U.S. patent application number 10/012008 was filed with the patent office on 2002-05-02 for medical device for removing thromboembolic material from cerebral arteries and methods of use.
This patent application is currently assigned to CoAxia, Inc.. Invention is credited to Barbut, Denise R..
Application Number | 20020052620 10/012008 |
Document ID | / |
Family ID | 22858322 |
Filed Date | 2002-05-02 |
United States Patent
Application |
20020052620 |
Kind Code |
A1 |
Barbut, Denise R. |
May 2, 2002 |
Medical device for removing thromboembolic material from cerebral
arteries and methods of use
Abstract
The invention provides a medical device having an elongate
catheter, a balloon occluder mounted on a distal end of the
catheter, and optionally a chopping mechanism associated with an
aspiration port of the catheter. Continuous or intermittent suction
can be applied to the aspiration port which is distal to the
occluder to dislodge thromboembolic material in a carotid or
cerebral artery. Oxygenated blood or other fluid, which may be
hypothermic, can be perfused through at least one perfusion port
proximal to the occluder to maintain and augment perfusion of the
collateral vasculature proximal to the occlusive lesion. The flow
rate of blood or fluid can be controlled by rotating two
cylindrical members. Neuroprotective agents or t-A can also be
infused distal to the occluder through the aspiration port or an
infusing port. Methods of using the devices in treating patients
with acute stroke or occlusive cerebrovascular disease are also
disclosed.
Inventors: |
Barbut, Denise R.; (New
York, NY) |
Correspondence
Address: |
LYON & LYON LLP
633 WEST FIFTH STREET
SUITE 4700
LOS ANGELES
CA
90071
US
|
Assignee: |
CoAxia, Inc.
10900 73rd Avenue North, Suite 102
Maple Grove
MN
55369
|
Family ID: |
22858322 |
Appl. No.: |
10/012008 |
Filed: |
October 29, 2001 |
Related U.S. Patent Documents
|
|
|
|
|
|
Application
Number |
Filing Date |
Patent Number |
|
|
10012008 |
Oct 29, 2001 |
|
|
|
09547951 |
Apr 12, 2000 |
|
|
|
09547951 |
Apr 12, 2000 |
|
|
|
09228718 |
Jan 12, 1999 |
|
|
|
Current U.S.
Class: |
606/190 |
Current CPC
Class: |
A61B 17/320758 20130101;
A61B 2017/22082 20130101; A61B 2017/320716 20130101; A61B
2017/22067 20130101; A61B 17/22 20130101 |
Class at
Publication: |
606/190 |
International
Class: |
A61B 017/00 |
Claims
What is claimed is:
1. A method for treating a carotid or cerebral artery, comprising
the steps of: inserting a distal end of a catheter into the carotid
or cerebral artery, the catheter having a proximal end, a distal
end, an expandable occluder mounted on the distal end, an
aspiration port distal the occluder, and an aspiration lumen
communicating with the port; expanding the occluder to occlude the
carotid or cerebral artery; applying a negative pressure to the
aspiration port; and removing an occlusion from the carotid or
cerebral artery.
2. The method of claim 1, further comprising the step of perfusing
oxygenated medium into the artery through a perfusion port proximal
the occluder.
3. The method of claim 1, wherein the occlusion is a thromboembolic
material, and wherein the thromboembolic material is engaged by the
aspiration port.
4. The method of claim 1, wherein the catheter further comprises at
least one perfusion port proximal to the occluder and communicating
with a perfusion lumen.
5. The method of claim 1, wherein the carotid artery is the common
carotid artery.
6. The method of claim 1, wherein the carotid artery is selected
from the group consisting of the internal carotid artery and
carotid siphon.
7. The method of claim 1, wherein the artery is the middle cerebral
artery.
8. The method of claim 1, wherein the artery is the anterior
cerebral artery.
9. The method of claim 1, wherein the occluder is a balloon which
communicates with an inflation lumen.
10. The method of claim 1, wherein the catheter further comprises a
chopping mechanism for removing the occlusion from the carotid or
cerebral artery.
11. The method of claim 4, wherein the catheter further comprises a
second balloon occluder proximal the perfusion port.
12. The method of claim 2, wherein the oxygenated medium is
hypothermic.
13. The method of claim 1, further comprising the step of infusing
pharmaceutical agent into the carotid artery through the aspiration
port.
14. The method of claim 1, further comprising the step of
localizing the thromboembolic material with intravascular
ultrasound.
15. The method of claim 1, further comprising the step of
localizing the thromboembolic material with carotid doppler.
16. The method of claim 1, further comprising the step of
localizing the atheroma and establishing the direction of flow with
transcranial doppler.
17. The method of claim 2, wherein the oxygenated medium is blood.
Description
[0001] This is a continuation of U.S. application Ser. No.
09/547,951, filed Apr. 12, 2000, which is a continuation of U.S.
application Ser. No. 09/228,718, filed Feb. 24, 1999, now U.S. Pat.
No. 6,165,199, all of which are expressly incorporated herein by
reference in their entirety.
FIELD OF THE INVENTION
[0002] The present invention generally relates to medical devices
useful in treating patients with acute stroke or occlusive
cerebrovascular disease. More specifically, the invention provides
an extra/intracranial balloon occlusive device with suction to
remove a thrombus or embolus lodged in a cerebral vessel and a
means of maintaining and augmenting perfusion of the collateral
vasculature proximal to the offending lesion. The device may employ
a chopping mechanism, vasodilator, hypothermic perfusion or local
administration of t-PA and optionally an extracorporeal pumping
mechanism to remove a vascular occlusion and reestablish cerebral
perfusion.
BACKGROUND OF THE INVENTION
[0003] Stroke is the third most common cause of death in the United
States and the most disabling neurologic disorder. Approximately
700,000 patients suffer from stroke annually. Stroke is a syndrome
characterized by the acute onset of a neurological deficit that
persists for at least 24 hours, reflecting focal involvement of the
central nervous system, and is the result of a disturbance of the
cerebral circulation. Its incidence increases with age. Risk
factors for stroke include systolic or diastolic hypertension,
hypercholesterolemia, cigarette smoking, heavy alcohol consumption,
and oral contraceptive use.
[0004] Hemorrhagic stroke accounts for 20% of the annual stroke
population. Hemorrhagic stroke often occurs due to rupture of an
aneurysm or arteriovenous malformation bleeding into the brain
tissue, resulting in cerebral infarction. The remaining 80% of the
stroke population are ischemic strokes and are caused by occluded
vessels that deprive the brain of oxygen-carrying blood. Ischemic
strokes are often caused by emboli or pieces of thrombotic tissue
that have dislodged from other body sites or from the cerebral
vessels themselves to occlude in the narrow cerebral arteries more
distally. When a patient presents with neurological symptoms and
signs which resolve completely within 1 hour, the term transient
ischemic attack (TIA) is used. Etiologically, TIA and stroke share
the same pathophysiologic mechanisms and thus represent a continuum
based on persistence of symptoms and extent of ischemic insult.
[0005] When a patient presents with neurological deficit, a
diagnostic hypothesis for the cause of stroke can be generated
based on the patient's history, a review of stroke risk factors,
and a neurologic examination. If an ischemic event is suspected, a
clinician can tentatively assess whether the patient has a
cardiogenic source of emboli, large artery extracranial or
intracranial disease, small artery intraparenchymal disease, or a
hematologic or other systemic disorder. A head CT scan is often
performed to determine whether the patient has suffered an ischemic
or hemorrhagic insult. Blood would be present on the CT scan in
subarachnoid hemorrhage, intraparenchymal hematoma, or
intraventricular hemorrhage.
[0006] Traditionally, emergent management of acute ischemic stroke
consists of mainly general supportive care, e.g. hydration,
monitoring neurological status, blood pressure control, and/or
anti-platelet or anti-coagulation therapy. In June 1996, the Food
and Drug Administration approved the use of Genentech Inc.'s
thrombolytic drug, tissue plasminogen activator (t-PA) or
Activase.RTM., for treating acute stroke. In a randomized,
double-blind trial, the National Institute of Neurological
Disorders and t-PA Stroke Study, there was a statistically
significant improvement in stoke scale scores at 24 hours in the
group of patients receiving intravenous t-PA within 3 hours of the
onset of an ischemic stroke. Since the approval of t-PA, an
emergency room physician could, for the first time, offer a stroke
patient an effective treatment besides supportive care.
[0007] However, treatment with systemic t-PA is associated with
increased risk of intracerebral hemorrhage and other hemorrhagic
complications. Patients treated with t-PA were more likely to
sustain a symptomatic intracerebral hemorrhage during the first 36
hours of treatment. The frequency of symptomatic hemorrhage
increases when t-PA is administered beyond 3 hours from the onset
of a stroke. Besides the time constraint in using t-PA in acute
ischemic stroke, other contraindications include the following: if
the patient has had a previous stroke or serious head trauma in the
preceding 3 months, if the patient has a systolic blood pressure
above 185 mm Hg or diastolic blood pressure above 110 mmHg, if the
patient requires aggressive treatment to reduce the blood pressure
to the specified limits, if the patient is taking anticoagulants or
has a propensity to hemorrhage, and/or if the patient has had a
recent invasive surgical procedure. Therefore, only a small
percentage of selected stroke patients are qualified to receive
t-PA.
[0008] New devices and methods are thus needed in treating patients
with acute ischemic stroke and occlusive cerebrovascular disease,
in treating symptomatic patients with embolization or hemodynamic
compromise, or in stroke prevention, e.g., patients with incidental
finding of asymptomatic carotid lesion, which improve a patient's
neurological function and quality of life without causing
significant side effect, and can be used in patients with
contraindication to using t-PA.
SUMMARY OF THE INVENTION
[0009] The invention provides devices and methods for treatment of
acute ischemic stroke and occlusive cerebrovascular disease by
taking advantage of the collateral cerebral circulation.
Anastomoses between the cerebral arteries provide alternative
pathways in which blood can reach a given region of the brain
besides the predominant supplying artery. At the base of the brain
close to the sella turcica, circulus arteriosus cerebri, or circle
of Willis, connects the vertebral and internal carotid arteries to
each other and to the vessels of the opposite side. When occlusion
of a blood vessel interrupting the flow of blood to a specific
region of the brain occurs, survival of the brain tissue and
therefore severity of a patient's neurological deficit depend on
the number and size of its collateral arteries. The devices of the
present invention utilize pressure generated by collateral cerebral
circulation to facilitate removal of thromboembolic material in an
occluded carotid or cerebral artery.
[0010] A first embodiment of the medical device comprises an
elongate catheter, a balloon occluder, and a chopping mechanism.
The catheter has a proximal end, a distal end and a lumen which
communicates with an aspiration port at the distal end. The balloon
occluder, which communicates with an inflation lumen and may
comprise an elastomeric balloon, is mounted on the distal end of
the catheter proximal to the aspiration port. The chopping
mechanism is operated to chop away any particulate matter engaged
by suction through the aspiration port.
[0011] In another embodiment, the catheter has an additional lumen
that communicates with a port distal to the balloon occluder for
infusing blood and pharmaceutical agents, such as a vasodilator or
t-PA. Vasodilator, such as nifedipine or nitroprusside, is used to
reverse any vascular spasm which occurs as a result of
instrumentation. The chopping mechanism may comprise an abrasive
grinding surface or a rotatable blade which operates within a
housing, as described in Barbut et al., U.S. Pat. No. 5,662,671,
incorporated herein by reference in its entirety.
[0012] In still another embodiment, the catheter includes a
perfusion lumen which communicates with one or a plurality of
perfusion ports and is adapted for infusion of oxygenated blood.
The perfusion ports may be located on two cylindrical members which
can be rotated relative to each other so that maximum blood flow
through the catheter is achieved when the perfusion ports on the
two members are aligned. Alternatively, the two cylindrical members
can be rotated so that the perfusion ports on the two members are
partially aligned to limit blood flow, or completely misaligned to
achieve no blood flow. In this manner, the flow rate of blood or
fluid through the perfusion ports can be varied by controlling the
rotation of the two cylindrical members.
[0013] In still another embodiment, a manometer is mounted distal
to the balloon occluder to monitor pressure within the chamber
created by the inflated occluder and the embolic or thromboembolic
occlusion.
[0014] In still another embodiment, a second balloon occluder is
mounted on the catheter proximal to the perfusion ports. The second
occluder, when inflated, reduces run-off of oxygenated blood from
the perfusion ports back down into the aorta, thereby improving
perfusion to the ischemic area by collateral circulation.
[0015] The invention also provides methods for removing atheroma
from an extracranial or intracranial cerebral artery in a patient
with occlusive cerebrovascular disease using the devices described
above. The methods can be used to treat a wide spectrum of
patients, including patients who are symptomatic due to
embolization of a cerebral artery lesion or hemodynamic compromise
caused by the lesion and asymptomatic patients who are found
incidentally to have the lesion during nonneurological procedures
such as cardiac catheterization and/or angiogram.
[0016] In a first method, the distal end of the catheter is
inserted through an incision on a peripheral artery, such as a
femoral artery, and advanced into the symptomatic carotid or
cerebral artery. The site of vessel occlusion is localized with an
angiogram or intravascular ultrasound (IVUS). In an emergency, the
catheter can also be inserted into the patient's carotid artery as
a direct stick after localizing the occlusion with the assistance
of IVUS or standard carotid doppler and transcranial doppler (TCD).
The distal end of the catheter can be advanced as far as the
occlusion which could be in the common carotid artery, internal
carotid artery, middle cerebral artery, anterior cerebral artery,
carotid siphon, terminal internal carotid artery, or any other part
of the cerebral vasculature. After the distal end of the catheter
is positioned proximal to the occluding lesion, the balloon
occluder is inflated to occlude the arterial lumen, thereby
creating a closed chamber between the balloon and the
thromboembolic occlusion. A pressure differential is created since
the pressure within the chamber is lower than the pressure distal
to the occlusion. Using the balloon occlusion therefore enhances
contralateral hemispheric blood flow, helping to reverse the flow
across the Circle of Willis, thereby providing retrograde arterial
collateral enhancement to the ischemic area distal the occlusion.
The catheter is attached to a vacuum and a negative pressure is
applied to the aspiration port. Blood within the chamber may be
completely aspirated. With continued suction, the thromboembolic
materials engaged by the aspiration port under negative pressure.
Occlusion of the port by the thromboembolic material and activation
of the chopper mechanism thereby removes at least a portion of the
occluding material.
[0017] In another method, intermittent suction is used instead of
the continuous suction. The alternating negative-positive pressure
gradient may dislodge the atheroma onto the aspiration port. The
chopping mechanism subsequently removes the atheroma.
[0018] In still another method, after the distal end of the
catheter is inserted and the occluder is inflated proximal to the
intracranial or carotid occlusion, pulsatile or continuous
perfusion is initiated through at least one perfusion port proximal
to the occluder. In this manner, perfusion to the ischemic area
distally is improved by opening and recruiting collateral vessels
which supply the ischemic territory, thereby providing antegrade
collateral enhancement. The more distal the occlusion in the
cerebral circulation, the larger the number of collateral arteries
available for recruitment by the proximal perfusion. Flow rate
through the perfusion ports is adjusted by rotation of two
cylindrical members of the catheter. As a result of increased
perfusion distal to the occlusion, the pressure differential across
the occlusive site increases, thereby facilitating dislodgment of
the thromboembolic material onto the aspiration port. The atheroma
is then removed under vacuum as the catheter is withdrawn, by a
chopping mechanism, an atherectomy device coupled to the aspiration
port, or by local administration of t-PA through an additional
perfusion lumen distal to the occluder.
[0019] It will be understood that there are several advantages in
using the devices and methods disclosed herein for management of
acute stroke. For example, the devices can be used (1) in a
majority of stroke patients, including those with contraindication
to using systemic t-PA, (2) to administer neuroprotective agents
and t-PA locally into an occluded vessel, thereby providing greater
local benefit and fewer systemic side effects, (3) to infuse
hypothermic fluid or blood to the ischemic area, thereby providing
protective focal hypothermia, (4) with standard atherectomy to
remove remaining arterial atheroma, (5) as an angioplasty device by
inflating the balloon over the stenotic arterial lumen to enlarge
the luminal diameter, (6) in other vascular procedures, such as in
treatment of occlusive peripheral vascular disease, (7) by any
invasive radiologist or cardiologist, (8) in the angiogram suite
available in most hospitals, (9) in treating acute stroke patients
with few systemic side effects, (10) to treat asymptomatic high
grade stenotic lesions found incidentally, e.g., during cardiac
catheterization and/or angiogram, (11) to treat symptomatic
vertebral artery occlusion, and (12) to maintain perfusion to the
distal ischemic area, even without removal of the occlusion, to
minimize neurologic damage while alternative intervention is being
considered.
BRIEF DESCRIPTION OF THE DRAWINGS
[0020] FIG. 1 depicts a normal cerebral circulation in the Circle
of Willis.
[0021] FIG. 2 depicts a reversed circulation in the Circle of
Willis to compensate for an occlusion in the left carotid siphon
artery.
[0022] FIG. 3 depicts an embodiment of the medical device for
treatment of acute stroke according to the present invention.
[0023] FIG. 4A depicts the device of FIG. 3 inserted proximal to an
occlusive lesion.
[0024] FIG. 4B depicts thromboembolic material being removed by the
device shown in FIG. 3.
[0025] FIG. 5 depicts another embodiment of the device for
treatment of acute stroke.
[0026] FIG. 6 depicts another embodiment of the device having
perfusion ports proximal to the balloon occluder.
[0027] FIG. 7A depicts complete misalignment of the perfusion ports
on two cylindrical members.
[0028] FIG. 7B depicts partial alignment of the perfusion ports on
two cylindrical members.
[0029] FIG. 7C depicts complete alignment of the perfusion ports on
two cylindrical members.
[0030] FIG. 8A depicts still another embodiment of the device
having two balloon occluders and a chopping mechanism.
[0031] FIG. 8B depicts the device of FIG. 8A inserted proximal to
an occlusive lesion.
[0032] FIG. 9 depicts the device of FIG. 3 inserted into a right
vertebral and left subclavian artery.
[0033] FIG. 10 depicts different peripheral artery access sites for
insertion of the device.
DETAILED DESCRIPTION
[0034] The cerebral circulation is regulated in such a way that a
constant total cerebral blood flow (CBF) is generally maintained
under varying conditions. For example, a reduction in flow to one
part of the brain, such as in acute stroke, may be compensated by
an increase in flow to another part, so that CBF to any one region
of the brain remains unchanged. More importantly, when one part of
the brain becomes ischemic due to a vascular occlusion, the brain
compensates by increasing blood flow to the ischemic area through
its collateral circulation.
[0035] FIG. 1 depicts a normal cerebral circulation and formation
of Circle of Willis. Aorta 100 gives rise to right brachiocephalic
trunk 82, left common carotid artery (CCA) 80, and left subclavian
artery 84. The brachiocephalic artery further branches into right
common carotid artery 85 and right subclavian artery 83. The left
CCA gives rise to left internal carotid artery (ICA) 90 which
becomes left middle cerebral artery (MCA) 97 and left anterior
cerebral artery (ACA) 99. Anteriorly, the Circle of Willis is
formed by the internal carotid arteries, the anterior cerebral
arteries, and anterior communicating artery 91 which connects the
two ACAs. The right and left ICA also send right posterior
communicating artery 72 and left posterior communicating artery 95
to connect, respectively, with right posterior cerebral artery
(PCA) 74 and left PCA 94. The two posterior communicating arteries
and PCAs, and the origin of the posterior cerebral artery from
basilar artery 92 complete the circle posteriorly.
[0036] When an occlusion occurs acutely, for example, in left
carotid siphon 70, as depicted in FIG. 2, blood flow in the right
cerebral arteries, left external carotid artery 78, right vertebral
artery 76, and left vertebral artery 77 increases, resulting in
directional change of flow through the Circle of Willis to
compensate for the sudden decrease of blood flow in the left
carotid siphon. Specifically, blood flow reverses in right
posterior communicating artery 72, right PCA 74, left posterior
communicating artery 95. Anterior communicating artery 91 opens,
reversing flow in left ACA 99, and flow increases in the left
external carotid artery, reversing flow along left ophthalmic
artery 75, all of which contribute to flow in left ICA 90 distal
the occlusion to provide perfusion to the ischemic area distal to
the occlusion.
[0037] FIG. 3 depicts an embodiment of the medical devices for
treatment of acute stroke or symptomatic occlusive disease
according to the present invention. The device comprises catheter
1, which has a proximal end (not shown), distal end 2, and lumen 5.
Lumen 5 communicates with the proximal end, adapted for attachment
to a vacuum, and distally to aspiration port 6. The lumen may also
be adapted for infusion of blood, fluid, or pharmaceutical agent,
such as a vasodilator. Balloon occluder 12, communicating with
inflation lumen 11, is mounted on distal end 2 of the catheter
proximal to aspiration port 6. The device further comprises
chopping mechanism 7 which is closely associated with the
aspiration port, so that occlusion of the aspiration port by any
material will activate the chopping mechanism. Manometer 10 is also
mounted on the distal end of the catheter distal to balloon
occluder 12 for monitoring pressure distal to the occluder. It will
be understood that balloon occluder 12 in FIG. 3 and in all other
embodiments described herein can be substituted for any other
expandable occlusive device, e.g., a pair of nested cones rotatable
relative to one another, and each having a plurality of holes which
pass into and out of alignment during such rotation. Such a system
of nested cones is described in greater detail in Barbut, U.S. Pat.
No. 6,231,551, incorporated herein by reference.
[0038] In use, the distal end of the catheter is inserted through
an incision on a peripheral artery into a more distal carotid or
intracranial artery, such as the terminal ICA, carotid siphon, MCA,
or ACA as depicted in FIG. 4A. Thromboembolic material 202 is shown
occluding the lumen of a cerebral artery narrowed by atheromatous
plaque 200. The occlusion site can be localized with cerebral
angiogram or IVUS. In emergency situations, the catheter can be
inserted directly into the symptomatic carotid artery after
localization of the occlusion with the assistance of IVUS or
standard carotid doppler and TCD. Balloon occluder 12 is then
positioned approximately 1 to 3 cm proximal to the thromboembolic
occlusion and inflated to occlude the arterial lumen. Closed
chamber 50 is created between occluder 12 and thromboembolic
occlusion 202. A vasodilator, e.g., nifedipine or nitroprusside,
may be injected through lumen 5 and port 6 to reverse vascular
spasm induced as a result of instrumentation and to reduce pressure
in the closed chamber. Pressure within the chamber is monitored by
manometer 10 and can be altered by applying vacuum to the proximal
end of the catheter. A pressure dial, which may be included in the
proximal end of the catheter, allows suction within the chamber to
be regulated according to the vessel size cannulated. With suction,
blood is initially aspirated from chamber 50. When continuous
negative pressure is applied, occluding material 202 is dislodged
onto and occludes aspiration port 6, thereby activating chopping
mechanism 7 to remove the occlusion, as depicted in FIG. 4B. Blood
can then be perfused through lumen 5 and port 6 to determine the
extent of reperfusion distal to the occluded site.
[0039] If the occlusion is not removed by the above continuous
suction method, intermittent suction can be used to create an
alternating negative-positive pressure gradient, which may dislodge
the thromboembolic occlusion. Alternatively, a thrombolytic agent,
e.g., t-PA may be infused through lumen 5 and port 6 to lyse the
occlusion if soft thrombus is suspected. Standard atherectomy or
angioplasty with or without stent placement can also be performed
on atheromatous plaque 200 after removal of the occlusion if
perfusion through the diseased artery is still inadequate. Balloon
occluder 12 can be used as an angioplasty balloon to enlarge the
luminal diameter of the stenotic artery, thereby establishing
reperfusion.
[0040] FIG. 5 depicts another embodiment of the device. Catheter 1
has a proximal end adapted for attachment to a vacuum, distal end
2, and lumen 5 which communicates with aspiration port 6. Balloon
12 is mounted on distal end 2 and communicates with inflation lumen
11. Chopping mechanism 7 is closely associated with aspiration port
6 to remove any material occluding the port. The device further
comprises infusion lumen 15, which communicates with port 16, for
infusion of fluid, blood, or pharmaceutical agent.
[0041] In use, distal end 2 of the catheter is inserted into a
carotid or cerebral artery as described above in the method of
using the device of FIG. 3. Balloon occluder 12 is inflated
proximal to an occlusion. The balloon occlusion may improve
contralateral blood flow to the distal ischemic area by reversing
blood flow across the Circle of Willis. In incomplete occlusive
lesions or partially removed occlusions, retrograde arterial flow
distal the occlusion can further be improved by infusing a
vasodilator through lumen 15 and port 16. Vasodilatation distal to
the balloon occluder reduces pressure within the closed chamber and
increases the pressure differential across the occlusion. Lumen 15
and port 16 can also be used to infuse t-PA to lyse the occlusion
or perfuse blood or other fluid distally after the occlusion is
removed by suction and chopping mechanism 7.
[0042] FIG. 6 depicts still another embodiment of the device having
perfusion ports proximal the balloon occluder. The device comprises
a catheter, perfusion lumen 19, and balloon occluder 12, which is
mounted on distal end 2 of the catheter and communicates with
inflation lumen 11. The catheter has a proximal end (not shown),
distal end 2, and lumen 5, which communicates with port 6. The
proximal end and the lumen are adapted for aspiration or infusion
of fluid or blood. Perfusion lumen 19 has two concentric
cylindrical members and communicates with 1, 2, 3, 4, 5, 6, or
other number of perfusion ports. Perfusion ports 25 and 26 are
located respectively on first member 20 and second member 21. The
second member can be rotated relative to the first member so that
the perfusion ports on the first member align with the perfusion
ports on the second member.
[0043] In use, distal end 2 of the catheter can be inserted
directly into a symptomatic carotid artery in the emergency room,
after the occlusion is localized with IVUS and regular carotid
doppler. The catheter can also be inserted through a guide wire as
distal as the occlusion in a cerebral artery, e.g., the ICA,
terminal ICA, carotid siphon, MCA, or ACA in an angiogram suite
ideally within a few hours of stroke symptom but up to 18 to 24
hours after. Balloon occluder 12 is inflated proximal to the
occlusion to create a closed chamber between the occluder and the
occlusion. Second member 21 is rotated relative to first member 20
so that perfusion ports 25 and 26 are in complete alignment. High
pressure, pulsatile or nonpulsatile perfusion, which involves flow
rates of approximately 200 to 300 cc/min, is initiated through
lumen 19 and perfusion ports 25 and 26, thereby opening ipsilateral
collateral arteries. This enhanced antegrade circulation thus
provides improved perfusion to the ischemic area distally and an
increased pressure gradient across the occlusion, which may result
in dislodgment of the occlusion onto port 6. The more distal the
occlusion, the larger the number of potential collateral arteries
are available for recruitment, and the higher the likelihood a
patient will benefit from the devices and methods. A vasodilator
can be infused or vacuum can be applied through lumen 5 and port 6
to reduce pressure in the closed chamber, thereby enhancing
retrograde arterial collateral circulation and facilitating
dislodgment of the occlusion. The occlusion is removed from the
artery by removing the catheter under continuous suction. Focal
hypothermia, which has been shown to be neuroprotective, can be
administered by perfusing hypothermic oxygenated blood or fluid.
Perfusion through perfusion ports 25 and 26 or port 6 distally can
be achieved by withdrawing venous blood from a peripheral vein and
processing through a pump oxygenator, or by withdrawing oxygenated
blood from a peripheral artery, such as a femoral artery, and
pumping it back into the carotid artery.
[0044] The flow rate of blood through the perfusion ports can
easily be controlled by rotating second member 21 relative to first
member 20 as depicted in FIGS. 7A, 7B, and 7C. In FIG. 7A, the
second member is rotated so that ports 25 and 26 are completely
misaligned, thereby achieving no flow through the ports. As second
member 21 is rotated clockwise relative to first member 20 in FIG.
7B, ports 26 on the second member become partially aligned with
ports 25 on the first member, thereby achieving some flow through
the ports. In FIG. 7C, with continuing clockwise rotation of the
second member, ports 26 become completely aligned with ports 25,
thereby achieving maximum flow through the ports.
[0045] The device of FIG. 6 may further comprise manometer 10
mounted distal to occluder 12, chopping mechanism 7 associated with
port 6 of the catheter, and second balloon occluder 30 as shown in
FIG. 8A. Balloon occluder 30 is mounted proximal to the perfusion
ports and communicates with inflation lumen 29. In use, a distal
end of the catheter is inserted into a cerebral artery and balloon
occluder 12 is inflated proximal to occlusion 202 as depicted in
FIG. 8B. Balloon occluder 30 is inflated prior to or during
high-pressure perfusion of blood through perfusion ports 25 and 26
to reduce run-off of perfused blood proximally, thereby maintaining
perfusion pressure to collateral artery 75. When cessation or
reduction of perfusion is desired, occluder 30 can be deflated in
addition to rotating the second cylindrical member relative to the
first member to misalign the perfusion ports. By applying
high-pressure perfusion through ports 25 and 26 for antegrade
collateral enhancement and suction to lumen 5 and port 6 to reduce
pressure within the closed chamber for retrograde collateral
enhancement, pressure distal the occlusion is greater than the
pressure proximal the occlusion. This pressure differential may
dislodge occlusion 202 onto port 6, whereupon the chopping
mechanism 7 is automatically or otherwise activated to remove the
occlusion. With occluder 30 inflated, occluder 12 may be
intermittently deflated and inflated to create alternating negative
and positive pressure within the closed chamber, similar to an
intra-aortic balloon pump (IABP), to facilitate dislodgment of the
occlusion.
[0046] If suction fails to dislodge the occlusion, a thrombolytic
agent, e.g., t-PA, can be infused through lumen 5 and port 6 to
lyse any thrombotic material with greater local efficacy and fewer
systemic complications. Administration of thrombolytic agent,
however, may not be recommended for devices which are inserted
directly into the carotid artery due to increased risk of
hemorrhage. If perfusion through ports 25 and 26 are continued for
more than a few minutes, removal of excess fluid from the
circulation is required to avoid fluid overload. Fluid can be
withdrawn from a jugular vein or from any other peripheral vein or
artery, e.g., the femoral vein or artery, and re-introduced into
the symptomatic artery. Moderate hypothermia, at approximately 32
to 34.degree. C., can be introduced during the fluid
recirculation.
[0047] In patients with vertebral artery occlusions, treatment with
angioplasty often results in disastrous complications due to
embolization of the occlusive lesion downstream to the basilar
artery. Emboli small enough to pass through the vertebral arteries
into the larger basilar artery are usually arrested at the top of
the basilar artery, where it bifurcates into the posterior cerebral
arteries. The resulting reduction in blood flow to the ascending
reticular formation of the midbrain and thalamus produces immediate
loss of consciousness. The devices described in FIG. 3 and FIG. 6
can be used to (1) remove thromboembolic material from the
vertebral artery by utilizing the concept of reversing cerebral
blood flow by ipsilateral occlusion, or (2) provide protection
during angioplasty and/or stenting by occluding the artery to
prevent distal blood flow carrying, emboli from progressing through
the basilar artery. In using the device of FIG. 3, the occlusion
site is first localized with transcranial doppler and angiogram.
The catheter can be inserted through an incision on a peripheral
artery into the symptomatic vertebral artery or the subclavian
artery. In FIG. 9, distal end 6 of catheter 1 is shown inserted
proximal to thromboembolic material 202 in right vertebral artery
87 and left subclavian artery 84. Balloon occluder 12 is then
inflated to occlude the arterial lumen, thereby reducing flow in
the symptomatic vertebral artery. Alternative approaches involve
deployment of the occluder positioned in brachiocephalic artery 82,
or in subclavian artery 83. In this manner, blood flow is diverted
from the contralateral vertebral artery down the symptomatic
vertebral artery. When continuous or intermittent suction is
applied to the distal end of the catheter, the pressure gradient
across the occluding lesion increases and thromboembolic material
202 may be dislodged and captured by the aspiration port. The
thromboembolic material may be removed by the chopping mechanism or
by removing the catheter under continuous suction, thereby reducing
the risk of embolization to the basilar artery.
[0048] FIG. 10 depicts different sites of entry for the devices
disclosed herein. An incision can be made on a peripheral artery,
such as right femoral artery 122, left femoral artery 120, right
radial artery 116, left radial artery 115, right brachial artery
112, left brachial artery 110, right axillary artery 126, left
axillary artery 115, right subclavian artery 142, or left
subclavian artery. An incision can also be made on right carotid
artery 132 or left carotid artery 130 in emergency situations.
[0049] The length of the catheter will generally be between 20 to
100 centimeters, preferably approximately between 30 and 60
centimeters. The inner diameter of the catheter will generally be
between 0.2 and 0.6 centimeters, preferably approximately 0.4
centimeters. The diameter of the inflated balloon occluder will
generally be between 0.3 and 2 centimeters, preferably
approximately 0.5 and 1.0 centimeters. The foregoing ranges are set
forth solely for the purpose of illustrating typical device
dimensions. The actual dimensions of a device constructed according
to the principles of the present invention may obviously vary
outside of the listed ranges without departing from those basic
principles.
[0050] Although the foregoing invention has, for the purposes of
clarity and understanding, been described in some detail by way of
illustration and example, it will be obvious that certain changes
and modifications may be practiced which will still fall within the
scope of the appended claims.
* * * * *