or overdrives the
heart at a rate slightly higher than its normal, intrinsic rate.
Overdriving the heart enables the device to control the heart rate
and, thereby, suppress potential episodes of AF.
[0009] Another alternative treatment for AF is surgery. In general,
an electrophysiology study is first performed to characterize the
arrhythmic event. This study usually includes mapping the exact
locations of the electrical impulses and conduction pathways along
the cardiac chambers using conventional mapping techniques. After
locating the cardiac tissue that is causing the arrhythmia, the
tissue is then surgically altered or removed to prevent conduction
of aberrant electrical impulses in the heart. One example of a
surgical procedure used to treat cardiac arrhythmias is the Maze
procedure.
[0010] The Maze procedure is an open-heart or percutaneous surgical
procedure designed to interrupt the electrical patterns or
conduction pathways responsible for cardiac arrhythmia. Originally
developed by Dr. James L. Cox, the Maze procedure involves
carefully forming a "maze" of surgical incisions (from which the
procedure's name is derived) in both atria to prevent the formation
and conduction of errant electrical impulses, while still
preserving the function of the atria. The incisions channel or
direct the electrical impulses along the heart to maintain
synchrony of contraction between the atria and ventricles of the
heart, thereby producing a normal heartbeat. In addition, resulting
scar tissue generated by the incisions also prevents formation and
conduction of aberrant electrical signals that cause AF, thereby
eradicating the arrhythmia altogether.
[0011] Although surgical intervention, such as the Maze procedure,
has proven successful in treating AF, these procedures are highly
invasive, generate many postoperative complications, require
lengthy patient recovery times and are quite costly. As a result,
minimally invasive ablation techniques have become more popular and
have been offered as an alternative treatment to surgical
intervention for patients suffering from AF.
[0012] Cardiac ablation techniques typically involve the removal or
destruction of cardiac tissue and the electrical pathways that
cause the abnormal heart rhythm. In general, cardiac ablation is
less costly, has fewer side effects and requires less recovery time
for the patient compared to more invasive procedures. There are
various methods by which a cardiac ablation procedure may be
performed. These methods and energy modalities include
cryoablation, radiofrequency (RF) ablation, laser ablation,
microwave, vaporization, balloon ablation, drug elution and
photodynamic therapy.
[0013] During an ablation procedure, an electrophysiology study is
first performed to characterize the arrhythmic event and map the
precise locations that exhibit the arrhythmia. Once these sites are
identified, an ablation catheter is maneuvered to each of these
sites and a sufficient amount of energy is delivered to ablate the
tissue. As a result, the energy destroys the targeted tissue and,
thus, makes it incapable of producing or conducting arrhythmia,
while leaving the adjacent healthy tissue intact and
functional.
[0014] In addition to ablating the specific arrhythmic tissue
sites, alternative ablation procedures, such as cardiac
segmentation procedures, have been developed to mechanically
isolate or re-direct errant electrical signals in the heart. These
procedures typically involve forming one or more linear or
curvilinear lesions in the wall tissue of the heart to segment the
cardiac chambers, similar to the above-described Maze procedure.
These segmented lesions are generally formed in the atrial tissue
of the heart, although accessory pathways, such as those through
the wall of an adjacent region along the coronary sinus, have also
been produced.
[0015] Advances in mapping and characterizing cardiac arrhythmias,
particularly AF, have provided much insight into the mechanism of
AF. Research has shown that there are at least six different
locations in the left and right atria of the heart where relatively
large, circular waves of continuous electrical activity (i.e.,
macro reentrant circuits) occur in patients suffering from AF.
Recently, it has been determined that these reentrant circuits or
wavelets may actually be confined to a limited area near the
pulmonary veins. In other words, some forms of AF may even be
triggered or maintained by a single focus of automatic firing. As a
result, several procedures have been developed whereby one or more
ablation segments or lesions are formed in tissue to isolate the
pulmonary veins and thereby block the electrical impulses that
cause AF.
[0016] Although catheter based ablation procedures are less
invasive than conventional surgical procedures, there are various
complications that may occur. Examples of possible complications
include ablation injuries, bleeding, hematoma, pericardial effusion
and cardiac tamponade, failure of the procedure, scar formation and
stenosis. In addition, the time course of lesion maturation and
scar formation following cardiac ablation procedures often result
in delayed onset of electrical isolation and high incidence of
post-operative atrial fibrillation.
[0017] In view of the above, there is a need for a minimally
invasive device and more effective and efficient methods to treat
cardiac arrhythmias. In particular, it is desirable that the
methods have a high success rate at treating arrhythmias, have
minimal to no side-effects or related complications, and can be
completed more rapidly than conventional methods. In addition, the
treatment methods should also reduce patient recovery times and
hospital costs. Overall, the method of treatment should also
improve the quality of life for patients.
BRIEF SUMMARY OF THE INVENTION
[0018] In general, the present invention contemplates an
implantable device and method for modifying conduction, electrical
connection and propagation properties in a tissue and/or treating
cardiac arrhythmias. The device comprises a structural platform
made of a biocompatible material, wherein the platform may be
conformable to a shape of a target tissue site. In addition, the
platform may also include a treatment component sized and shaped to
induce a fibrotic response in the target tissue. The treatment
component may also be configured to cause sufficient fibrotic
response so as to substantially eliminate cardiac arrhythmias.
[0019] The present invention also contemplates a method of treating
cardiac arrhythmias. In general, the method comprises delivering a
treatment device to a target site and manipulating the device to
conform a shape of the device to a shape of the target site. The
method may also include modifying a tissue makeup at the target
site and allowing the modification of tissue makeup to proceed so
as to induce a response that results in electrically decoupling the
tissue. The method may further include leaving the treatment device
implanted at the target site.
[0020] Additionally, the present invention contemplates a device
for modifying tissue at a target tissue site of an organ, wherein
the device comprises at least one deployment platform. The
deployment platform may include a treatment component configured to
induce a material tissue response at the target tissue site. In
addition, the treatment component may also be configured to induce
a material tissue response sufficient to modify local physiologic
properties of the organ so as to achieve a desired therapeutic goal
for the organ.
[0021] The present invention also contemplates a method of inducing
a material tissue response at a target site, wherein the method
includes delivering a treatment device to the target site and
ensuring contact of a treatment component of the treatment device
with tissue at the target site. The method may also include
inducing the material tissue response at the target site as a
result of ensuring contact of the treatment component with the
tissue and allowing the material tissue response to continue at the
target site at least until a therapeutic goal is substantially
achieved.
BRIEF DESCRIPTION OF THE DRAWINGS
[0022] Other features and advantages of the present invention will
be seen as the following description of particular embodiments
progresses in conjunction with the drawings, in which:
[0023] FIG. 1 is a cross-sectional diagram of a normal, healthy
heart;
[0024] FIG. 2A illustrates another embodiment of the device in
accordance with the present invention;
[0025] FIGS. 2B and 2C are sectional views of other embodiments of
an implanted device in accordance with the present invention;
[0026] FIGS. 3A-3C illustrate sectional views of various
embodiments of an implanted device in accordance with the present
invention;
[0027] FIG. 4A illustrates the various layers of a vessel;
[0028] FIG. 4B illustrates areas of high sheer at various tissue
points in accordance with the present invention;
[0029] FIGS. 5A and 5B illustrate other embodiments of the device
in accordance with the present invention;
[0030] FIGS. 6A and 6B are sectional views of various embodiments
of an implanted device in accordance with the present
invention;
[0031] FIG. 7 is a perspective view of an embodiment of the device
in accordance with the present invention;
[0032] FIGS. 8A-8C illustrate perspective views of other
embodiments of the device in accordance with the present
invention;
[0033] FIGS. 8D and 8E illustrate sectional views of various
embodiments of an implanted device in accordance with the present
invention;
[0034] FIGS. 9A and 9B illustrate perspective views of various
embodiments of an implanted device in accordance with the present
invention;
[0035] FIGS. 10A and 10B illustrate perspective views of various
embodiments of an implanted device in accordance with the present
invention;
[0036] FIG. 11 illustrates a perspective view of a ring-shaped
embodiment of the device in accordance with the present
invention;
[0037] FIGS. 12A-12C illustrate sectional views of various
embodiments of an implanted device in accordance with the present
invention;
[0038] FIG. 12D illustrates a perspective view of an embodiment of
an implanted device in accordance with the present invention;
[0039] FIG. 12E illustrates a section view of an embodiment of a
device implanted on an internal surface of a vessel in accordance
with the present invention;
[0040] FIG. 12F illustrates a perspective view of an embodiment of
a device implanted on an external surface of a vessel in accordance
with the present invention; and
[0041] FIG. 12G illustrates a perspective view of an embodiment of
an implanted device in accordance with the present invention.
DETAILED DESCRIPTION OF THE INVENTION
[0042] In one preferred embodiment of the invention, a stent-shaped
device 30 may be used to treat, prevent and/or terminate
arrhythmias. It should be noted that use of the term "stent" is not
meant to be limiting but, rather, is used for reader convenience
and brevity. In general, the device 30 resembles an "inverse sock"
fabricated from a fine netting material (e.g., Nitinol.RTM.,
spring-tempered stainless steel, cloth fiber, etc.). The netting
material may be self-expandable, causing the device 30 to tightly
conform to the structure into which it is placed. In one
embodiment, a high spatial frequency of fine material (i.e., fine
fibers, elongate elements (discussed in further detail below) or
strands) is used to fabricate the device 30. This design provides
the device 30 with added axial conformability and trans-axial
capabilities, resulting in improved tissue adhesion and fit.
[0043] The device or deployment platform 30 of the present
invention may also be characterized by its ability to bend
longitudinally and trans-axially. This capability enables the
device 30 to conform to any desired biologic shape, including, but
not limited to, the wall of an artery, vein, cardiac chamber or
other biologic target structure. In addition, the device 30 may
also be characterized by its ability to expand in a radial
direction, and continue to conform to a shape that may change. In
one embodiment, the device 30 may have a maximum size, beyond which
the device 30 does not expand. This configuration prevents the
tissue structure 36, into which the device 30 is placed, from
growing or expanding above a predetermined size.
[0044] As shown in FIG. 2A, one or more hollow protrusions 34
(discussed in further detail below) lie on an external surface of
the device 30. Upon radial expansion of the device 30, via
self-expansion, balloon expansion, or other means, the protrusions
34 pierce or embed into the tissue 36 target site of the lumen, as
illustrated in FIG. 2B. The protrusions may penetrate the vessel
wall either partially or completely (as shown in FIGS. 2B and 2C),
gaining access to any cells at any location in or on the structure.
The protrusions may also be solid rather than hollow, as may be
desirable if drug delivery is not contemplated. In addition to
anchoring the device 30, the protrusions also serve various other
functions as described in further detail below.
[0045] In one embodiment, injection from a drug delivery balloon
(not shown) causes the hollow protrusions 34 to conduct the drug to
the adventitial surface of the lumen or vessel. The drug may then
cause cell death, fibrosis or inflammation, all of which may be
used to combat arrhythmia depending on the type of drug used and
desired tissue response.
[0046] As disclosed in further detail below, the device 30 of the
present invention and its methods of use are designed to achieve a
variety of therapeutic goals including, but not limited to,
prevention, treatment and/or elimination of arrhythmias. Studies
have shown that some forms of AF originate in the pulmonary veins
44 or coronary sinus. More specifically, it has been determined
that sources of AF originate in atrial tissue that is on the
surface or ingrown into the vessel as it enters the left atrium
(i.e., at or near the ostium of the vessel entrance into the
atrium). Although further references will be made specific to the
pulmonary veins 44, it is understood that other vessels (e.g.,
coronary sinus, aorta, abdominal aorta, pulmonary artery, atrium,
cerebral vessels, etc.) are also included within the scope of the
present invention.
[0047] When positioned at this target site, the device 30,
preferably in an expanded state, eliminates or neutralizes the
electrical activity and conductivity of the atrial cells on the
pulmonary vein so that AF stimulation is either prevented (by
ablating the atrial cells) or the impulses are prevented from
propagating into the atrium. In principle, it is distortion of the
anatomy, such as the ostium, by a luminal or extra-luminal device
30 that permits sclerosis, cell death, scar formation, mechanical
injury, laceration or any combination of these results to attack
impulse stimulation and conduction. The following are but a few
examples of atrial tissue ablation methods. It is understood that
other tissue modification and ablation methods though not
specifically disclosed herein are also included within the scope of
the claimed invention.
[0048] In one embodiment, the device 30 (with or without grasping
members, as discussed in further detail below) is radially
expanded, for example via self-expansion and/or balloon expansion,
in the lumen or outside the lumen (e.g., on the adventitia) of the
pulmonary vein 44. Alternatively, the device 30 may be expanded on
an endocardial 40 or epicardial 42 surface of the heart. Expanding
the device 30 sufficiently beyond the normal diameter of the
pulmonary vein 44 causes the vessel to severely stretch, which
induces cellular changes that alter the biologic behavior of the
tissue 36.
[0049] In particular, the fine network of blood vessels called the
"vasa vasorum," which are located on the outer surface of many
blood vessels and supply the vessel wall itself with blood, are
subsequently compressed by this over-stretching, resulting in
fibrosis. This vessel over-stretch may further produce
tissue/vessel ischemia and other tension effects that may also
induce fibrosis. The fibrosis may be induced by many mechanisms
including, but not limited to, growth factors (Hypoxia Inducible
Factor-1 alpha (HIF-1alpha), Vascular Endothelial Growth Factor
(VEGF), etc.) and cytokines.
[0050] Lack of blood to the atrial cells combined together with the
fibrosis induced by the over-stretching renders the atrial cells
inactive. However, any unaffected cells upstream from the
over-stretched area can still produce the stimulatory potentials.
While these cells may still produce a stimulus, it cannot be
propagated through the fibrotic area in and/or on the vein due to
the fibrosis electrically decoupling the affected cells.
[0051] Vessel over-stretch, or other mechanical tissue change, is
accomplished initially by deployment of the device 30. However,
continued or chronic over-stretch may be achieved by simply
maintaining the oversized device 30 within the vessel. As such, the
over-stretch itself may also be enough to induce adventitial and/or
medial fibrosis simply due to the stretch process.
[0052] The purpose of the fibrosis induced by the device 30 may be
several-fold. In one embodiment, the fibrosis may serve to
mechanically prevent organ or gross body expansion. For example,
the structural component of the device 30 may be tailored to expand
only to a certain degree. Fibrosis formed in the tissue 36
functions to tightly attach or "glue" the device 30 to the tissue.
Moreover, the fibrosis serves to anchor the tissue of interest to
the supporting structure/device 30, and even integrate the device
completely into the tissue. As such, further expansion of the
biological structure is prevented due to the mechanical properties
of the device 30 and due to the fibrosis itself (which may develop
and grow to contain collagen that will further inhibit mechanical
expansion).
[0053] Alternatively, the fibrotic response from the expandable
device 30 may enable the tissue 36 to retain sufficient pliability
to maintain normal tissue (or body organ) function, yet increase
its overall structural strength. For example, fibrosis may be
induced to strengthen the wall of a cardiac ventricle when the
device 30 is placed on the inside of the chamber/structure, while
still allowing the ventricle to contract, move and fulfill its
normal function. However, the fibrosis also prevents ventricular
expansion beyond a certain predetermined size. In general, the
material make-up of this type of pliable fibrous tissue comprises
more elastin and other pliable materials than collagen.
[0054] Alternatively, the fibrotic response may be stimulated to a
severe degree causing a process of negative remodeling or
contraction. This response, well known by those skilled in the art,
results in natural scar formation that promotes wound contraction
or shrinkage. The amount of fibrosis contraction may be
controllable, via device materials, structure and other components,
and may range from no remodeling to a small/medium/large amount of
negative remodeling (resulting in contraction). This would be of
particular use in preventing expansion of an aneurysm, as in the
abdominal aorta or the cerebral vessels. The degree of remodeling
is based upon the pre-selected application and desired
response.
[0055] In addition to device expansion, device materials and
structure may also be used to biologically guide the cellular and
biologic features of the eventual tissue response and/or
therapeutic goal. For example, the device 30 may be configured to
induce elastance in the tissue or an elastin-rich fibrosis (e.g.,
stimulate elastin synthesis and cellular growth) that is quite
flexible and visco-elastic. Alternatively, the device may be
configured to stimulate growth of densely packed collagen that may
mimic the need for such bioabsorbable tissue 36. In the case of
collagen, the induced tissue 36 is quite inelastic and, thus,
prevents tissue and device expansion. As such, inducing a
simultaneous combination of elastin and collagen may simulate any
range of mechanical properties for both tissue 36 and device
30.
[0056] In an alternate embodiment, the device 30 may be configured
to control the biologic features of the fibrosis and its
cellularity. For example, a highly cellular scar may be formed or,
alternatively, less cellular tissue may be produced due to device
structure and/or materials. In another embodiment of the invention,
the device 30 may be coated with a material to stimulate less
collagen or elastin growth and increased glycose-aminoglycan and
other components of extra cellular matrix production.
[0057] There are numerous additional methods by which to induce
fibrosis, thereby preventing aberrant impulse conduction through
tissue 36. In addition to over-stretch injury, inflammation and
toxicity may also be used, as discussed further below.
[0058] Inflammation induced fibrosis may be accomplished using an
embodiment of the device 30 having prongs or tissue grabbers 34
that penetrate partially into or completely through the vessel. A
chemical irritant located on the surface of the prongs 34 causes
the desired inflammation and, thereby, induces fibrosis in the
atrial tissue 36. In general, the fibrosis occurs in and around the
three-dimensional structure and, thus, it is the structural
configuration of the device 30 that guides/determines the eventual
fibrosis configuration. As discussed in further detail below, the
device 30 may be configured in any arbitrary shape, size and
density and may include one or more of a variety of
chemicals/agents/substances. Alternatively, the device 30 may be
placed only against the interior surface and tissue ablation may
still occur on the outer surface of the biologic structure.
[0059] In an alternate embodiment, only the tips of the prongs 34
are coated with a chemical irritant, the remainder of the stalk of
each prong 34 being uncoated and, thus, inactive. Further, the
interior of the prongs 34 may house additional chemical irritant
that elutes out into the outer regions of the vein, thereby
gradually inducing a fibrotic response that prevents initiation or
propagation of the arrhythmia. Examples of such chemical irritants
include, but are not limited to, metallic copper, zinc, talc,
polymers, drug-eluting polymers, tetracycline or other
fibrosis-inducing substances.
[0060] In another embodiment of the invention, a toxic substance
may also be used to induce fibrosis. The substance is released into
the tissue 36 by the device 30, via a delivery device and/or any of
the previously disclosed methods, and either kills atrial cells or
prevents their depolarization and/or conduction. Thus, the
resulting fibrosis or scarring inhibits cell stimulation and/or
impulse propagation and, thereby, prevents or terminates the
arrhythmia. Examples of toxic substances include, but are not
limited to, metallic copper, zinc, polymers, poly-lactic acid,
poly-glycolic acid, tetracycline, talc or any other
chemicals/agents/substances capable of fibrosis induction.
[0061] Use of a conventional stent-shaped device 30 near the atrial
entrance of the pulmonary vein 44, or entrance of any other vessel,
generally distorts the ostium-atrial entrance geometry in a radial
(i.e., outward, trans-axial) direction. As previously discussed,
this configuration may be effective in attacking arrhythmias since
cell/tissue death or fibrosis may successfully interrupt the
conduction/stimulation of AF. In some instances, there may be cells
extending up and down the ostial wall that may escape the fibrotic
process. In such an instance, a flared device may be used.
[0062] Referring to FIGS. 3A and 3B, an alternate embodiment of the
device 30 of the present invention includes one or more outwardly
flared portions 46. When positioned within a patient, the flared
end 46 is located at or near the ostium or vein-atrial interface.
In addition to anchoring the device 30, this device configuration
also draws tissue into the ostium and, in so doing, causes the
cells to cease conduction, either by death or fibrosis. Inevitably,
distortion of the ostium prevents propagation or conduction of
impulses into the atrial tissue 36 and, thereby, terminates
arrhythmias.
[0063] This mechanical distortion of the tissue and/or ostium
geometry, in effect, brings the ostium into the lumen of the device
30. In other words, cells that were previously within the atrium at
the ostial site are relocated within the new lumen created by the
mechanical support of the device 30.
[0064] In another embodiment, illustrated in FIG. 3C, the flared
end 46 of the device 30 may further include a lip or ring 48 that
extends out into the atrium 50. As such, the ring 48 functions to
prevent conduction and/or generation of impulses beyond the ostium
and, in so doing, terminates AF or prevents its conduction into the
atrial tissue.
[0065] In general, the device 30 of the present invention functions
to stretch not only the vein, but also the ostium. This stretch
causes tension in the vessel wall and compression of blood supply
in either capillary form or vasa vasorum. The resulting compression
may further produce tissue ischemia and other tension effects and
induce fibrosis and/or collagen/matrix formation to interrupt
electrical impulse generation and conduction. As disclosed in
further detail below, toxic or inflammatory agents may also be
included with the device of the present invention to prevent, treat
and/or terminate arrhythmias.
[0066] Although compression forces alone may induce an inflammatory
response, the anatomy of a device-tethered vein in communication
with a free atrial wall and the relative motion between the two
structures may also induce irritability and inflammation.
Alternatively, the device 30 may also prevent or change this
relative motion. However, even in these instances, impulse
induction and conduction may still be interrupted or
eliminated.
[0067] In addition to inducing fibrosis via tissue compression,
tissue injury or chemical/agent inducement, the device 30 of the
present invention may also be used to stimulate proliferation of
cells in the adventitial or outside region of a vein or artery,
where electrically active cells reside and/or conduction occurs. An
illustration of the various tissue layers of an artery/vein is
shown in FIG. 4. In general, the vessel 52 includes three layers or
"tunics." The tunica intima 54 comprises an inner endothelial cell
layer 56 (i.e., the endothelium), a subendothelial connective
tissue 58 and a layer of elastic tissue 60 (i.e., the elastica
interna). In contrast, the tunica media 62 comprises smooth muscle
and the tunica adventitia 64 comprises connective tissue.
[0068] Cell proliferation, stimulated by the device 30 and/or
methods of the present invention, consists of fibrous tissue,
fibroblasts, myofibroblasts and other extra-cellular matrix
elements that serve to isolate the electrically active cells that
cause the arrhythmia. As such, cells are not necessarily killed or
injured, as with ablation techniques. Moreover, the proliferation
and stimulation of fibrosis (including fibroblasts, fibrocytes,
collagen and extra cellular matrix formation) occurs throughout the
vessel wall (i.e., a transmural effect), including within the
intima 54.
[0069] Cell proliferation and other transmural effects occur from
stretch and tension induced in the wall of the artery or vein. The
tension within the vessel wall, assuming the wall is relatively
thin, is governed by LaPlace's Law: T=P.times.R (wherein: T=wall
tension, P=pressure within the structure, and R=radius of the
structure).
[0070] As previously disclosed, tension can cause collapse of
arterial or venous vasa vasorum, thereby making the vessel
ischemic. Also, if the tension is too high, injury or laceration
(small to large, depending on the tension applied) to the vessel
may occur. However, it has been shown that such tension may also
actually stimulate proliferation of fibrous tissue. Therefore, by
controlling the amount of tension or injury (with or without tissue
laceration), the degree of fibrosis and proliferation can also be
controlled. Moreover, the tissue proliferation is typically
proportional to the tension and injury created.
[0071] Unlike conventional ablation technologies which promote
widespread cell death and cause the intima 54 to thicken to the
point where vascular stenosis occurs (an additional complication of
ablation procedures), the device 30 of the present invention
carefully controls the injury and, thus, does not stimulate such
stenosis. For example, the transmural effects of the device 30 and
associated methods may affect the adventitia with fibrosis;
however, the inner lumen remains relatively unaffected. Moreover,
the mechanical and/or structural support offered by the implant 30
further limits or eliminates the problem of fibrosis restricting
the lumen (which generally also induces stenosis).
[0072] For example, high shear at sharp points (such as those shown
by reference numeral 66) can be placed at various points on the
tissue 36 using the device 30, as shown in FIG. 4A, thus creating
localized fibrosis that extends transmurally from intima 54 to
adventitia 64. These focal areas can then be used to create
conduction isolation/blocks, due to the
non-arrhythmic/non-conductive nature of the fibrous tissue and
matrix. Thus, it is the fibrotic tissue that prevents conduction or
generation of arrhythmic impulses.
[0073] Alternatively, the device 30 can also be used to induce
fibrosis by inflammation induction. It has been determined that
subsequent healing of the inflammation is a long-term cause of
fibrosis. This inflammation can be purely mechanical (e.g., stress;
tension) or chemical (e.g., copper and/or zinc coating;
inflammatory agent coating). As disclosed in further detail below,
a chemical agent could also be delivered to the target site by a
local delivery mechanism (such as a local drug delivery balloon)
prior to or following device delivery. The body's response to the
inflammation is to attack the inflammation, thereby producing
excess interstitial fibrous tissue which prevents conduction or
generation of irregular signals.
[0074] In addition to inducing fibrosis, the present invention may
also be used to induce calcification of the adventitial region
within a vessel, such as the pulmonary vein 44. The calcification
process functions to harden soft tissue which interrupts electrical
conduction of atrial impulses and, thus, prevents AF impulses from
spreading to the atrium. Further, calcification of the coronary
sinus can also be performed, in the event that the coronary sinus
is involved in the arrhythmic circuit. In general, calcification
may be induced in practically any tissue region exhibiting
arrhythmia.
[0075] One method of inducing calcification is to take blood
directly from a patient and inject it into the vascular wall.
Alternatively, the blood may be concentrated, for example, by
methods of centrifugation or sedimentation by gravity. Since the
red blood cells are the apparent inducers of calcification, the
blood is first concentrated to separate out these red blood cells.
Next, a sufficient amount of red blood cells are then injected
directly into the wall of the vessel. Consequently, the tissue 36
becomes relatively hardened or inflexible due to calcification,
thereby suppressing or terminating irregular rhythm conduction.
[0076] The above-discussed injection may be accomplished using a
local drug delivery catheter such as the Infiltrator (manufactured
by Boston-Scientific Corp.). The Infiltrator has small needles
capable of delivering injectate through the needles and into the
wall of the vessel. However, care should be taken so that the
needle does not dissect the vessel wall during the injection
process. As such, small dissections may be more beneficial and
induce a higher calcific volume compared to larger dissections.
[0077] In an alternate embodiment of the invention, the device 30
may also be used to prevent or slow growth/expansion of aneurysms.
In general, the device 30 creates fibrosis and collagen deposition
and promotes cellularity of the aneurysms to hemodynamically
stabilize them, thereby preventing growth and rupture. This is
accomplished by initially generating a temporary inflammatory
reaction that heals with a fibrotic layer. The resulting fibrosis
contains cellularity, a feature that sustains the fibrosis,
attaches the device 30 to the artery wall, and provides for
long-term stabilization of the biologic-technologic hybrid
combination.
[0078] This embodiment of the device 30 comprises a percutaneous
implant that expands, either through a self-expanding mechanism
(similar to those described previously and in further detail below)
or via a balloon-expanding mechanism. The device 30 may further
exhibit excellent longitudinal and trans-axial flexibility,
enabling it to optimally conform to the vessel wall. As such, the
device 30 provides a supporting structure that effectively presses
the device 30 against the wall of the aneurysm, preventing both
expansion and rupture of the aneurysm. The fibrosis serves to
irreversibly attach the device to the vessel wall.
[0079] In general, a variety of device configurations may be used
to treat, prevent and terminate aneurysms. For example, the device
30 may be coated with a chemical (similar to those described
previously and in further detail below) that induces an
inflammatory response. In addition, the device 30 may also include
a large structural component combined with a fine netting or mesh.
This configuration may provide improved coverage of the internal
surface of the aneurysm. As such, when the inflammatory material is
pressed against or contacts the intima of the vessel, this induces
a subsequent inflammatory response. Additionally, the material may
be made to expand only to a certain point, and then become quite
stiff/rigid, thereby limiting further expansion of the device 30
and/or aneurysm.
[0080] In an alternate embodiment, the material structure or
configuration of the device 30 alone may be sufficient to stimulate
a thickened response (e.g., cellularity) or create tension that
makes the adventitia ischemic. These mechanisms may be similar to
those by which a stent induces fibrosis and neointimal thickening
in a vessel. Thus, in some instances, the device 30 simply needs to
be pressed against the wall of the vessel to induce the desired
fibrotic response. Alternatively, it may be the intimal placement
of the mesh/inflammatory coating of the device 30 that generates
the desired adventitial inflammatory response.
[0081] The above-described device 30 (and additional embodiments
further disclosed below) may be used to treat a variety of
aneurysms, such as abdominal aortic aneurysms, cerebral aneurysms
and all peripheral aneurysms of arterial or venous structures. For
example, the device 30 may be positioned in the abdominal aorta of
a patient with a small to moderate sized aneurysm. This device 30
may also be configured to prevent radial expansion both by
mechanical features of the strut and also by the fibrous structure
of the induced tissue response. As a result, the device 30 fibroses
the aortic wall, gives it a cellular nature, thickens the wall,
increases the structural integrity of the organ/abdominal aorta at
the aneurysm site, attaches to the wall and/or prevents expansion.
The aneurysm is thus "frozen" in size and cannot continue to grow
(i.e., limited device expansion also limits aneurysm expansion).
This result eliminates the need for future surgical repair and,
further, is prophylactic for aneurysm growth.
[0082] Similar to the above-described abdominal aneurysm, cerebral
aneurysms may also be treated using the device 30 of the present
invention. The device 30, generally smaller in size, strengthens
the structural integrity of the organ at the aneurysm site and,
thus, prevents both expansion and rupture due to the resulting
thickened wall structure (i.e., cellularity).
[0083] The device 30 of the present invention may be used in a
variety of additional applications. In one embodiment, the device
30 may be placed in a vein graft (e.g., saphenous vein graft) that
is beginning to degenerate. The device 30 functions to "reline" the
vein graft with a layer of device material and/or tissue 36. In
general, the density of material determines the amount of
cellularity and neointima produced.
[0084] In an alternate embodiment, the device 30 may be placed in a
vein to "shrink" the venous size, thereby restoring venous valve
patency. In yet another embodiment, the device 30 is positioned to
encircle the entire atrium, thus providing full internal support as
the fibrous tissue develops and restoring/maintaining normal atrial
contraction. In another embodiment, the device 30 may be positioned
internally of the heart as one or more atrial rings. Fibrous tissue
growth induced by the device 30 may not only prevent undesired
atrial expansion but, further, may terminate AF. In an alternate
embodiment, the internally implanted device 30 promotes formation
of an endocardial encircling ring that prevents ventricular infarct
expansion and, in some instances, ventricular remodeling.
[0085] In another embodiment, the device 30 of the present
invention may be an elastic band, passive (i.e., requires no
energy) and percutaneously implantable device 30 that functions as
an arterial shock absorber when implanted at a target site. For
example, when placed in an artery or other structure, the device 30
modifies the elasticity of that structure (i.e., the
pressure-volume relationship of the structure in a fixed manner
that may be linear, or any other simple mathematical function).
[0086] To better understand the mechanisms and functional
characteristics of this embodiment of the device 30, a general
review of blood flow and blood pressure and their affects on
vessels/organs is helpful.
[0087] In general, blood pressure and flow are in phase (i.e., the
phase angle between them is zero) when pulsatile flow is instituted
in a purely resistive structure. However, blood flow within the
human vasculature is further complicated by curves, bifurcations
and vessel compliance. As such, the normal human aorta and large
capacitance vessels are not purely resistive structures. The
pressure-flow relationship in these organs is partially capacitive,
since the walls of these organs expand and contract with the
pumping of blood. As a result, pressure and flow differ in phase
and, in particular, flow typically leads pressure for pulsatile
waveforms, such as those induced by a bolus of blood ejected by the
heart into the aorta with each cardiac cycle.
[0088] As the human vessel ages it becomes significantly stiffer,
resulting in a more purely resistive (less compliant) structure.
This means that the blood pressure rises simply because of the
arterial stiffness. The heart must expend more work on each
heartbeat to pump the blood throughout the body at the higher
pressure. Arterial stiffness is a major cause of high blood
pressure and, in the long turn, heart failure if the hypertension
is not treated. Literally millions of people are under treatment
(typically with medication) for hypertension and heart failure.
[0089] The device 30 of the present invention, when elastic and
placed in the aorta or great vessels, restores elasticity (as
previously described and discussed in further detail below) to
aging cardiovascular systems that have become stiff, rigid, and
cause hypertension. If the applied pressure-volume relationship of
the implantable device 30 is appropriately nonlinear, the device
becomes a "blood pressure regulator." As such, the device 30 allows
any blood pressure up to a pre-defined limit, but prevents higher
blood pressures than that limit by expanding to accommodate the
volume of ejected blood and prevent pressure rises. By restoring a
capacitive vector to the central circulation, the device 30
actually lowers blood pressure without pharmacology.
[0090] In general, the device 30 functions as a passive, hydraulic
system that absorbs volume in proportion to pressure and has a
rapid frequency response. In one embodiment, the device 30 is
configured as a scaffold (with, for example, a stent-like
configuration) that grows into the artery and becomes part of the
vessel. In effect, the device 30 functions as an "arterial shock
absorber" after implant. The following are several examples of
various embodiments of the device 30 used to treat
hypertension.
[0091] In one embodiment, shown in FIG. 5A, the stent-like device
30 includes two concentric, tubular-shaped members 68, 70 that
function as a shock-absorber to blood flow/pressure. For example,
as a bolus of blood is pumped out of the heart and into the target
site where the device 30 is positioned, the inner member 68 of the
device 30 compresses against the outer member 70, thereby
absorbing, partially or totally, the volume of ejected blood to
maintain normal pressure within the system. Generally, the amount
of compression is proportional to the pressure; however, nonlinear
compression-pressure relationships may also be desirable (as
described above) to generate unique properties, such as blood
pressure regulation. In some instances, the volume of fluid/blood
absorbed may be up to 20% or more of the stroke volume.
[0092] In an alternate embodiment, the device 30 may be a fiber
band on a circumferential support structure that stimulates elastin
growth. As shown in FIGS. 8C-8E, the device 30 may be partially or
completely covered with elastin or an elastin epitope. In this
configuration, the device 30, in essence, functions to restore the
capacitive vector to the vessel/organ 36. For example, as the heart
ejects a bolus of blood into, for example, the aorta, the elastin
expands to partially accept the volume, thereby preventing the
blood pressure from rising as high as would be the case were the
vessel rigid (i.e. without the device 30). In general, the amount
of expansion is proportional to the pressure.
[0093] As discussed in further detail below, the device 30 may be
fabricated from a variety of materials and configured into various
designs. In one embodiment, the device 30 may be completely
elastic, due to its material and/or structural characteristics.
Alternatively, the device 30 may be elastic and include pores that
promote cellular in growth so that the device 30 becomes a living
structure within the body.
[0094] By restoring the elastic pressure-volume capacitive
relationships, the device 30 is useful as a passive (e.g.
non-powered), non-pharmacologic method for treating heart failure.
This is true not only because blood pressure is lowered, but also
because the energy of the failing heart is more efficiently coupled
to the arterial system via the compliant nature of the device 30.
Thus, if the device 30 functions with minimal energy loss, then the
energy is more efficiently coupled.
[0095] For example, in one embodiment of the invention, illustrated
in FIG. 5B, one or more springs 72 (e.g., Nitinol.RTM. springs) are
located between the two membranes 68, 70 of the device 30. The
springs enable the device 30 to function with minimal energy loss
such that the resulting system actually conserves energy, an
important feature/attribute for cases with failing hearts.
[0096] In an alternate embodiment (not shown), the biocompatible
device 30 includes inflammation inducing features (e.g.,
structural, chemical, etc.) either on the entire device 30 or on a
portion of the device 30. The inflammation may further induce
fibrosis which functions to "glue" the device 30 to the inside of
an artery or other organ.
[0097] In yet another embodiment, the device 30 may also be
configured to function as a bladder-like system. This system may
include compressibility features that decrease volume with
increasing blood pressure.
[0098] Although generally passive, the device 30 may include
certain features or mechanisms that are externally programmable.
Examples of such features/mechanisms include, but are not limited
to, variable compliance, variable compressibility, and variable
expandability. For example, referring to FIG. 5B, one or more
Nitinol.RTM. springs of the device 30 may be heated externally in
order to change the spring constant. Changing the spring constant
may increase (or decrease, depending on the type of change) the
amount of device compressibility to that which is more proportional
to the hypertension. The ability to transcutaneously heat
Nitinol.RTM. may yield other programmable features, not disclosed
herein but known to those skilled in the art, which are also
included within the scope of the claimed invention.
[0099] In another embodiment of the invention, the device 30 may
include feedback capabilities. For example, the device 30 of the
present invention may measure and transmit pressure readings to
another implantable device, such as a biventricular pacing system.
This configuration permits literal and real-time feedback to
optimize energy transfer and heartbeat within the system.
[0100] As previously described, the device 30 is generally a
passive, non-powered device. However, these communication or
sensing features of the device 30 may require a source of power in
order to properly function. In one embodiment, this can be
accomplished via the compression/expansion capabilities of the
device 30. As the blood pressure causes the device 30 to
compress/expand, this energy, in turn, can be captured to generate
electrical energy which can then be transferred to power the
system. Alternate energy generating systems and means, not
disclosed herein but known to those skilled in the art, may also be
used and are also included within the scope of the claimed
invention.
[0101] Referring to FIGS. 6A, 6B and 7, an alternate embodiment of
the implantable device 30 in accordance with the present invention
includes at least one elongate element 32 and one or more
protrusions or grasping members 34 that extend into or through
tissue 36. In general, the device 30 comprises a sterile
biocompatible material and may be percutaneously or surgically
implanted on either an endocardial or epicardial surface of the
heart. In an alternate embodiment, the device 30 may be implanted
within a lumen of the heart. The size and configuration of the
device 30, including the materials from which it is made, are
tailored to properly conform to tissue requirements and desired
device-induced results. Although the invention as disclosed herein
generally refers to the heart, other body organs and cavities, such
as pulmonary veins, coronary artery, coronary vein, renal artery,
renal vein, aorta, cerebral vessels, coronary sinus or other
similar cavities/organs, are also included within the scope of the
present invention.
[0102] As shown in FIG. 8A, an alternate embodiment of the device
30 of the present invention may include a plurality of elongate
elements 32 configured to form a mesh-shaped device 30. This device
30 configuration not only increases the surface area of the device
30 that contacts tissue 36, but may also enhance the structural
integrity, flexibility and tissue adhesion characteristics of the
device 30.
[0103] In an alternate embodiment, shown in FIG. 8B, the elongate
elements 32 may be rod-shaped to form a type of fiber. The
fiber-shaped element 32 may be used alone or in combination with
other devices. For example, referring to FIG. 8C, the fiber-shaped
element 32 may be combined with a fabric or net 38, thereby
functioning as a structural component of the resulting device 30.
During use, the device 30 produces the desired fibrotic response
through proper tissue contact, shown in FIG. 8D, and/or by becoming
integrated within, the tissue 36, as shown in FIG. 8E. Additional
details concerning device structure and tissue response are
described in further detail below.
[0104] One or more of the elongate elements 32 or simply portions
of the elongate elements 32 may also be configured to an increased
thickness/diameter, which may provide increased strength and
structural integrity to the overall device 30. Additional device 30
configurations including, but not limited to, ribbon-shaped,
spherical, cubical, tubular, rod-shaped, net-shaped, ring-shaped,
sheet-shaped and woven, including combinations thereof, are also
within the scope of the claimed invention.
[0105] The grasping members 34 of the present invention are
generally designed to be pushed into and attached to tissue 36,
such as muscle, as described in further detail below. These
grasping members 34 anchor the device 30 to the tissue 36 and,
thus, prevent the device 30 from slipping/dislodging or causing
embolization within the patient. As such, the grasping members 34
may be configured as darts, studs, barbs, prongs, pointed
structures, capped rods and other designs for secure attachment to
and/or permanent placement within tissue 36.
[0106] A variety of methods may be used to urge the grasping
members 34 into the tissue 36. Examples of such methods include,
but are not limited to, a radially expanding balloon, a
self-expanding device 30 (due to material characteristics of the
device 30 or structural characteristics, such as internal struts),
an expanding tool, or mechanical force by a physician.
[0107] Although the device 30 illustrated in FIGS. 6A-8E includes
at least one grasping member 34 designed to penetrate partially or
completely through tissue 36, the device 30 may also be configured
to include no grasping members 34. Tissue adhesion or attachment
may be accomplished via structural or chemical characteristics of
the device 30. For example, the device 30 may be configured to
conform and, thereby, adhere to an internal or external area of a
body cavity. Alternatively, the device 30 may be fabricated from
porous materials that promote tissue adhesion and subsequent
biological anchoring. Permanent cellular in-growth may further
transform the device 30 into a living structure. As such, the
living nature of the device 30 permits it to become integrated and
thereby last for long periods of time within the body.
[0108] Examples of porous materials used with the device 30 of the
present invention include, but are not limited to, ceramics,
alumina, silicon, Nitinol.RTM., stainless steel, titanium, porous
polymers, such as polypropylene, ePTFE, silicone rubber,
polyurethane, polyethylene, acetal, nylon, polyester, and any
combination of such materials. Although these materials (and others
not specifically described, but included in the scope of the
claimed invention) may not be inherently porous, various
manufacturing and processing techniques may be used to give the
materials the desired porosity characteristics.
[0109] In one embodiment of the invention, the device 30 is made of
a conductive material, such as stainless steel. Alternative
biocompatible materials including, but not limited to, metals,
ceramics, plastics, bioabsorbable materials, bioresorbable
materials, biostable materials, absorbable materials,
non-absorbable materials or biomaterials, either alone or in
various combinations, may also be used.
[0110] In general, the device 30 of the present invention is used
to treat, prevent and/or terminate arrhythmias. In one embodiment
of the invention, the device 30 is made of a conductive material,
such as a metal, and functions as a voltage clamp to short circuit
an arrhythmia. During use, the grasping members 34 of the device 30
are pushed into the target cardiac tissue 36. A single device 30 or
multiple devices 30 may be placed over a portion or
circumferentially around a cardiac chamber, such as the atrium or
ventricle, depending on the type and location of the arrhythmia.
For example, in the case of multiple devices 30, the devices 30 may
be placed in parallel (i.e., multiple equatorial bands, shown in
FIGS. 9A and 9B) or combined to form equatorial and polar rings,
shown in FIGS. 10A and 10B, respectively.
[0111] After the grasping members 34 are inserted into tissue 36,
the metallic properties of the device 30, particularly the grasping
members 34 which are also made of metal, cause the device 30 to
hold the intramyocardial tissue 36 at the same isoelectric
potential across the entire device 30. Additionally, when the
grasping members 34 of the device 30 extend through the cardiac
tissue 36, the isoelectric potential also extends through the
entire transmural muscle. As such, since all device-contacted
muscle must be isoelectric, the device 30 short-circuits the
arrhythmia. Examples of arrhythmias that may be short-circuited by
the device 30 include, but are not limited to, atrial fibrillation,
reentrant supraventricular tachycardia (SVT), ventricular
tachycardia (VT) and Junctional Tachycardia.
[0112] In an alternate embodiment, the device 30 of the present
invention may also be used to isolate localized sources of
arrhythmias. As previously discussed in the Background of the
Invention, some arrhythmias may be triggered or maintained by a
single focus of automatic firing. To prevent the aberrant signal
from propagating throughout the cardiac muscle, the elongate member
32 is configured into a generally ring-shaped device 30, as
illustrated in FIG. 11. However, it is understood that other device
configurations optimized to isolate the particular arrhythmia at a
specific tissue site may also be used and are hereby included
within the scope of the claimed invention.
[0113] The device 30 is then positioned to contact the tissue 36
and surround that portion of muscle from which the arrhythmia
originates. For example, the device 30 may be located on a portion
of either an endocardial 40 or epicardial 42 surface of an atrium,
ventricle or vessel (such as a pulmonary vein), shown in FIGS. 12A,
12B, 12C and 12D. Alternatively, as illustrated in FIGS. 12E, 12F
and 12G, the device 30 may be positioned to surround one or more of
the pulmonary veins 44 on either an endocardial 40 or epicardial 42
surface of the heart. As another example, the device 30 may be
placed on an internal surface or an external surface of a pulmonary
vein 44. The metallic nature of the device 30 together with its
tissue-contacting characteristics create a block thereby preventing
conduction of the impulse beyond the confines of the device 30 and,
ultimately, short-circuiting the arrhythmia.
[0114] In another embodiment of the invention, one or more
biologics, drugs or other chemicals/agents may also be included
with the device 30. The chemical may be bound, for example, to at
least a portion of the surface and/or interior of the elongate
members 32 and/or grasping members 34 of the device 30. For
example, the grasping members 32 may be hollow allowing the
chemical to elute from the hollow area of the grasping members 34
and into the tissue 36. Alternatively, if the device 30 is
fabricated from porous materials (as discussed above), the chemical
may be contained within and released from the pores and into the
tissue 36.
[0115] During use, the chemical/agent is released into the
myocardial tissue 36 or simply interfaces with the tissue 36 as it
contacts the device 30. In an alternate embodiment, the chemical,
which may be a coating that is bioabsorbable (or biostable),
dissolves or erodes and disappears over time. In yet another
embodiment, the chemical promotes formation of an endothelial
lining and, eventually, a neointimal layer, thereby encasing the
device within the tissue. Alternatively, the chemical may be an
anti-thrombotic material that functions to prevent clot formation
and/or embolization from the implanted device 30.
[0116] As a result, the chemical may depress or prevent conduction
of aberrant impulses, affect the electrophysiology of the heart to
maintain normal sinus rhythm, act as a therapeutic agent, terminate
arrhythmias or induce other desired tissue and system responses.
Examples of these chemicals/agents include, but are not limited to,
blood, copper, zinc, nickel, polylactic acid, polyglycolic acid,
heparin, platelet glycoprotein IIb/IIa inhibiting agent,
tetracycline, lidocaine, starch, paclitaxel, adriamycin, alcohol,
fibrosis inducing agents, inflammatory inducing agents,
anticoagulants, polymers, drug-eluting polymers, macrophage
chemoattractant protein, chemoattractants, therapeutic drugs and
other agents/chemicals.
[0117] In addition to providing an effective means of treating
arrhythmias, the device 30 and methods of use of the present
invention effectively reduce pain, infections and postoperative
hospital stays. Further, the various treatment methods also improve
the quality of life for patients.
[0118] Although the invention has been described in terms of
particular embodiments and applications, one of ordinary skill in
the art, in light of this teaching, can generate additional
embodiments and modifications without departing from the spirit of
or exceeding the scope of the claimed invention. Accordingly, it is
to be understood that the drawings and descriptions herein are
proffered by way of example to facilitate comprehension of the
invention and should not be construed to limit the scope
thereof.
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