U.S. patent application number 12/541112 was filed with the patent office on 2009-12-03 for ventricular infarct assist device and methods for using it.
This patent application is currently assigned to The Foundry, LLC. Invention is credited to Bernard H. Andreas, Hanson S. Gifford, III.
Application Number | 20090299133 12/541112 |
Document ID | / |
Family ID | 25508088 |
Filed Date | 2009-12-03 |
United States Patent
Application |
20090299133 |
Kind Code |
A1 |
Gifford, III; Hanson S. ; et
al. |
December 3, 2009 |
VENTRICULAR INFARCT ASSIST DEVICE AND METHODS FOR USING IT
Abstract
This relates to surgical devices and methods of using them. In
particular, the devices are used to support and to reform
myocardial tissue in the region of and across an infarct. The
devices provide tension across the infarct in varying degrees by
attachment of the device to the myocardium at sites adjacent the
infarct. A support-providing component across the infarct, between
the heart attachment sites, provides support to the myocardial wall
and support across the infarct. Optionally, but preferably, the
support-providing component includes a time-delay element that
variously may allow the device to be introduced onto the myocardial
surface and to change the support of the support element over
time.
Inventors: |
Gifford, III; Hanson S.;
(Woodside, CA) ; Andreas; Bernard H.; (Redwood
City, CA) |
Correspondence
Address: |
TOWNSEND AND TOWNSEND AND CREW, LLP
TWO EMBARCADERO CENTER, EIGHTH FLOOR
SAN FRANCISCO
CA
94111-3834
US
|
Assignee: |
The Foundry, LLC
Menlo Park
CA
|
Family ID: |
25508088 |
Appl. No.: |
12/541112 |
Filed: |
August 13, 2009 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
10695649 |
Oct 27, 2003 |
|
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|
12541112 |
|
|
|
|
09964070 |
Sep 25, 2001 |
6685620 |
|
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10695649 |
|
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Current U.S.
Class: |
600/37 |
Current CPC
Class: |
A61B 2017/0419 20130101;
A61F 2/2481 20130101; A61B 17/00234 20130101; A61B 17/0401
20130101 |
Class at
Publication: |
600/37 |
International
Class: |
A61F 2/00 20060101
A61F002/00 |
Claims
1. A device for reforming the shape of a beating heart, said device
comprising: a first anchor adapted to adhere directly to a first
surface of the heart, the first surface adjacent the damaged
tissue; a second anchor adapted to adhere directly to a second
surface of the heart, the second surface adjacent the damaged
tissue, and opposite the first surface; and a resiliently
elongatable support member having a first end and a second end
opposite the first end, wherein the first anchor is coupled to the
first end, and the second anchor is coupled to the second end, the
support member adapted to resiliently contract from an elongated
configuration to a contracted configuration so as to decrease
distance between the first and the second ends over a period of
time following implantation in the heart tissue.
2. The device of claim 1, wherein the first anchor comprises a
fastener coupled therewith and adapted to penetrate at least
partially into the heart so as to secure the first anchor
thereto.
3. The device of claim 1, wherein the second anchor comprises a
fastener coupled therewith and adapted to penetrate at least
partially into the heart so as to secure the second anchor
thereto.
4. The device of claim 1, further comprising an adhesive, wherein
the adhesive adheres at least one of the anchors to its respective
surface.
5. The device of claim 1, wherein the support member comprises a
first spring.
6. The device of claim 5, wherein the first spring comprises a flat
spring or a coil spring.
7. The device of claim 5, wherein the support member comprises a
second spring.
8. The device of claim 7, wherein the second spring comprises a
flat spring or a coil spring.
9. The device of claim 1, wherein the support member comprises a
time delay member coupled with the support member, the time delay
member having a first state in which contraction of the support
member is prevented, and a second state in which the support member
can contract.
10. The device of claim 9, wherein the time delay member comprises
a biodegradable polymer.
11. The device of claim 1, further comprising a radiopaque marker
attached to one or more of the anchors or to the support
member.
12. The device of claim 1, further comprising a bioactive agent
coupled with at least one of the anchors or the support member, the
bioactive agent adapted to be delivered therefrom to facilitate
healing of the damaged tissue.
13. The device of claim 12, wherein the bioactive agent promotes
angiogenesis in the damaged tissue and in tissue adjacent
thereto.
14. A method for reforming the shape of a beating heart, said
method comprising: providing a support device having first and
second anchors and a support member therebetween; attaching the
first anchor directly to a first sufficiently healthy surface of
the heart, wherein the first surface is adjacent the damaged
tissue; attaching the second anchor directly to a second
sufficiently healthy surface of the heart, wherein the second
surface is adjacent the damaged tissue, and opposite the first
surface; resiliently contracting the support member to draw the
first and the second sufficiently healthy surfaces together over a
period of time following attachment of the first and second anchors
thereby reforming the shape of the heart.
15. The method of claim 14, wherein the first anchor comprises a
fastener and the step of attaching the first anchor comprises
positioning the fastener at least partially into the heart.
16. The method of claim 14, wherein the second anchor comprises a
fastener and the step of attaching the second anchor comprises
positioning the fastener at least partially into the heart.
17. The method of claim 14, wherein the step of attaching the first
anchor or the step of attaching the second anchor comprises bonding
one of the anchors to its respective surface.
18. The method of claim 14, wherein the step of drawing the first
surface to the second surface comprises providing a time delay
member coupled with the support member, the time delay member
having a first state in which contraction of the support member is
prevented, and a second state in which the support member can
contract.
19. The method of claim 18, wherein the step of drawing the first
surface to the second surface comprises biodegrading the time delay
member.
20. The method of claim 14, further comprising delivering a
bioactive agent from the support device to the damaged tissue, the
bioactive agent adapted to facilitate healing of the damaged
tissue.
21. The method of claim 20, wherein the bioactive agent promotes
angiogenesis in the damaged tissue and in tissue adjacent
thereto.
22. The method of claim 14, wherein the heart is reformed so as to
reduce mitral regurgitation.
Description
CROSS-REFERENCES TO RELATED APPLICATIONS
[0001] This application is a continuation of U.S. patent
application Ser. No. 10/695,649 (Attorney Docket No.
020979-002310US), filed Oct. 27, 2003, which is a continuation of
U.S. patent application Ser. No. 09/964,070 (Attorney Docket No.
020979-002300US), filed on Sep. 25, 2001, the full disclosures of
which are incorporated herein by reference.
FIELD OF THE INVENTION
[0002] This invention relates to surgical devices and to methods of
using them. In particular, the devices are used to support and to
reform myocardial tissue in the region of and across an infarct.
The devices provide support to the infarct in varying degrees by
attachment of the inventive device to the myocardium at sites
adjacent the infarct. A supporting component across the infarct,
between the heart attachment sites, provides support to the
myocardial wall and to the infarcted region. Optionally, but
preferably, the supporting component includes a time delay element
that variously may allow the device to be safely manipulated and
introduced onto the myocardial surface and then to change the
distance between the ends of the support member or the amount of
infarct support over time.
BACKGROUND OF THE INVENTION
[0003] This invention relates to devices and processes for
treating, in particular, ischemic heart diseases, particularly
myocardial infarction. The term "myocardial infarction" generally
refers to the death of that tissue resulting from either inadequate
blood supply or an absolute lack of blood supply to that tissue
region. Classically, a "heart attack" occurs with the sudden onset
of specific symptoms, followed by a specific series of
electrocardiographic changes and a rise in serum levels of enzymes
released from the myocardium. Total occlusion of a major coronary
artery by thrombosis creates an infarcted area involving virtually
the full thickness of the ventricular wall in the region of the
heart supplied by the blocked artery. The occlusion of the coronary
artery may occur more slowly and not completely block the artery.
The resulting infarction then occurs over a significant period of
time and may be less localized.
[0004] In the United States, myocardial infarction occurs in
upwards of two million people a year. Less than half of those
persons are hospitalized and a quarter to a third of them die
suddenly outside of the hospital.
[0005] Coronary artery thrombosis almost always occurs at the site
of an atheromatous plaque. Although plaque is present, it does not
typically severely narrow the lumen of the affected artery before
the thrombosis occurs. The formation of the thrombus is caused by a
variety of events and likely may be considered to be the formation
of a breakage in the intimal lining or hemorrhage within the
plaque. Generally, plaques that are amenable to such fissuring are
soft, rich in lipid, and formed in such a way that a fibrous cap
overlies the softer lipid material. The fissure frequently occurs
at the junction of the fibrous cap and a normal intima. As is a
case with any vascular injury of this type, the response is an
aggregation of platelets. The platelets begin a cascade of the
release of thromboxane, promoting further platelet aggregation,
coronary vasoconstriction, further reduction of blood flow, and
formation of a thrombus. These coronary occlusions occur without
warning signs in most instances, although physical activity and
stress may have some role in causation.
[0006] In any case, these coronary accidents are easily detectable
by electrocardiogram. Similarly, the treatment of acute myocardial
infarction is typically via medication. Treatment of pain, perhaps
by administering sublingual nitroglycerin is common. The goal of
medicinal therapy in such cases is the opening of the partially
closed artery. Administration of thrombolytics such as
streptokinase, alteplace (recombinant tissue plasminogen
activator-rt-PA), and anistreplase (anisoylated plasminogen
streptokinase activated complex or APSAC) may be had. In some
instances, angioplasty is administered, typically without
thrombolysis, but on rare occasions with such a drug.
[0007] It is uncommon to treat infarcts with surgery unless there
have been anatomic complications of the myocardial infarction,
e.g., ventricular septal rupture, mitral regurgitation, ventricular
aneurysms, ATC. Two procedures for dealing with myocardial infarcs
via surgery are the Batista Procedure and the Dor Procedure, named
after the surgeons who first performed them. In the Batista
Procedure, the surgeon resects a portion of the heart to change its
shape to a more correct cone shape. The Batista Procedure removes
both healthy tissue and tissue not so healthy. The procedure is
said not to be in favor due to high complication rates.
[0008] The Batista Procedure was replaced by a surgery known as the
Dor Procedure. The Dor Procedure is less aggressive and apparently
more effective. The Dor Procedure is typically used after an
aneurysm forms following the presence of an infarct. The Dor
Procedure is also called "endoventricular circular patch plasty" or
EVCPP. The procedure creates a looped stitch pattern around a dead,
scarred aneurysm to shrink the dead area. Any remaining defect may
be covered by a patch made from DACRON or tissue. The aneurysm scar
is closed over the outside of the patch to make the overall site
more stable.
[0009] A variation of the Dor Procedure is called the SAVR
Procedure, which stands for Surgical Anterior Ventricular
Remodeling. This procedure opens the affected ventricle through the
"akinetic" segment. A surgeon feels the beating heart and detects,
using the fingers, where the heart muscle is not working. A suture
is placed at the junction of a beating muscle and non beating
muscle that is typically semicircular, purse string suture shape. A
patch is then installed.
[0010] There are a variety of devices which are applied to the
heart for treatment of congestive heart failure (CHF). Patents
owned by Abiomed (U.S. Pat. Nos. 6,224,540; 5,800,528; 5,643,172)
show a girdle like device situated to provide structure to a
failing heart. U.S. patents owned by Acorn Cardiovascular, Inc.
(U.S. Pat. Nos. 6,241,654; 6,230,714; 6,193,648; 6,174,279;
6,169,922; 6,165,122; 6,165,121; 6,155,972; 6,126,590; 6,123,662;
6,085,754; 6,077,218; 5,702,343) show various devices, also for
treatment of CHF, which typically include a mesh sock-like device
placed around the myocardial wall. U.S. patents to Myocor, Inc.
(U.S. Pat. Nos. 6,264,602; 6,261,222; 6,260,552; 6,183,411;
6,165,120; 6,165,119; 6,162,168; 6,077,214; 6,059,715; 6,050,936;
6,045,497; 5,961,440) show devices for treatment of CHF generally
using components which pierce the ventricular wall.
[0011] None of the devices described in any of these patents
suggests the devices and methods disclosed here.
BRIEF SUMMARY OF THE INVENTION
[0012] This invention is a heart tissue supporting device
comprising a.) at least one first heart tissue adherence region
(each adapted to adhere to selected first heart tissue regions on a
heart surface), b.) at least one second heart tissue adherence
region, separated from the first heart tissue adherence regions and
each adapted to adhere to selected second heart tissue regions on a
heart surface, and c.) at least one support providing member
situated variously to maintain support to the tissue located
between the first heart tissue adherence regions and the second
heart tissue adherence regions.
[0013] The first and second heart tissue adherence regions may be
at least partially surrounded by a region that is substantially non
adhering to heart tissue. The tissue support maintaining member is
sized and placeable to maintain the distance between the first and
second heart tissue contact regions. The device may include a
connector strap that is substantially non adhering to heart tissue
and is configured to connect the first and second heart tissue
adherence regions around the heart not adjacent the infarct to form
a loop surrounding the heart. The portions of the device that do
not adhere to heart tissue may be made from non adherent materials
such as woven or non woven polymeric fabrics, e.g.,
polyfluorocarbons and polyolefins, such as polytetrafluoroethylene
(PTFE or TFE), ethylene-chlorofluoroethylene (ECTFE), fluorinated
ethylene propylene (FEP), polychlorotrifluoroethylene (PCTFE),
polyvinylfluoride (PVF), polyvinylidenefluoride (PVDF),
polyethylene (LDPE, LLDPE, and HDPE), and polypropylene.
[0014] The portions of the device that should adhere to the heart
may be made of materials known to adhere, adhering materials
selected to allow ingrowth such as woven or non woven polymeric
fabrics desirably selected from polyethyleneterephthalate, cotton,
and expanded polyfluorocarbons having internodal spacing suitable
for intergrowth.
[0015] The device includes at least one support maintaining member,
often having a spring with opposing ends attached between the at
least one first heart tissue adherence region and the at least one
second heart tissue adherence region. The springs may be coiled or
flat or other suitably shape. The support maintaining member
further desirably includes a time delay member adapted to provide a
period of time between the introduction of the device onto the
heart and the initiation of a movement of the first heart tissue
adherence region towards the second and/or to provide a period of
time over which the distance between the first heart tissue
adherence region and the second heart tissue adherence region
varies.
[0016] The time delay member may be coated with, embedded in, or be
formed of a suitable biodegradable material.
[0017] The first or second heart tissue adherence regions may have
surfaces selected to allow or enhance ingrowth of heart tissue into
those regions. The regions may be, e.g., not smooth, roughened,
nubbed, perforated, etc.
[0018] As appropriate, the surfaces of the device, e.g., the heart
tissue supporting member, the time delay member, and the first and
second heart tissue adherence regions, may be treated with at least
one angiogenesis composition.
[0019] The first and second heart tissue adherence regions may be
made to adhere to the heart tissue in a variety of ways, e.g., by
mechanical fasteners, by ingrowth, by adhesives, or other
materials, devices or procedures that cause the device component to
adhere to the heart.
[0020] The invention includes methods for use of the device itself,
methods of supporting a localized or regional area of a heart
particularly where that region includes an infarct or region that
has been surgically altered. Procedures typically include the steps
of adhering a first tissue contact area of a supporting member to
the myocardial wall at a first tissue site adjacent the infarct or
other region to be supported, adhering a second tissue contact area
of the supporting member to the myocardial wall at a second tissue
site adjacent the infarct or other region to be supported but
adapted for positioning the supporting member across the region of
concern, and maintaining the distance between or advancing the
first tissue contact area towards the second tissue contact area.
The procedures may involve adhesively connecting the first and
second tissue contact areas respectively to first and second tissue
sites or by allowing ingrowth or by mechanically fastening a
contact area to the tissue site. The step of advancing the two
tissue contact area towards each other may take place as a result
of the erosion of a bioerodible material situated between those
first and second tissue contact areas. The advancing step may
comprise eroding a bioerodible material time delay member
associated with the support maintaining member in such a way that
it tends to tend to hold the spring in extension until after
functional biodegradation in the human body. The advancing step may
include eroding the support maintaining member itself when that
member is made up of a bioerodible material.
[0021] Finally, the invention includes a fastener made up of a
shaft terminating at one end in a tissue piercing end and having a
collar end at the opposite end, a collar slidable on the shaft, and
a braided member concentric to the shaft, affixed to the shaft
substantially adjacent the tissue piercing end. The fastener
operates in the following way. The collar on the on the shaft
slides towards the tissue piercing end and expands the braided
member. The region between the collar and the braided member is
appropriate for fastening. The braided member may be affixed to the
collar at the end opposite the tissue piercing end. Desirably, the
fastener includes a stop for affixing the shaft to the collar after
the braided member has been expanded.
BRIEF DESCRIPTION OF THE DRAWINGS
[0022] FIG. 1 shows an anterior view of a human heart having a
ventricular infarct region.
[0023] FIGS. 2A and 2B show placement of two variations of the
inventive device around an infarcted region. The views are both of
an anterior view of the heart.
[0024] FIGS. 3A, 3B, and 3C show cross sectional views of a
myocardial wall, placement of a variation of the inventive device,
and the effect resulting from use of that device.
[0025] FIGS. 4A, 4B, and 4C are similar to FIGS. 3A 3C but depict a
differing use of the time delay element of the inventive
device.
[0026] FIGS. 5 and 6 show variations of the inventive device.
[0027] FIG. 7A shows a variation of the device including a band to
be wrapped around a diseased heart. FIG. 7B shows the device shown
in FIG. 7A without the support inducing element.
[0028] FIGS. 8A, 9A, and 10A show front views of various supporting
members made according to the invention. FIGS. 8B, 9B, and 10B show
cross sections, respectively, of the springs shown in FIGS. 8A, 9A,
and 10A.
[0029] FIGS. 11 and 12 show a number of surfaces for the tissue
adherence regions of the inventive device.
[0030] FIGS. 13A to 13D show a procedure for introducing a
mechanical fastener onto a myocardial wall to cause the inventive
device to adhere to that wall.
[0031] FIGS. 14A to 14F show a procedure for introducing the
inventive device to the heart via a subxiphoid approach.
DETAILED DESCRIPTION OF THE INVENTION
[0032] This invention deals, in general, with devices for
supporting and reforming myocardial tissue in the region of and
across an infarct. Generally, the device adheres to the myocardial
tissue adjacent the infarcted region. The devices also provide
support across and to the infarct preferably in a way that varies
with time to allow the injured area to reform and generally to
allow surrounding tissue to strengthen. In some instances, the
tissue may merge opposing areas of substantially healthy myocardial
tissue across an infarct location. Used in such a way, the device
also prevents resulting injuries such as ventricular aneurysms.
[0033] Although the device is preferably introduced onto the heart
without removal of the infarcted tissue, the device may also be
used after surgical removal of infarcted tissue. The device may be
introduced onto the myocardial surface using percutaneous or
minimally intrusive procedures. Open chest surgery is also suitable
but is not preferred.
[0034] Preferably, the inventive device includes a support region
generally suitable for placement exteriorly to an infarct that 1.)
allows placement of the inventive device onto the heart using
selected procedures (e.g., minimally invasive, etc.), and 2.) later
(preferably through the use of a temporally biodegradable
component) varies the geometry of the support component, e.g., by
drawing the ends of the support component together as a function of
time, to support the infarcted region and allow reformation of the
adjacent myocardial tissue. As noted elsewhere, the ends of the
supporting area functionally adhere to healthy myocardial tissue at
sites beyond the periphery of the infarcted region.
[0035] FIG. 1 shows an anterior view of the heart (100). The right
ventricle (102) and right auricle (104) may be seen in this view.
The arch of the aorta (106) and pulmonary trunk (108) may also be
seen. Also seen from this view is the site of an infarct (110).
This injury is typical of those found in the myocardial wall after
occlusion of a coronary artery. The infarct (110) shown in this
depiction is one that might occur due to the occlusion of some
portion of the anterior interventricular branch of the left
coronary artery (112). The occlusion typically would reside at or
near the site marked (114). The infarct itself generally is
considered to have three zones of influence. The first is the zone
of infarction (116) and is considered to be simply dead heart
muscle tissue. Electrocardial measurements taken over this zone (in
a conceptual sense) "see through" the zone of infarction and record
electrical activity on the other side of the heart. Surrounding the
zone of infarction (116) is the zone of injury (118). Injured
cardiac muscle has a cell membrane which is never fully polarized
and potentially may be recoverable with the passage of time.
Finally, the zone of ischemia (120) surrounds the zone of injury
(118). Diagnoses of the scope of these regions is well documented
and are determined using electrocardiograms and similar
devices.
[0036] FIG. 2A depicts, in concept, the desired effect of one
variation of the inventive device and a specific procedure for
using the device. In particular, schematized inventive device (200)
is shown situated about the heart (100). In concept, the device
(200) is placed about the infarct (shown in FIG. 1 as (110)) and
allowed to adhere to comparatively healthy regions of tissue (205,
207) that are adjacent to the infarct so that upon activation of
the device (200), those comparatively healthy regions (205, 207)
regions are drawn towards each other thereby tending to shrink the
infarct. The springs (202, 204) which act as the support inducing
and maintaining members across the infarct are also shown. The goal
in this variation is to create a region about the infarct in which
sufficiently healthy myocardial tissue on one side of the infarct
is either 1.) held in a generally static position with respect to
sufficiently healthy myocardial tissue on the other side of the
infarct and with support for a period of time sufficient to allow
wall thickening of some portion of that adjacent tissue and
preferably shrinkage of the infarct region and or 2.) moved as a
function of time with respect to sufficiently healthy myocardial
tissue on the other side of the infarct to reach the same
result.
[0037] Desirably two or more adherent regions (204) of the
inventive device (200) will be put together in such a way that they
adhere to the myocardial wall (via mechanical connection or
intergrowth with the tissue of the heart). An optional band (206)
may be used to maintain position of the inventive device on the
selected site.
[0038] FIG. 2B shows another variation of the inventive device as
placed on the ventricular wall of a heart (100). The variation of
the inventive device (210) shown in FIG. 2B does not utilize a band
about the heart (100) but instead relies on direct adherence of the
device sections (212) and (214) to the ventricular surface across
the infarct region (216). Adherent regions or portions (212) and
(214) may variously be caused to be adherent to the ventricular
surface by intergrowth as mentioned above, by a mechanical
fastener, as will be discussed below, or by biocompatible adhesives
such as cyanoacrylate or fibrin based glues or by other suitable
procedures. Further, the variation shown in FIG. 2B shows the use
of flat springs (218) as the support inducing members in device
(210). In this variation, springs (218) are coated with a
biodegradable or bioabsorbable material which allows the overall
distance between the ends of the springs slowly to decrease. As the
stiff coating erodes away, the springs themselves decrease in
length (end to end) and tend, therefore, to pull the edges of the
infarct region (216) towards each other. In this variation of the
invention, the device is intended to decrease the distance between
the ends over a chosen or specified length of time, allowing
reformation of tissue in the infarct regions, support of the
ventricular wall, e.g., to prevent ventricular aneurysms.
[0039] FIGS. 3A, 3B, and 3C show the conceptual operation of the
variation of the inventive device as shown in FIG. 2A.
[0040] FIG. 3A shows a cross sectional portion of the myocardial
wall (300) and an infarct (302). Peripherally adjacent the infarct
(302) are regions (304) of sufficiently healthy myocardial tissue.
By "sufficiently healthy" is meant that the tissue is not in the
"infarct region" discussed above and will regenerate or reform in
time. FIG. 3A shows the inventive device of (306) shortly after its
placement on the ventricular wall (300). Included in this schematic
depiction are two or more regions (308) that are adapted to adhere
to the myocardial wall at about the positions shown in the Figure.
Surrounding the adhering regions (308) are regions (310) of the
inventive device that generally do not adhere to the heart.
[0041] Band (312) is shown in FIG. 3A although other ways of
maintaining the inventive device in position until (and after) it
is operative are included in the scope of this invention. The
support maintaining member (314) is here shown to be made up of a
coil spring (316) and a time delay member (318). In function, time
delay member (318) may comprise, for instance, a biodegradable
plastic which after some period of time erodes to the point where
it allows spring (316) to collapse and pull the edges of infarct
(302) incrementally towards each other. FIG. 3A shows, as mentioned
above, the placement of inventive device (306) shortly after
introduction to the heart surface.
[0042] FIG. 3B shows the placement of the inventive device (306)
after ingrowth of myocardial tissue into the heart tissue adherence
regions (308) or other fixation of the adherence regions (308) onto
the heart tissue.
[0043] Finally, FIG. 3C shows the approach of the myocardium
regions and the eventual collapse of the spring to its lowest
energy configuration. A region of reformed tissue (318) may be
produced depending upon a wealth of variables such as the health of
the patient and the heart, the speed with which the springs (316)
moved the affected tissue, the size of the infarct, etc. This
region of reformed tissue (318) has been created by the
disappearance of the time delay member (318) (shown in FIGS. 3A and
313) from the center of spring (316). Spring (316) then pulls
together the two opposing portions of the inventive device (306)
and maintains an appropriate support to the tissue between the two
opposing tissue regions (304).
[0044] A substantial but desirable variation of the invention is to
form the springs (316) from a material, typically polymeric, having
both sufficient bio degradability and springiness to act as the
time delay component discussed above and as the component that
provides movement between the opposing adherence regions of the
inventive device, such as may be provided by the springs (316)
above. This variation allows a major component of the device to be
absorbed into the body after the end of its functional life.
Oriented polyglycolide and polylactide-based polymers (and other
polymeric materials listed below) that have been sized and formed
into spring structures are particularly suitable for this
variation.
[0045] In any case, the associated covering or composition
preferably is a polymeric material such as a biodegradable polymer,
e.g., polyglycolic acid, polylactic acid, reconstituted collagen,
poly-p-dioxanone, and their copolymers such as poly(glycolide
lactide) copolymer, poly(glycolide-trimethylene carbonate)
copolymer, poly(glycolide-.epsilon.-caprolactone) copolymer,
glycolide-trimethylene carbonate triblock copolymer, and the like.
Mixtures of the noted polymers, e.g., of polylactide and
polyglycolide may also be used.
[0046] The various time delay components discussed here may be
produced using materials that are biocompatible and preferably
either metallic or polymeric. Acceptable polymeric compositions are
discussed just above. Appropriate materials for these inventive
devices include alloys such as super-elastic alloys. Super-elastic
or pseudoelastic shape recovery alloys are well known in this art.
For instance, U.S. Pat. Nos. 3,174,851; 3,351,463; and 3,753,700
each describe one of the more well known super elastic alloys,
known as Nitinol. These alloys are characterized by their ability
to be transformed from an austenitic crystal structure to a
stress-induced martensitic (SIM) structure at certain temperatures
and then to return elastically to the austenitic shape when the
stress is removed. These alternating crystal structures provide the
alloy with its super-elastic properties. The alloy mentioned in the
three patents just above, is a nickel-titanium alloy. It is readily
commercially available and undergoes the austenitic-SIM austenitic
transformation at a variety of temperatures between -20.degree. C.
and +30.degree. C.
[0047] These alloys are especially suitable because of their
capacity to recover elastically, almost completely, to the initial
configuration once the stress is removed. Typically, in services
such as are described here, there is little permanent plastic
deformation even at relatively high strains. This ability allows
the time delay component to retainer device to undergo substantial
bending both during delivery through various minimally invasive
devices and to return to its least stressed form and contract the
nearby infarct as any time-delay polymeric covering reacts,
dissolves, or is absorbed.
[0048] The transition temperature of this material is not
particularly important, but it should be reasonably below the
typical temperature of the human body so to allow it to be in its
austenitic phase during use. The diameter of the wires or ribbons
making up the various time-delay element but are typically smaller
than about 0.010 inches in diameter. However, they need only be
sized appropriately for the production and maintenance of the
infarct support as specified elsewhere.
[0049] Super-elastic alloys are not always suitably visible under
fluoroscopy as it is used on the human body. Consequently it may be
desirable to add a covering of some kind to improve the
radio-opacity of the component. Radio-opaque metals such as gold
and platinum are well known. They may be added the various elements
of this inventive device by such widely recognized methods as by
plating or by wrapping the element in a radio-opaque wire or
ribbon.
[0050] Specific members of other classes of suitable super-elastic
alloys include: Monel alloys such as MP35N, SYNTACOBEN, and
cobalt/chromium alloys such as ELGILOY, etc.
[0051] Although we have discussed producing the spring member from
super elastic alloys, other metals may in certain circumstances be
appropriate. Such metals include a number of the stainless steels
(for instance, SS308, SS304, SS318, etc.) and other highly elastic,
if not super-elastic, alloys. The support inducing member may
further be produced from other metals or alloys known as suitable
springs, e.g., tantalum, tungsten, titanium, silver, gold,
platinum, and alloys of these materials.
[0052] FIGS. 4A, 4B, and 4C show, in concept, the proposed
operation of the device such as depicted in FIG. 2B.
[0053] In this variation, the device employs mechanical fasteners
(320) that penetrate the ventricular wall (322) to hold the
inventive device (324) in place about infarct (326). The spring
(328) in this variation is coated with a biodegradable or
bioerodable covering or, as an alternative, comprises a
biodegradable polymer. In the latter case, as the bioerodable
covering thins, spring (128) decreases in length between the two
depicted fasteners (320) and provides support to the tissue between
those fasteners (320).
[0054] FIG. 4B shows the infarct (326) site at a later time. The
regions of comparatively healthier myocardial tissue (330) have
thickened and the distance between two fasteners (32) has decreased
as the covering on spring (328) has eroded.
[0055] FIG. 4C shows a still further stage in recovery of the
ventricular wall (322) and the specific region (330) interior to
infarct (326).
[0056] As noted elsewhere, the inventive device desirably includes
at least three components: at least a first heart tissue adherence
region, at least one second heart tissue adherence region that is
either separable or separated from the first tissue adherence
region, and at least one tissue supporting member situated (with
respect to the first and second heard tissue adherence regions) so
to maintain support to the tissue (usually containing an infarcted
area) between the first and second tissue adherence regions when
the device has been introduced onto the heart surface. Highly
preferable is a variation of the tissue supporting member that
involves a "time delay" feature. This feature permits a change of
the spring length between the first and second heart tissue
adherence regions with time.
[0057] It is desirable that the inventive device be adapted to
promote angiogenesis in the myocardial wall both adjacent the
various tissue contact regions and throughout the pericardial
space. Angiogenesis promoting materials, particularly those that
promote growth of microvasculature, whether synthetic or natural
may be infused into the various components of the inventive device
or introduced into the pericardial space during placement of the
device. Introduction of angiogenesis promoting materials into the
supporting region, into or onto the polymers acting as time-delay
coatings or springs, and generally placed adjacent the infarct
regions and their peripheries is seen to be a desirable enhancement
of the healing process. Angiogenic materials include, e.g.,
collagen, fibrinogen, vitronectin, other plasma proteins, various
appropriate growth factors (e.g., vascular endothelial growth
factor, "VEGF"), and synthetic peptides of these and other similar
proteins. Other components having a specific role may be included,
e.g., genes, growth factors, biomolecules, peptides,
oligonucleotides, members of the integrin family, RGD-containing
sequences, oligopeptides, e.g., fibronectin, laminin, bitronectin,
hyaluronic acid, silk-elastin, elastin, fibrinogen, and the
like.
[0058] Other bioactive materials which may be used in the invention
include, for example, pharmaceutically active compounds, proteins,
oligonucleotides, ribozymes, and anti-sense genes. Desirable
additions include vascular cell growth promoters such as growth
factors, growth factor receptor antagonists, transcriptional
activators, and translational promoters; vascular cell growth
inhibitors such as growth factor inhibitors, growth factor receptor
antagonists, transcriptional repressors, translational repressors,
replication inhibitors, inhibitory antibodies, antibodies directly
against growth factors, bifunctional molecules consisting of a
growth factor and a cytotoxin, bifunctional molecules consisting of
an antibody and a cytotoxin; cholesterol-lowering agents;
vasodilating agents; agents which interfere with endogenous
vasoactive mechanisms, and combinations thereof.
[0059] In addition, polypeptides or proteins that may be
incorporated into or onto the inventive device, or whose DNA can be
incorporated, include without limitation, proteins competent to
induce angiogenesis, including factors such as, without limitation,
acidic and basic fibroblast growth factors, vascular endothelial
growth factor (including VEGF-2, VEGF-3, VEGF-A, VEGF-B, VEGF-C)
hif-1 and other molecules competent to induce an upstream or
downstream effect of an angiogenic factor; epidermal growth factor,
transforming growth factor .alpha. and .beta., platelet derived
endothelial growth factor, platelet derived growth factor, tumor
necrosis factor .alpha., hepatocyte growth factor and insulin like
growth factor; cell cycle inhibitors including CDK inhibitors;
thymidine kinase ("TK") and other agents useful for interfering
with cell proliferation, and combinations thereof.
[0060] By the term "adherence," we mean that the noted heart tissue
adherence region of the inventive device is substantially immobile
with respect to its related heart tissue. That is to say that a
tissue adherence region may be adhesively connected to the tissue,
mechanically attached to the tissue, ingrown with the tissue,
connected using specific mechanical connectors, or other methods of
or means for preventing relative motion between the device
component and the tissue wall.
[0061] We consider it generally undesirable to incur adhesion of
the device to the myocardium and to the pericardium except in the
areas specifically selected for adhesion. A variety of methods are
appropriate for preventing such adhesion. However, one highly
effective way is to select materials of construction that do not
usually adhere to heart tissue. Such materials include polymers
such as polyfluorocarbons and polyolefins particularly those
selected from the group consisting of polytetrafluoroethylene (PTFE
or TFE), ethylene chlorofluoroethylene (ECTFE), fluorinated
ethylene propylene (FEP), polychlorotrifluoroethylene (PCTFE),
polyvinylfluoride (PVF), polyvinylidenefluoride (PVDF),
polyethylene (LDPE, LLDPE, and HDPE), and polypropylene.
[0062] FIG. 5 shows a variation (350) of the inventive device
having a first tissue contact pad (352) which, of course, makes up
the first heart tissue adherence region, and a second tissue
contact pad (354), typically of a similar composition and size to
the first contact pad (352). The two pads are shown in FIG. 5 to be
separated and to be separable.
[0063] Also shown in FIG. 5 are two spring support maintaining
members (356). In this instance, they comprise springs (356) that
are fixedly attached to each of the tissue contact pads (352, 354).
Each of tissue contact pads (352, 354) may be made to adhere to the
heart by any of the methodologies discussed above and discussed in
more detail below. For instance, the pads may be glued to the
myocardial surface suing appropriate adhesives such as fibrin based
glues or cyanoacrylates. Other suitable biological adhesives would
obviously also be useful on these devices. As is the case with each
of the tissue contact pads listed in the variations discussed
below, the pads may be held in a position to allow to intergrow
with heart tissue if suitable treatment permits long-term placement
of the device in alleviating the injury. The contact pads may be
mechanically fastened to the heart muscle by mechanical fasteners
as discussed elsewhere.
[0064] The nature of the support inducing members, shown as springs
(356), is not critical in that the member or members may be
polymeric or rubbery materials but preferably are springs as shown
in the figure. The springs (356) shown in FIG. 5 are flat springs
to minimize the overall thickness of the device and the U shaped
turns of the springs provide a substantially linear spring rate
upon spring compression. As discussed elsewhere, the depicted
springs (356) may include coatings to permit change of spring
length over time.
[0065] FIG. 6 shows a variation of the inventive device (360)
similar in overall function and view to that found in FIG. 5. It
includes a first tissue contact region (362) and a second tissue
contact region (364) separated from the first. The support
inducement and maintenance components (366) in this variation are
shown to be embedded springs (368) having a biodegradable or
bioerodable overall covering (370), as also discussed elsewhere.
These support inducing members are intended to provide a constant
stiffness between the two tissue contact surfaces (362, 364). This
means that the springs are somewhat stretched during placement into
the covering material (370). As the covering (370) erodes, the
embedded springs (368) are allowed to relax and the spring length
becomes shorter, thereby all the while providing a specific
rigidity to the infarcted tissue region between the ends of the
inventive device.
[0066] FIG. 7A shows a variation (380) of the inventive device
having dual heart tissue contact regions at (382) and a support
inducing member (384), here depicted as a coil spring. In addition,
this variation includes a band (386) which extends from one tissue
contact region (382) to the other tissue contact region (382). The
band (386) is used to surround the heart and to position the
various active components of inventive device (380) properly about
the infarct region. The band (386) is typically made of a material
which tends not to allow intergrowth or adhesion to heart
tissue.
[0067] FIG. 7B shows the device (380) without the spring (384).
This portion of the device shows an inner contact region (392)
which may be adapted to aid with biologic or chemical adhesion of
device (390) to heart tissue.
[0068] FIGS. 8A and 8B show side view and cross sectional views of
one variation of springs (400) useful as a support inducing member
and as a time delay element. In this variation, the spring (402) of
a bioerodable or biodegradable material. Suitable coverings include
polymeric materials such as a biodegradable polymer, e.g.,
polyglycolic acid, polylactic acid, reconstituted collagen,
poly-p-dioxanone, and their copolymers such as
poly(glycolide-lactide) copolymer, poly(glycolide-trimethylene
carbonate) copolymer, poly(glycolide-c-caprolactone) copolymer,
glycolide-trimethylene carbonate triblock copolymer, and the like.
Copolymers, mixtures, and alloys of the noted polymers, e.g., of
polylactide and polyglycolide may also be used. The turns in this
spring are flat and approximately "U"-shaped.
[0069] FIG. 9A shows a side view of a combination support inducing
member and time delay member (406) made up of a spring (408) and
its attendant bioerodable or biodegradable covering (410). In this
variation, the covering is cast generally as a slab with the spring
inside. In this variation, the spring (408) is flat and has loops
at the end of the coil undulations. Again, this spring form
provides a reasonably linear rate/spring length relationship.
[0070] FIGS. 10A and 10B show a coil spring (416) which an interior
time delay element (418). The time delay element (418) in this
variation is a composite component having an inner stripe of
biodegradable or bioerodable polymer (420) and an outer partial
covering of nonerodable material (422). The partial outer covering
(422) may be considered a U-shaped component having an erodable
polymer inside the arms of the U. This variation allows degradation
or erosion of the inner polymer along the exposed edge and the
inner stiffener (418) will bend with time allowing the spring to
collapse and pull and shorten.
[0071] FIG. 11 shows the inner surface of a variation of the
inventive device (430). Surface (432) is the heart tissue contact
surface. This surface (432) is roughened and will allow creation of
a biological bond with the heart muscle it contacts given the
appropriate amount of time.
[0072] Similarly, FIG. 12 shows a device 434 having a surface (436)
having small "nubs" (438) which are small hillocks which tend to
promote mechanical attachment to heart muscle. In the variation
shown in FIGS. 11 and 12, it is highly desirable that the contact
areas (432) in FIG. 11 and (436) in FIG. 12 be surrounded by (or at
least partially surrounded by) material which tends not to adhere
to or create biological adherence to the heart muscle.
[0073] FIGS. 13A to 13D show a procedure for introducing a
mechanical tissue fastener (450) through the inventive device (452)
and the myocardial wall (454).
[0074] As shown in FIG. 13A, the fastener (450) and contact region
(452) are positioned appropriately at the site chosen on myocardium
(454). In FIG. 13B, the mechanical fastener (450) having a
penetrating shaft (451) ending in a piercing end (462) has
penetrated the myocardial wall (454) and the contact region (452)
has been snugged down against the myocardial wall (454).
[0075] FIG. 13C shows the spreading of braid (456) interior to
myocardial wall (454). This mechanical adhering device (450) has an
inner shaft (458), a collar (460), and a piercing end (462). The
inner shaft (458) may be moved against the collar (460) to expand
braid (456) to allow the device to be held against the inner heart
wall.
[0076] FIG. 13D shows the final step in which the braid (456) is
flattened against the inner wall of the myocardium (454). The inner
shaft (458) has been removed and collar (460), in conjunction with
braid (456), holds the device in position for use.
[0077] This inventive device is quite tidy and because it generally
has but a localized placement on the heart, is suitable for
placement on the myocardium via any number of procedures, ranging
from the most invasive--open chest surgery--to those that are much
less invasive. A preferred procedure for placing the device is via
a percutaneous approach through the diaphragm beneath the xiphoid
process. It is direct and uses short instruments for ease and
accuracy. Such a process is outlined in FIGS. 14A-14F.
[0078] Shown in FIG. 14A is a heart (500) having an infarct (502)
in the right ventricular wall. The heart (500) is surrounded by a
pericardial space (504) holding pericardial fluid and all is
enclosed by the pericardium (506). Also shown is the muscle sheet
known as the diaphragm (508). For the purposes of depicting the
spatial relationships in this procedure, also shown (in shadow) is
the xiphoid process (510) and some nearby rib and sternal
structure. Much of the extraneous body structure not otherwise
needed for explanation of the procedure has been omitted for
clarity.
[0079] Also shown in FIG. 14A is the first step of the procedure. A
suitably large hollow needle (512) and a guidewire (514) passing
through the lumen of the needle (512) have been introduced below
the xiphoid process (510) and through the diaphragm (508). The
needle (512) and the guidewire (514) are shown having penetrated
the pericardium (506).
[0080] FIG. 14B shows that the needle has been removed from the
guidewire (514) and the distal end (515) of the guidewire (514) has
been manipulated to pass by the infarcted region (502). An
introducer or cannula (516) is shown being passed up the guidewire
(514).
[0081] FIG. 14C shows placement of the introducer or cannula (516).
The tip of delivery catheter (518) is shown passing up the
guidewire (514) and towards the lumen of introducer or cannula
(516).
[0082] FIG. 14D shows placement of the delivery catheter (518)
through the introducer or cannula (516) and up onto the region of
the heart having the infarct (502). The guidewire (514) has been
removed.
[0083] FIG. 14E depicts the step of deploying the inventive device
(520) across the infarct (502). In this variation, the inventive
device (520) is introduced into the lumen of the delivery catheter
(518) and pushed through the catheter (518) by use of a pusher
(522).
[0084] FIG. 14F shows the final positioning of the inventive device
(520) over the infarct (502) on the heart (500). The support
inducing and maintenance member (522) may be seen extending over
the opposing sides of the periphery of the infarct (502).
[0085] Not discussed with relation to FIGS. 14A-14F is a step of
affixing the inventive device (522) to the heart (500). However,
the procedures discussed with relation to FIGS. 13A-13D may be
applied independently, for instance, to so cause adherence between
the device and the heart. Separate tubing members for introduction
of adhesives to the appropriate regions of the heart or device are
also suitable.
[0086] Many alterations and modifications may be made by those of
ordinary skill in this art, without departing from the spirit and
scope of this invention. The illustrated embodiments have been
shown only for purposes of clarity and the examples should not be
taken as limiting the invention as defined in the following claims.
Which claims are intended to include all equivalents, whether now
or later devised.
* * * * *