Note: Descriptions are shown in the official language in which they were submitted.
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ENDOVASCLTLAR PROSTHESIS
TECHNICAL FIELD
In one of its aspects, the present invention relates to an endovascular
prosthesis. In another of its aspects, the present invention relates to a
method of
treating an aortic disease condition in a patient.
BACKGROUND ART
Stents are generally known. Indeed, the term "stent" has been used
interchangeably with terms such as "intraluminal vascular graft" and
"expandable
prosthesis". As used throughout this specification the term "stent" is
intended to
have a broad meaning and encompasses any expandable prosthetic device for
implantation in a body passageway (e.g., a lumen or artery).
In the past ten years, the use of stents has attracted an increasing amount
of attention due the potential of these devices to be used, in certain cases,
as an
alternative to surgery. Generally, a stent is used to obtain and maintain the
patency of the body passageway while maintaining the integrity of the
passageway. As used in this specification, the term "body passageway" is
intended to have a broad meaning and encompasses any duct (e.g., natural or
iatrogenic) within the human body and can include a member selected from the
group comprising: blood vessels, respiratory ducts, gastrointestinal ducts and
the
like.
Stent development has evolved to the point where the vast majority of
currently available stents rely on controlled plastic deformation of the
entire
structure of the stent at the target body passageway so that only sufficient
force to
maintain the patency of the body passageway is applied during expansion of the
stent.
Generally, in many of these systems, a stent, in association with a balloon,
is delivered to the target area of the body passageway by a catheter system.
Once
the stent has been properly located (for example, for intravascular
implantation
the target area of the vessel can be filled with a contrast medium to
facilitate
visualization during fluoroscopy), the balloon is expanded thereby plastically
deforming the entire structure of the stent so that the latter is urged in
place
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against the body passageway. As indicated above, the amount of force applied
is
at least that necessary to expand the stent (i.e., the applied the force
exceeds the
minimum force above which the stent material will undergo plastic deformation)
while maintaining the patency of the body passageway. At this point, the
balloon
is deflated and withdrawn within the catheter, and is subsequently removed.
Ideally, the stent will remain in place and maintain the target area of the
body
passageway substantially free of blockage (or narrowing).
An alternate approach is the. so-called "self-expanding" stents. In this
approach, the stent is compressed in a sheath. The stent/sheath combination is
delivered to the body passageway of interest and, thereafter, the sheath is
retracted. As the stent is exposed, potential energy stored in the stent is
converted
to kinetic energy and the stent expands. This is a common approach with
conventional wire stents and nitinol stents.
See, for example, any of the following patents:
United States patent 4,733,665 (Palmaz),
United States patent 4,739,762 (Palmaz),
United States patent 4,800,882 (Gianturco),
United States patent 4,907,336 (Gianturco),
United States patent 5,035,706 (Gianturco et al:),
United States patent 5,037,392 (Hillstead),
United States patent 5,041,126 (Gianturco),
United States patent 5,102,417 (Palmaz),
United States patent 5,147,385 (Beck et al.),
United States patent 5,282,824 (Gianturco),
United States patent 5,316,023 (Palmaz et al.),
United States patent 5,755,771 (Penn et al.),
United States patent 5, 906,640 (Penn et al.),
United States patent 6,217,608 (Penn et al.),
United States patent 6,183,506 (Penn et al.),
Canadian patent 1,239,755 (Wallsten), and
Canadian patent 1,245,527 (Gianturco et al.),
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for a discussion on some previous stent designs and deployment systems.
To date, most stent development has focused on the .so-called coronary
stents. While a number of advances in art of coronary stent development have
been made, there is room for improvement.
One area which has received little or no attention is the area of
endovascular treatment of aortic disease. At this point it is useful to review
diseases of the aorta.
Aortic diseases contribute to the high overall cardiovascular mortality.
Relatively new imaging modalities (e.g., transesophageal echocardiography,
magnetic resonance tomography, helical computed tomography, electron beam
computed tomography) have been introduced during the last decade. These new
imaging techniques facilitate better and/or earlier diagnosis of aortic
diseases,
even in emergency situations. These new imaging techniques have had an effect
on patient management during recent years allowing more rapid diagnosis and
decision making.
Generally, aortic disease is caused by mechanisms which weaken the
strength of the aortic wall, particularly, the aortic media. Such wall
weakening
leads to higher wall stress, which can induce aortic dilatation and aneurysm
formation, eventually resulting in aortic dissection or rupture. The various
categories of aortic disease are summarized in Figure 1.
Diseases of the aorta are a significant problem in medicine. There are
two general approaches: drug treatment and surgery. Drug treatment is used to
lower blood pressure - this approach is disadvantageous since, at best, it
modulates the effect of the disease while still leaving the patient at
significant
risk. Surgery is disadvantageous due to the high mortality and morbidity, even
in
centers of excellence. The increasing age of the population is resulting in an
increased incidence of aortic disease as it is a degenerative disease.
Further,
aortic stiffness increases with age thereby reducing coronary and other artery
perfusion.
There are three (3) indications of aortic disease which are regularly of
clinical interest: (1) aortic dissection, (2) blunt chest trauma (with
consequential
=
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trauma to the aorta), and (3) aortic sclerosis.
Aortic dissection is known to occur in approximately 15-20 cases/1
million inhabitants/year with .a mortality of 50% in the first year and 5% per
hour
for the first 5 hours after the onset of symptoms. It results in a splitting
of the
aortic wall, a bleeding into the wall with formation of a true and false (new)
lumen separated by a flap called "intima" with tear or "rupture point". In
patients
with involvement of the ascending aorta, surgery is performed and drug
treatment preferred in patients with involvement of the descending aorta. As
stated above, despite surgery, mortality is still high. The main problem is
the
organ perfusion of the abdomen which results in shock and multiorgan failure.
Relatively recent studies have demonstrated that intramural hemorrhage,
intramural hematoma and aortic ulcer may be signs of evolving dissections or
dissection subtypes. Currently, the various forms of dissection may be
classified
as follows:
Class 1 (Figure 2a): Classical aortic dissection with an
intimal flap between true and false lumen;
Class 2 (Figure 2b): Medial disruption with formation of
intramural hematoma! hemorrhage;
Class 3 (Figure 2c): Discrete/subtle dissection without
hematoma, eccentric bulge at tear site;
Class 4 (Figure 2d): Plaque rupture leading to aortic
ulceration, penetrating aortic atherosclerotic ulcer with
surrounding hematoma, usually subadventitial; and
Class 5 (Figure 2e): Iatrogenic and traumatic dissection.
Each of these classes of dissection can be seen in their acute and chronic
stages; chronic dissections are considered to be present if more than 14 days
have
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elapsed since the acute event.
Classic Aortic Dissection (Class 1 - Figure 2a)
Acute aortic dissection is characterized by the rapid development of an
intimal flap separating a true lumen and false lumen. Due to the pressure
= difference the true lumen is usually smaller than the false lumen.
Intimal flap
tears characterize communicating dissections. However, tears are not always
found and non-communicating dissections are not uncommon. The dissection
can spread from diseased segments of the aortic wall in an antegrate or
retrograde
fashion, involving side branches and causing other complications.
Intramural Hematoma/Hemorrhage (Class 2 - Figure 2b)
An intramural hematoma is believed to be the initial lesion in the majority
of cases of cystic medial degeneration leading to aortic dissection in which
the
intimal tear seems to be secondary to preceding intramural dissection.
Intramural
hematoma may be the result of ruptured normal-appearing vasa vasorum which
are not supported by the surrounding aortic media or the result of rupture of
diseased vasa vasorum. As a dissecting hematoma extends along the aorta the
weakened inner wall is subjected to the elongating force of the diastolic
recoil.
Differences in elasticity between the aortic fibrous adventitia and the inner
more
elastic media may play an additional role.
In autopsy studies, dissecting aneurysms without tears have been found in
up to 12% of 311 autopsies. Others studies have reported an incidence of 4% in
505 cases. In a series of sudden deaths, 67 % of patients with dissections did
not
have tears. The incidence of intramural hemorrhage and hematoma in patients
with suspected aortic dissection, as observed by various new imaging
techniques,
seems to be in the range of 10-30 %.
There are two distinct types of intramural hematoma and hemorrhage.
Type I intramural hematoma and hemorrhage shows a smooth inner aortic
lumen, the diameter is usually less than 3.5 cm, and the wall thickness
greater
than 0.5 cm. Echo free spaces (seen echocardiographically) as a sign of
intramural hematoma are found in only U of the patients. The mean longitudinal
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extent of the hematoma is about 11 cm and the echo free spaces show minimal or
no signs of flow.
Type II intramural hematoma and hemorrhage occurs in aortic
arteriosclerosis. A rough inner aortic surface with severe aortic sclerosis is
characteristic, the aorta is dilated to more than 3.5 cm and calcium deposits
are
frequently found. Mean wall thickness is 1.3 cm with a range of from about 0.6
to about 4 cm, and echo free spaces are found in 70 % of the patients studied.
The longitudinal extension has a similar range as in Type I hematoma, usually
about 11 cm. Intramural hemorrhages are more often found in the descending
than in the ascending aorta.
The fact that intramural hemorrhage and hematoma can lead to aortic .
dissection has only be demonstrated in follow-up studies. Acute aortic
dissection
= as a consequence of intramural hemorrhage and hematoma develops in from
about 28% to about 47 % of the patients. It is associated with aortic rupture
in
from about 21% to about 47 %; and regression is seen in about 10% of the
patients.
Subtle-Discrete Aortic Dissection (Class 3 - Figure 2c)
The structural weakness can either lead to clinically undetected disease or
minor forms of aortic dissection. Subtle dissection has been described as a
partial
stellate or linear tear of the vessel wall, covered by thrombus. After the
partial
tear forms a scar, this constellation is called abortive, discrete dissection.
Partial
ruptures of the inner layer of the aorta allow the blood to enter the already
damaged media and thus cause dissection of the aortic wall, eventually leading
to
a second lumen within the wall, to a rupture or healing during follow-up.
Plaque Rupture/Ulceration (Class 4 - Figure 2d)
Ulceration of atherosclerotic aortic plaques can lead to aortic dissection or
aortic perforation. This was first observed by computed tomography.
Innovations in imaging techniques (e.g., intravascular ultrasound, spiral
computed tomography and magnetic resonance imaging) provide new insight.
The ability to diagnose aortic ulceration has thereby been improved and
further
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insight into the pathophysiology of this condition was gained. The ulcers seem
to
affect the descending thoracic aorta, as well as the abdominal aorta, and are
usually not associated with an extensive longitudinal propagation or branch
vessel compromise. Valvular, pericardial or other vascular complications seem
to
be rare. The ulcer may penetrate beyond the intimal border, often with an
nipple-
like projection with subjacent Type II intramural hematoma formation. The
continuous erosion of the atherosclerotic plaque may eventually violate the
internal elastic membrane. False aneurysms, aortic rupture or dissections may
Aortic sclerosis is normally divided into four grades from thickening of
the intima (Grade I) up to the development of free floating thrombi (Grade IV)
with the danger of embolism. In elderly patients, the incidence of the Grade
IV
aortic sclerosis is increasing. This has lead to a significant occurrence of
stroke in
patients. Thus, if a treatment of aortic sclerosis Grade IV with thrombi free
floating in the aortic lumen could be developed, this wOuld likely obviate or
mitigate the consequential occurrence of stroke.
Currently, there is no reliable treatment approach for aortic sclerosis,
particularly the Grade IV type. Anticoagulation is a known approach, however
this treatment must be accepted with the danger of hemorrhagic strokes,
particularly in the older patients Further, the therapy is very difficult to
monitor.
Surgery is very complicated and has a high mortality and morbidity. Currently,
surgery is not seen as a desirable altenative to anticoagulation therapy.
=
Traumatic/Iatrogenic Aortic Dissection (Class 5 - Figure 2e)
Blunt chest trauma usually causes dissection of the ascending aorta and/or
the region of the ligamentum Botalli at the aortic isthmus. Iatrogenic
dissection
of the aorta may rarely occur during heart catheterization. It is regularly
seen
following angioplasty of an aortic coarctation, but can also be observed after
cross clamping of the aorta and after the use of intraaortic balloon pumping.
Most catheter-induced dissections are retrograde dissections. They will
usually
decrease in size as the false lumen thromboses. Proximal progression of the
coronary dissection into the aortic root may be observed. In blunt chest
trauma,
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the large acceleration of the aorta is leading to an intimal, medial or
transsection
of the aorta particularly at the adjunction at the aortic arch and the
descending
aorta (15-20% of blunt chest trauma cases are related to aortic injury). As a
consequence of this blunt chest trauma, mediastinal hematoma can occur with
abrupt death of the patient. The blunt chest trauma is known to occur in
accidents
involving heavy motorcycles and cars, as well as in other chest traumas. The
diagnosis is very difficult but has been improved by transesophageal
echocardiography. Typically, the damage to the aorta is limited to a small
portion
comprising 3 cm to 5 cm of the aorta. Conventionally, surgery was the only
treatment to stabilize these patients. A mortality rate of 90% has been seen
if
surgery was not timely preformed. Even if surgery was timely performed, there
is a significant mortality rate.
Most prior art attempts to improve surgical techniques to treat aortic
dissection have not be particularly successful.
It is also worth pointing out that the so-call "stent grafts" are not well
suited for treating diseases of the aorta. As is known in the art, a stent
graft is a
prosthesis having a stent portion and a cover portion, each of which are
tubular.
In use, they will cover the entire interior surface of the lumen in which they
are
deployed. While this is not problematic in certain coronary applications, this
can
lead to catastrophic results in the treatment of aortic diseases since there
is a
significant likelihood of side branch arterial occlusion by the graft portion.
A
block of such arteries supplying the spinal cord can occur leading to
paraplegia
which has been observed when current stent grafts have been used in the
treatment of aortic dissection.
Thus, despite the advances made in the art, there is still a need for an
endovascular prosthesis capable obviates or mitigates at least one of the
above-
mentioned disadvantages of the prior art.
DISCLOSURE OF THE INVENTION
It is an object of the present invention to provide a novel endovascular
prosthesis which obviates or mitigates at least one of the above-mentioned
disadvantages of the prior art.
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Accordingly, in one of its aspects, the present invention provides an
endovascular prosthesis for implantation in a body passageway, the prosthesis
comprising a tubular wall, the tubular wall comprising an annular portion for
occlusion of a section of the body passageway, the annular portion comprising
a
first porous section and a non-porous section.
In another of its aspects, the present invention provides a method for
endovascular blocking of an aortic disease condition in a body passageway of a
patient with an endovascular prosthesis comprising an elongate tubular wall,
the
tubular wall comprising an annular portion for occlusion of the aortic disease
condition, the annular portion comprising a first porous section and a non-
porous
section, the method comprising the steps of:
disposing the prosthesis in a catheter;
inserting the prosthesis and catheter within a body passageway by
catheterization of the body passageway;
translating the prosthesis and catheter to a target body passageway at
which the aortic disease condition is located;
positioning non-porous section such that it is substantially aligned with
the aortic disease condition;
exerting a radially outward expansive force on the tubular wall such that
the tubular wall is urged against the target body passageway; and
urging the non-porous section against the aortic disease condition thereby
blocking the aortic disease condition.
Thus, the preferred form of the present endovascular prosthesis device is a
stent system with partially radially, covered by a non-porous or graft
material.
Generally, the present prosthesis can be advantageously used to treat the
indications of aortic disease referred to hereinabove.
With reference to aortic dissection, the present prosthesis normally will be
implanted at the side of the intima tear in order to block the flow from the
true
lumen into the false lumen at the dissection connection. The present
prosthesis
may be advantageously used in dissection of the descending part of the aorta.
A feature of the present endovascular prosthesis is that it has only a
partial, radial non-porous or graft covering. Placement and positioning of the
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device can be facilitated by intravascular ultrasound and transesophageal
echocardiography blocking the tear and while obviating or mitigating covering
the entire aortic wall - e.g., the portion of the aortic wall possibly
containing
important side branches.
An advantage of the present endovascular prosthesis is that it allows flow
from the proximal to the distal aorta even during the implantation of the
device
due to the unique design. In contrast, conventional stent grafts must be used
with
the concurrent danger of abrupt rise of blood pressure leading to an extension
and
enlargement of the dissection.
The present endovascular prosthesis may be used advantageously to block
the tear, thereby obviating or mitigating flow from the true lumen to the
false
lumen. Thus, the healing process begins which, in the successful cases, will
lead
during follow-up within 6 months to total obliteration of the false lumen and
strengthening of the aortic wall. In addition the pressure in the false lumen
is
reduced or eliminated and thereby, the true lumen can expand and improve the
organ perfusion.
When properly deployed, the present endovascular prosthesis will protect
the diseased part of the aorta, so that little or no blood is escapes from the
lumen
to the mediastinum and thereby, the patient is stabilised in the acute phase
of the
aortic injury. Using intravascular ultrasound and transesophageal
echocardiography, the present endovascular prosthesis may be appropriately
navigated to block the damage of the aorta. Again as in treatment of aortic
dissection, it - is important to avoid blockage of multiple arteries which are
supplying the spinal cord since this can lead to paraplegia with enormous
consequences for the patient.
Indeed, to the knowledge of the present inventors, the present
endovascular device is the first such device to be useful in reliable
treatment of
aortic diseases. Thus, with the present endovascular device, blockage of the
aortic flow is obviated or mitigated and abrupt blood pressure increases
(which
could lead to a fatal event) are avoided. Further, since the present device
may be
deployed endovascularly (i.e., non-surgically), it is generally safer for the
patient
and is less of a burden on public health systems.
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.
The present endovascular prosthesis may be used advantageously to wrap
the intimal flaps and thrombi to the aortic wall and thereby obviate or
mitigate the
danger of stroke and emboli without the need for anticoagulation. As the
prosthesis covers only a radial portion of the aortic circumference, blocking
of
side arteries, which are supplying the spinal cord, is obviated or mitigated.
As the
present prosthesis is open and not blocking the flow from the proximal and
distal
aorta during the implantation, a blood pressure increase is obviated or
mitigated.
Thus, a unique advantage of the present prosthesis is that it can be used even
in
multiple places of the aorta when more parts of the aorta are showing thrombus
formation.
BRIEF DESCRIPTION OF THE DRAWINGS
Embodiments of the present invention will be described with reference to
the accompanying drawings, in which:
Figure 1 illustrates a summary of the various categories of aortic disease;
Figures 2a-2e illustrate various categories of dissection of the aorta;
Figure 3 illustrates a perspective view of a preferred embodiment of the
present endovascular prosthesis;
Figure 4 illustrates a schematic, cross-sectional view of the human heart
and various anatomy connected thereto;
Figures 5-13 illustrate various views of a preferred embodiment of the
present endovascular prosthesis being deployed to occlude a Class 4 aortic
dissection (in theseFigures, Figure 11 is a section along line XI-XI in Figure
10).
BEST MODE FOR CARRYING OUT THE INVENTION
Thus, with reference to Figure 3, there is illustrated an endovascular
prosthesis 10. An endovascular prosthesis 10 comprises a tubular wall 15.
Tubular wall 15 comprises a porous section shown generally at 20 and a non-
porous section 25.
As will be appreciated by those of skill in the art, the terms "porous" and
"non-porous" are used throughout the present specification in a relative
sense.
Thus, the term "non-porous" section is intended to mean a section of
expandable
=
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prosthesis 10 which will cause thrombosis or clotting of bodily fluid (e.g.,
blood)
located exteriorly adjacent to expandible prosthesis 10. Specifically, most
aortic
diseases subsist by receiving a regular flow of bodily fluid (e.g., blood).
The
aortic disease may be effectively occluded by impeding this regular fluid of
bodily fluid. Thus, those of skill in the art will recognize that the "non-
porous"
section of expandable prosthesis 10 need not necessarily be fluid impermeable
provided it provides sufficient impedance to the flow of bodily fluid
therethrough.
Porous section 20 may be any conventional stent design which is
preferably optimized to facilitate navigation of prosthesis 10 to the target
site in
the anatomy. The preferred design for non-porous section 20 is that disclosed
in
the Penn et al. International patent applications referred to above. Of
course,
those of skill in the art will recognize that the present endovascular
prosthesis is
not restricted to the use of the specific stent designs for porous section 20
and that
any generally suitable stent design may be used.
As illustrated, non-porous section 25 is disposed on tubular wall 15. The
nature of the material used in non-porous section 25 is not particularly
restricted
provided that it is generally biocompatible and that the physical nature
thereof
does not impede delivery, deployment and general efficacy of the endovascular
prosthesis after it has been implanted.
In one embodiment, non-porous section 25 comprises a sheet material
such as DacronTM, GortexTM, other polymeric materials, bovine pericardium and
the like. The nature of the material used for this purpose is not particularly
restricted. Non-porous section may also be derived from a silicone-based
material such as those commercially available from NuSil Technology
(Carpenteria, California). A non-limiting example of such material is derived
from a silicone-based dispersion commercially available from NuSil Technology
under trade name MED-6640. This material is usually obtained as a liquid
dispersion in an organic insolvent such as xylene. The dispersion may be used
as
such or the viscosity thereof may be altered as desired by addition of further
solvent.
Preferably, the cover material is attached to an otherwise tubular stent
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structure. The means by which attachment may be achieved is not particularly
restricted. For example, the cover material could be fixed to the appropriate
spot
on the stent using a suitable adhesive. Alternatively, the cover material
could be
sewn onto the stent. Those of skill in the art will conceive of a number of
other
means by which the cover material may be fixed to the stent structure.
In another embodiment, non-porous section 25 may be made of the same
material as porous section 20 but preferably suitably modified to comprises a
number of slits, microcuts, slots, apertures and the like to reconcile the
feature of
impeding bodily fluid (e.g., blood) therethrough with the feature of rendering
non-porous section 25 sufficiently flexible so as to permit delivery and
deployment of expandable prosthesis 10.
As shown in the embodiment illustrated in Figure 3, a portion of porous
section 20 is disposed both distal and proximal with respect to non-porous
section
25. Those of skill in the art will recognize that it is possible to dispose
non-
porous section 25 on tubular wall 15 in a manner such that one or both of the
proximal and distal edges of the cover material are aligned with the proximal
and
distal edges, resPectively of tubular wall 15. Further, it is possible to vary
the
design of porous section 20 in the regions which surround the proximal distal
edges of the cover material compared to the remainder of porous section 20 of
tubular wall 15.
With further reference to Figure 3, endovascular prosthesis further
comprises a first set of radiopaque markers 30 which are disposed on the
distal
edge of tubular wall 15. Further, a second set of radiopaque markers 35 are
= disposed at points along the distal edge of non-porous section 25. The
use of
such radiopaque markers facilitates correct placement of endovascular
prosthesis
10 as will be described in more detail hereinbelow. The nature of radiopaque
markings 30,35 is not particularly restricted. For example, radiopaque markers
30,35 may be made from gold or any other material which is opaque to X-ray
radiation.
Preferably, non-porous section 25 spans a radial arc of from about 90 to
about 270 , more preferably from about 150 to about 250 , most preferably to
about 180 to about 240 , of an annular portion of tubular wall 15.
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Further, the longitudinal length of endovascular prosthesis 10 is selected
to correspond to the length of anatomy in which the device will be deployed.
For
. example, if the endovascular prosthesis is to be deployed in the descending
aorta,
it is appropriate for a non-porous section to have longitudinal length of in
the
range of from about 2 cni to about 30 cm, more preferably from about 2 cm to
about 25 cm, most preferably from about 2 cm to about 20 cm. In this preferred
embodiment, the overall length of the expandable prosthesis would be more than
this since it is preferred to have porous sections on opposite sides of the
distal and
proximal edges of the non-porous section.
Preferably, tubular wall 15 is constructed from a plastically deformable
material such as stainless steel, tantalum or the like. Alternatively, the
plastically
deformable material could be made from a radioopaque composite material such
as that in described in United States patent 5,858,556 [Eckert et al.] - this
could
obviate the use of radioopaque markers 30,35 described above. Generally, such
devices are expanded with a balloon catheter.
Alternatively, it is possible to produce tubular wall 15 from a so-called
"shape memory alloy" which will expand when a certain temperature is reached.
In this embodiment, the material may be a metal alloy (e.g., Nitinol) capable
of
self-expansion at a temperature of at least 30 C, preferably in the range of
about
30 to about 40 C.
With reference to Figure 4, it is appropriate to set out some basic
anatomical terms which are used throughout the present specification. Thus,
there is illustrated a heart 50. Heart 50 comprises right ventricle 52, right
atrium
54, left ventricle 56 and left atrium 58.
Emanating from heart 15 is ascending aorta 57 which transitions into
aortic arch 60 and then descending aorta 62. Emanating from aorta arch 60 is
left
subclavian artery 64, left common carotid artery 66 and innominate artery 68.
As illustrated, superior vena cava 66 and inferior vena cava 68 are in
communication with right atrium 54. Further, right innominate vein 70 and left
innominate vein 72 are in communication with right ventricle 52.
As shown, descending aorta 62 comprises a plurality of side branches 80.
It is important during use of the present endovascular prosthesis that these
side
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branches not be occluded as this can result in paralysis of the patient.
As shown, renal arteries 85 are in communication with descending aorta
62 and also should not be occluded during catheterization techniques employing
the present endovascular prosthesis.
With reference to Figures 5-11, deployment of endovascular prosthesis 10
will be illustrated. In the illustrated example, tubular wall 15 of
endovascular
prosthesis 10 is constructed from a plastically deformable material such as
NitinolTM.
Thus, with reference to Figures 5 and 6, there is illustrated an enlarged
portion of the descending aorta 62 illustrated in Region A in Figure 4. In the
illustrated embodiment, a blockage 90 has formed on a wall of descending aorta
62 opposite side branches 80. Blockage 90 may be manifested as a Class 4
dissection (e.g., aortic sclerosis).
As illustrated, the first step in deploying the endovascular prosthesis 10
involves a conventional catheterization step of navigating a guidewire 100
such
that the distal end thereof is distal blockage 90. Next, it is conventional to
insert
a guide catheter to appoint just proximal blockage 90. For clarity, this step
is not
shown. Thereafter, a sheath 105 encompassing endovascular prosthesis 10 is
navigated such that non-porous section 25 of endovascular prosthesis 10 is
aligned with blockage 90 and porous section 20 of endovascular prosthesis 10
is
aligned with side branches 80.
Once endovascular prosthesis 10 is correctly positioned, sheath 105 is
retracted in a direction of arrow B as shown in Figure 7. This results in
exposure
of endovascular prosthesis 10 to blood flow at the appropriate temperature
which
causes tubular wall 15 of endovascular prosthesis 10 to "self expand".
Thus, as shown in Figure 8, when sheath 105 has been retracted to expose
the entire endovascular prosthesis 10, the latter fully expands with non-
porous
section 25 occluding blockage 90 while permitting blood flow through porous
section 20 and into side branches 80 (arrows C) see, also, Figure 10.
With reference to Figures 10 and 11, the deployed endovascular prosthesis
10 is shown in perspective and sectional views, respectively.
With reference to Figures 12 and 13, there is shown, in schematic form,
CA 02428742 2003-05-14
WO 02/39924
PCT/CA01/01587
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adjustment of positioning of endovascular prosthesis 10 before it is fully
deployed. Thus, as described with reference to Figure 1, it is preferred that,
if
tubular wall 15 of endovascular prosthesis 10 is constructed from a radio
transparent material, discreet portions thereof be marked with a radiopaque
material.
In the embodiment illustrated in Figure 12, if endovascular prosthesis 10
were fully deployed as illustrated, non-porous section 25 would occlude side
branches 80 resulting in significant risk to the patient. In such a situation,
it is
possible to alter orientation of endovascular prosthesis 10 (and by inference,
non-
porous 25) by rotating sheath 105 in the direction of arrows D and or
extending/retracting sheath 105 in the direction of arrow E - see Figure 13.
Once
non-porous section 25 is properly positioned with respect to blockage 90,
sheath
105 is retracted as described above to deploy endovascular prosthesis 10.
The present endovascular prosthesis may further comprise a coating
material thereon. The coating material may be disposed continuously or
discontinuously on the surface of the prosthesis. Further, the coating may be
disposed on the interior and/or the exterior surface(s) of the prosthesis. The
coating material can be one or more of a biologically inert material (e.g., to
reduce the thrombogenicity of the prosthesis), a medicinal composition which
leaches into the wall of the body passageway after implantation (e.g., to
provide
anticoagulant action, to deliver a pharmaceutical to the body passageway and
the
like) and the like.
The present endovascular prosthesis is preferably provided with a
biocompatible coating in order to minimize adverse interaction with the walls
of
the body vessel and/or with the liquid, usually blood, flowing through the
vessel.
The coating is preferably a polymeric material, which is generally provided by
applying to the prosthesis a solution or dispersion of preformed polymer in a
solvent and removing the solvent. Non-polymeric coating material may
alternatively be used. Suitable coating materials, for instance polymers, may
be
polytetraflouroethylene or silicone rubbers, or polyurethanes which are known
to
be biocompatible. Preferably, however, the polymer has zwitterionic pendant
groups, generally ammonium phosphate ester groups, for instance phosphoryl
W002139924 CA 02428742 2007-06-06 PCT/C.401 /0 LW
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).
choline groups or analogues thereof. Examples of suitable polymers are
described in International Publication Numbers WO 93/16479 and WO 93/15775.
Polymers described in those specifications are hemo-compatible as well as
generally biocompatible and, in addition, are lubricious. It is important to
ensure
that the surfaces of the prosthesis are completely coated in order to minimize
unfavourable interactions, for instance with blood, which might lead to
thrombosis in the parent vessel and/or endoleaks therethrough.
This good coating can be achieved by suitable selection of coating
conditions, such as coating solution viscosity, coating technique and/or
solvent
removal step.
While this invention has been described with reference to illustrative
embodiments and examples, the description is not intended to be construed in a
limiting sense. Thus, various modifications of the illustrative embodiments,
as
well as other embodiments of the invention, will be apparent to persons
skilled in
the art upon reference to this description. It is therefore contemplated that
the
appended claims will cover any such modifications or embodiments.
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