U.S. patent application number 14/154088 was filed with the patent office on 2014-05-08 for methods and apparatus for reducing localized circulatory system pressure.
This patent application is currently assigned to V-WAVE LTD.. The applicant listed for this patent is V-WAVE LTD.. Invention is credited to Gad KEREN, Randy KESTEN.
Application Number | 20140128796 14/154088 |
Document ID | / |
Family ID | 25280294 |
Filed Date | 2014-05-08 |
United States Patent
Application |
20140128796 |
Kind Code |
A1 |
KEREN; Gad ; et al. |
May 8, 2014 |
METHODS AND APPARATUS FOR REDUCING LOCALIZED CIRCULATORY SYSTEM
PRESSURE
Abstract
The present invention is thus directed to methods and apparatus
for decreasing pressure in a first portion of a vessel of the
cardiac structure of a patient by implanting a shunt communicating
with an area outside said first portion, whereby a volume of blood
sufficient to reduce pressure in said first portion is
released.
Inventors: |
KEREN; Gad; (Kiryat Ono,
IL) ; KESTEN; Randy; (Mountain View, CA) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
V-WAVE LTD. |
Or Akiva |
|
IL |
|
|
Assignee: |
V-WAVE LTD.
Or Akiva
IL
|
Family ID: |
25280294 |
Appl. No.: |
14/154088 |
Filed: |
January 13, 2014 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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13708794 |
Dec 7, 2012 |
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14154088 |
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13107843 |
May 13, 2011 |
8328751 |
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13708794 |
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09839643 |
Apr 20, 2001 |
8091556 |
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13107843 |
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Current U.S.
Class: |
604/9 ;
604/8 |
Current CPC
Class: |
A61B 17/00234 20130101;
A61M 1/1008 20140204; A61B 2017/00243 20130101; A61M 27/002
20130101; A61M 1/125 20140204; A61M 1/1098 20140204; A61B
2017/00252 20130101; A61F 2/2493 20130101; A61M 27/006 20130101;
A61M 1/101 20130101; A61F 2/2412 20130101; A61M 1/122 20140204 |
Class at
Publication: |
604/9 ;
604/8 |
International
Class: |
A61M 27/00 20060101
A61M027/00 |
Claims
1. A system for delivering an implantable device to an atrial
septum, the system comprising: a sheath having a lumen and a distal
opening, the sheath sized for percutaneous advancement across the
atrial septum such that the distal opening is disposed within a
left atrium; a delivery catheter sized for advancement through the
lumen of the sheath; an implantable device configured to be coupled
to the delivery catheter and sized to be advanced through the lumen
of the sheath, the implantable device having a passageway
configured to permit passage of blood therethrough and first and
second self-expanding end regions; and a control wire coupled to
the implantable device, the control wire configured to permit
independent translational control of the implantable device within
the lumen of the sheath.
2. The system of claim 1, wherein the implantable device comprises
a shunt having a first end adapted to communicate with the left
atrium and a second end adapted to communicate with a right
atrium.
3. The system of claim 1, wherein the first and second
self-expanding regions are configured to be compressed in the lumen
of the sheath.
4. The system of claim 3, wherein the lumen of the sheath has a
lumen diameter and the first and second self-expanding regions each
have a diameter, and wherein the diameter is greater than the lumen
diameter.
5. The system of claim 1, wherein the implantable device has a
valve disposed therein, the valve configured to open to permit
blood to flow from the left atrium to a right atrium only when the
left atrial pressure exceeds a pressure in the right atrium.
6. The system of claim 1, further comprising radiopaque markers
disposed on at least one of the delivery catheter and the
sheath.
7. The system of claim 1, wherein at least one of the delivery
catheter and the sheath are configured to permit fluoroscopic
visualization thereof.
8. The system of claim 1, wherein the control wire is configured to
detach from the implantable device upon receipt of a prescribed
tension level.
9. The system of claim 1, further comprising at least one of a
needle and a guidewire configured for transseptal puncture.
10. The system of claim 1, wherein the first self-expanding end
region is configured to provide tactile feedback once deployed.
11. The system of claim 1, further comprising at least one of
hemodynamic and ECG monitoring equipment configured to measure
patient vital signs.
12. A method for delivering an implantable device to an atrial
septum in a patient, the method comprising: percutaneously
delivering a sheath across the atrial septum such that a distal
opening of the sheath is disposed within a left atrium; advancing a
delivery catheter coupled to an implantable device through a lumen
of the sheath; retracting the sheath such that a first
self-expanding end region of the implantable device expands in the
left atrium; further retracting the sheath such that a second
self-expanding end region of the implantable device expands in the
right atrium and the implantable device is secured at the atrial
septum to permit blood to flow through the implantable device; and
removing the sheath and the delivery catheter from the patient.
13. The method of claim 12, further comprising translating the
implantable device within the sheath using a control wire coupled
to the implantable device.
14. The method of claim 13, further comprising applying tension to
the control wire to detach the control wire from the implantable
device.
15. The method of claim 12, wherein percutaneously delivering
comprises percutaneously delivering the sheath via a femoral vein
access point.
16. The method of claim 12, further comprising, prior to
percutaneously delivering the sheath, percutaneously delivering at
least one of a needle and a guidewire to the atrial septum and
puncturing the atrial septum.
17. The method of claim 16, wherein the sheath is delivered over
the guidewire,
18. The method of claim 12, further comprising visualizing at least
one of the delivery catheter and the sheath prior to removing the
sheath and the delivery catheter.
19. The method of claim 12, further comprising, after retracting
the sheath such that the first self-expanding end region of the
implantable device expands, providing tactile feedback that first
self-expanding end region is seated against the atrial septum.
20. The method of claim 12, wherein the first and second
self-expanding end regions are configured to expand to engage
opposing sides of the atrial septum.
21. The method of claim 12, further comprising measuring patient
vital signs using at least one of hemodynamic and ECG monitoring
equipment.
Description
CROSS-REFERENCE TO RELATED APPLICATIONS
[0001] This application is a divisional under 35 U.S.C. .sctn.121
of U.S. patent application Ser. No. 13/107,843, filed May 13, 2011
and entitled "Methods and Apparatus for Reducing Localized
Circulatory System Pressure, the entire contents of which are
incorporated by reference herein, which is a continuation under 35
U.S.C. .sctn.120 of U.S. patent application Ser. No. 09/839,643,
filed Apr. 20, 2001, now U.S. Pat. No. 8,091,556 and entitled
"Methods and Apparatus for Reducing Localized Circulatory System
Pressure," the entire contents of which are incorporated by
reference herein.
FIELD OF THE INVENTION
[0002] The present invention relates to treatments for reducing
specific localized points of high pressure within the circulatory
system, and more particularly to methods and apparatus to either
acutely or chronically reduce left ventricular diastolic pressure
that is created as a result of congestive heart failure or similar
indications.
BACKGROUND OF THE INVENTION
[0003] Congestive heart failure (CHF) is recognized as the most
common cause of hospitalization and mortality in Western society.
CHF is an extremely serious affliction that has a great impact on
the quality of life; it involves the loss of heart rate variability
and rate responsive mechanisms in the heart, leading to impaired
ventricular relaxation and low exercise tolerance. The disease
afflicts about 4 million Americans in any given year; in the USA
alone, there are annually about 400,000 new cases, 1 million
hospital admissions, and $8 billion cost of care. Congestive heart
failure is a syndrome characterized by left ventricular
dysfunction, reduced exercise tolerance, impaired quality of life
and dramatically shortened life expectancy. Decreased contractility
of the left ventricle leads to reduced cardiac output with
consequent systemic arterial and venous vasoconstriction. CHF
develops generally in the course of months or years, and can be the
end stage of chronic hypertension, infarction, angina, or diabetes.
Heart failure, however caused, represents an intrinsic property of
the muscle, and slow relaxation due normal, healthy heart the
duration of contraction and relaxation decreases with increasing
heart rate. This ensures a diastolic period of sufficient duration,
which is important (a) for filling of the ventricle, and (b)
because coronary perfusion and myocardial oxygen supply occurs only
during diastole. The duration of contraction and relaxation is
determined by calcium removal from the contractile filaments,
mainly by the calcium pump in the sarcoplasmic reticulum Increased
heart rate causes more rapid relaxation due to increased activation
of the calcium pump. The latter mechanism is impaired in the
hypertrophied or failing heart due to reduced transcription of the
genes that supply the calcium pump proteins. Therefore, in heart
failure patients an increase of heart rate may almost abolish the
diastolic interval, which leads to reduced ventricular filling, and
reduces myocardial blood supply (Davies et al., 1995, "Reduced
Contraction and Altered Frequency Response of Isolated Ventricular
Myocytes From Patients With Heart Failure," Circulation 92:
2540-2549).
[0004] The syndrome of heart failure is a common course for the
progression of many forms of heart disease. Heart failure may be
considered to be the condition in which an abnormality of cardiac
function is responsible for the inability of the heart to pump
blood at a rate commensurate with the requirements of the
metabolizing tissues, or can do so only at an abnormally elevated
filling pressure. There are many specific disease processes that
can lead to heart failure with a resulting difference in
pathophysiology of the failing heart, such as the dilatation of the
left ventricular chamber. Etiologies that can lead to this form of
failure include idiopathic cardiomyopathy, viral cardiomyopathy,
and ischemic cardiomyopathy. The process of ventricular dilatation
is generally the result of chronic volume overload or specific
damage to the myocardium In a normal heart that is exposed to long
term increased cardiac output requirements, for example, that of an
athlete, there is an adaptive process of ventricular dilation and
myocyte hypertrophy. In this way, the heart fully compensates for
the increased cardiac output requirements. With damage to the
myocardium or chronic volume overload, however, there are increased
requirements put on the contracting myocardium to such a level that
this compensated state is never achieved and the heart continues to
dilate. The basic problem with a large dilated left ventricle is
that there is a significant increase in wall tension and/or stress
both during diastolic filling and during systolic contraction. In a
normal heart, the adaptation of muscle hypertrophy (thickening) and
ventricular dilatation maintain a fairly constant wall tension for
systolic contraction. However, in a failing heart, the ongoing
dilatation is greater than the hypertrophy and the result is a
rising wall tension requirement for systolic contraction. This is
felt to be an ongoing insult to the muscle myocyte resulting in
further muscle damage. The increase in wall stress is also true for
diastolic filling. Additionally, because of the lack of cardiac
output, there is generally a rise in ventricular filing pressure
from several physiologic mechanisms. Moreover, in diastole there is
both a diameter increase and a pressure increase over normal, both
contributing to higher wall stress levels. The increase in
diastolic wall stress is felt to be the primary contributor to
ongoing dilatation of the chamber.
[0005] Presently available treatments for CHF fall into three
generally categories: (1) pharmacological, e.g., diuretics; (2)
assist systems, e.g., pumps; and (3) surgical treatments. With
respect to pharmacological treatments, diuretics have been used to
reduce the workload of the heart by reducing blood volume and
preload. While drug treatment improves quality of life, it has
little effect on survival. Current pharmacological treatment
includes a combination of diuretics, vasodilators, inotropes,
.beta.-blockers, and Angiotensin-Converting-Enzy-me
(ACE)-inhibitors (Bristow & Gilbert, 1995, "Improvement in
Cardiac Myocyte Function by Biological Effects of Medical Therapy:
A New Concept in the Treatment of Heart Failure," European Heart
Journal 16, Supplement F: 20-31). The effect is a decrease of
symptoms, and improved quality of life, but little change in
mortality. Moreover, the exercise tolerance of most patients is
extremely low, as a consequence of limited oxygen supply through
the lungs. Long lasting lack of exercise and malnutrition may
contribute to the condition and partly explain the exercise
intolerance. Indeed, the lack of exercise and deterioration of
cardiac muscle may each contribute to each other, with a
snowballing effect (Coats et al., 1992, "Controlled Trial of
Physical Training in Chronic Heart Failure: Exercise Performance,
Hemodynamics, Ventilation, and Autonomic Function," Circulation 85:
2119-2131). Clinically, preload is defined in several ways
including left ventricular end diastolic pressure (LVEDP), or left
ventricular end diastolic volume (LVEDV). Physiologically, the
preferred definition is the length of stretch of the sarcomere at
end diastole. Diuretics reduce extra cellular fluid that builds in
congestive heart failure patients increasing preload conditions.
Nitrates, arteriolar vasodilators, angiotensin converting enzyme
inhibitors have been used to treat heart failure through the
reduction of cardiac workload through the reduction of afterload.
Afterload may be defined as the tension or stress required in the
wall of the ventricle during ejection. Inotropes such as digoxin
are cardiac glycosides and function to increase cardiac output by
increasing the force and speed of cardiac muscle contraction. These
drug therapies offer some beneficial effects but do not stop the
progression of the disease. Captopril, enalapril and other
inhibitors of angiotensin-converting enzyme (ACE) have been used to
treat congestive heart failure. See Merck Index, 1759 and 3521(11th
ed. 1989); Kramer, B. L. et al. Circulation 1983, 67(4):755-763.
However, such ACE inhibitors have generally provided only moderate
or poor results. For example, captopril therapy generally provides
only small increases in exercise time and functional capacity.
Captopril also has provided only small reductions in mortality
rates.
[0006] Assist devices used to treat CHF include, for example,
mechanical pumps. Mechanical pumps reduce the load on the heart by
performing all or part of the pumping function normally done by the
heart. Currently, mechanical pumps are used to sustain the patient
while a donor heart for transplantation becomes available for the
patient. There are also a number of pacing devices used to treat
CHF. However, in the chronic ischemic heart, high rate pacing may
lead to increased diastolic pressure, indicating calcium overload
and damage of the muscle fibers. Finally, there are at least three
surgical procedures for treatment of heart failure: 1) heart
transplant; 2) dynamic cardiomyoplasty; and 3) the Batista partial
left ventriculectomy. Heart transplantation has serious limitations
including restricted availability of organs and adverse effects of
immunosuppressive therapies required following heart
transplantation. Cardiomyoplasty includes wrapping the heart with
skeletal muscle and electrically stimulating the muscle to contract
synchronously with the heart in order to help the pumping function
of the heart. The Batista partial left ventriculectomy includes
surgically remodeling the left ventricle by removing a segment of
the muscular wall. This procedure reduces the diameter of the
dilated heart, which in turn reduces the loading of the heart.
However, this extremely invasive procedure reduces muscle mass of
the heart.
[0007] One category of CHF is diastolic heart failure (DHF), which
afflicts between 30% and 70% of those patients with heart failure.
DHF is an episodic clinical syndrome that can instigate pulmonary
edema, possibly necessitating hospitalization and ventilatory
support. The heart is a complex pump structured of two atria and
two ventricles that pump blood in parallel into the pulmonary
circulation at a relatively low pressure (right ventricle peak
systolic pressure is about 25 mmHg) and the systemic circulation
(left ventricle peak systolic pressure is about 120 mmHg). During
the diastolic phase of the cardiac cycle the ventricles of the
heart fill via the respective atria. The pressure differential that
propels blood from the respective venous circulations to the atria
and ventricles (systemic to the right ventricle and pulmonary to
the left ventricle) is low, less than about 5 mmHg. On the left
side, during diastole (when the mitral valve opens), pressure in
the left atrium normally is not more than 12 mmHg. Due to active
diastolic relaxation at the onset of diastole, the pressure
difference between the left atrium and the left ventricle is
augmented contributing to the early rapid diastolic filling of the
left ventricle. Diastolic pressures in the atrium and the ventricle
at this phase of the cardiac cycle drop quickly to less than 5 mmHg
and equalize. At this point during diastole, the process of filling
the left ventricle partially stops (diastiasis) and is renewed only
towards late diastole, when active contraction of the atrium
occurs, resulting in increased left atrial pressure and an
increased pressure differential between the atrium and the
ventricle. Atrial contraction is very important for maintaining
adequate left ventricular filling during exercise and other states
of increased cardiac output demand, or when the left ventricle
fails to relax normally such as during ischemia or LV hypertrophy.
Toward the end of diastole, pressure in the left ventricle (LVEDP)
is increased but is normally not more than 12 mmHg.
[0008] Disease states in which active and passive relaxation
properties of the left ventricle are disturbed, or the pumping and
emptying capacity of the ventricle is reduced, may be translated to
increased diastolic pressures in the left ventricle. The higher
pressures and distension of the left ventricle cause a rise in wall
stress and increased oxygen consumption. Up to a limit, the
increased diastolic pressure and increased ventricular size result
in augmented stroke volume. This compensatory mechanism is limited
and has a significant physiologic price mainly when the slope of
the pressure-volume curves turn steep, and left ventricular
diastolic pressures becomes markedly high (>20 mmHg). At this
point, a state of pulmonary congestion may ensue, turning later to
a life threatening state of pulmonary edema.
[0009] A number of cardiovascular diseases can cause significant
cardiac dysfunction and lead to the above-mentioned
pathophysiologic state and pulmonary edema. These include:
hypertension, ischemic heart disease state and post myocardial
infarction, idiopathic dilated cardiomyopathy, valvular heart
disease, including aortic stenosis, mitral stenosis, aortic
regurgitation, mitral regurgitation, and combined valvular heart
disease. Other primary myocardial diseases such as post partum and
hypertrophic cardiomyopathy may cause similar conditions. In all
these disease states with either decreased ability for the left
ventricle to pump blood (systolic dysfunction) or reduced fling
capacity (diastolic dysfunction) left ventricular diastolic
pressure rises. Increased diastolic pressure in the left ventricle
eventually in and of itself becomes a cause for greater degradation
in cardiac function than occurred as a result of the original
insult. The augmented pressures may cause as stated previously
pulmonary congestion and dyspnea. At extreme conditions the
clinical state may deteriorate to pulmonary edema.
[0010] There are several known techniques to attempt to overcome
the state of left ventricular dysfunction, increased diastolic left
ventricular pressures and pulmonary congestion. However, none are
fully satisfactory. For example, pharmacological treatments are the
only practical methods for chronic therapy for most of the
population with congestive heart failure. The pharmacological
agents used to treat congestive heart failure result in a reduction
in diastolic pressure and prevention of pulmonary and peripheral
congestion discussed above, diuretics, vasodilators and digoxin.
Diuretics reduce the volume load and thereby reduce preload and
diastolic wall stress. Vasodilators have a dual effect in reducing
arterial resistance as well as increasing venous capacitance,
thereby reducing preload and after load and wall stress throughout
the cardiac cycle. These drugs, either direct acting on the
vasculature or via neurohormonal mechanisms (ACE inhibitors), are
limited in their effect since they may cause hypotension in a
significant number of patients with myocardial dysfunction. These
pharmacological agents are of limited value mainly because of their
side effects. The use of diuretics is associated with side effects
related to the drugs and to the detrimental effect on renal
function. Vasodilators have also many side effects some of which
limit the use of the drugs and their efficacy including hypotension
in many patients. Drug therapy results in many of the patients in
relative clinical stability. However, episodes where
intraventricular diastolic pressure may rise above physiologic
needs for cardiac stroke volume augmentation and culminate into
pulmonary edema occur often and are very difficult to manage.
[0011] In extreme acute situations, temporary assist devices and
intraaortic balloons may be helpful. Cardiac transplantation and
chronic LVAD implants are solutions available for a small part of
the patient population and as last resort. However, all the assist
devices currently used are intended to improve pumping capacity of
the heart and increase cardiac output to levels compatible with
normal life. Finally, cardiac transplantation is another solution,
but is not a very practical and is limited to extreme cases and as
are the various assist devices. The mechanical devices were built
to allow propulsion of significant amount of blood (liters/min) and
this is also their main technological limitation. The need for
power supply, relatively large pumps and danger of hemolysis and
infection are all of significant concern.
[0012] Thus, there exists a long-felt and as of yet unsolved need
for a treatment that addresses the course of congestive heart
failure, and in particular the high pressure of the left ventricle
and the compounding factors that are associated with it. It would
therefore be desirable to provide methods, apparatus and treatments
that beneficially reduce and regulate the pressure within the left
ventricle. It is an object of the present invention to provide
methods and apparatus for reducing left ventricular end diastolic
pressure, and more particularly to provide methods and apparatus
without deleterious side effects. It is a further object of the
present invention to provide methods and apparatus that can be used
in a minimally invasive manner for both acute and chronic
treatments.
SUMMARY OF THE INVENTION
[0013] The present invention reduces the increased diastolic
pressure that can occur as part of the clinical syndrome referred
to as Congestive Heart Failure (CHF). Passive and semi-passive
devices to reduce left ventricular end-diastolic pressure are
disclosed, and in preferred embodiments, a shunt-type device allows
a small volume of blood to be released from the left ventricle to
reduce the pressure. Certain embodiments use a passive check-valve
that allows flow only above a given threshold pressure, while
others use a passive check-valve that allows flow only within a
window between a lower pressure threshold and a higher-pressure
threshold. Embodiments employing check valves prevent shunting
during left ventricular systole. Alternatively, semi-passive
embodiments have a valve activated by an external signal, such as
an intra-corporeal electrical battery or an externally coupled
energy source. A third type of preferred embodiment of the
invention employs an device such as a pump to actively move blood,
with the intent of preventing further deterioration of the
patient's heart failure or allowing for some reversal of the heart
failure. For example in patients presenting with diastolic heart
failure (DHF) the present invention prevents this occurrence by
reducing diastolic pressures in the left atrium below the excessive
levels that would otherwise have caused pulmonary edema.
[0014] The present invention is thus directed to methods and
apparatus for decreasing pressure in a first portion of a vessel of
the cardiac structure of a patient by implanting a shunt
communicating with an area outside said first portion, whereby a
volume of blood sufficient to reduce pressure in said first portion
is released. Preferably, the first portion comprises the left
ventricle and the pressure reduced is the end diastolic pressure,
which is accomplished by having the shunt communicate with the left
ventricle so a small volume of blood is released from the left
ventricle to reduce the end diastolic pressure. Most preferably,
the shunt selectively permits flow when a pressure differential
between the left ventricle and another chamber of a heart above a
threshold pressure, whereby shunting is prevented during left
ventricular systole, or, alternatively, selectively permits flow
when a pressure differential between the left ventricle and another
chamber of a heart is between a lower threshold and a higher
threshold, whereby shunting is again prevented during left
ventricular systole. In certain embodiments a semi-passive
check-valve is controlled and actuated by an external signal,
either using a signal generated by an intra-corporeal electrical
battery or an externally coupled energy source. In certain
embodiments, the shunt has a pump with an input connected to the
left ventricle, or other portion with excessive pressure, and an
output connected to a volume of lower pressure. The preferred
method of implanting the shunt to effect the present invention is
by deploying a tubular element having two ends and a tissue
affixation element disposed at each of said ends via a catheter,
preferably, the fixation element is a shape retaining metallic
material that returns to its original shape as part of the
retention aspect of its function. In preferred embodiments of the
apparatus, the tubular element is comprised of a biologically inert
non-metallic material.
BRIEF DESCRIPTION OF THE DRAWINGS
[0015] FIG. 1 is a perspective view of a first embodiment of an
implantable shunt made in accordance with the present
invention;
[0016] FIG. 2 is a side elevation view, in cross-section as shown
by lines 2-2 in FIG. 1, illustrating the placement of the shunt
shown in FIG. 1 in a septum, and showing diagrammatically the use
of a pump to augment flow in certain embodiments; and
[0017] FIGS. 3-5 are a cross sectional view of a patient receiving
a shunt made in accordance with the present invention via
percutaneous placement.
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
[0018] Referring now to FIG. 1, there is shown a perspective view
of a first embodiment of a shunt 100 made in accordance with the
present invention. The shunt 100 is comprised of a fixation element
110, which is shown as a planar circular element. It will be
understood, however, that the fixation element 110 can be circular,
polygonal, spiral or many other shapes. Moreover, the fixation
element can lie in a single plane or be curved in multiple planes,
such as in a helical configuration. It can be constructed of a
variety of materials that offer the elastic range and spring-like
characteristics that will enable passage through a catheter lumen,
or through the lumen of another implantation assistance device, in
a relatively straightened configuration and then recovery of its
fill fixation configuration shape. In certain embodiments, the
fixation element can be made of reduced size and then expanded
through the use of shape-memory alloys (SMA's), such as
nickel-titanium (NiTi, also known as nitinol), that change shape in
response to temperature changes and which are fabricated such that
the temperature change from below body temperature to body
temperature causes the shape conversion necessary for implantation.
If SMA materials are not used, suitable materials include
super-elastic metals, such as NiTi or stainless steel, such as the
alloy ELGILOY.RTM., commonly used for medical implants.
Additionally, polymeric materials can be used to form the fixation
element or as a coating over a metallic core. The fixation element
may be coated and/or textured as so as to increase its
biocompatability or to increase the degree to which it quickly
becomes endothelialized, which may be desired in some implantation
conditions.
[0019] As illustrated, the fixation element 110 surrounds and
positions the shunt tube element 120, which is provided so as to
enable passage of blood from a region of high pressure, such as the
left atrium, to a region of lower pressure, such as the right
atrium. The dimensions of the shunt tube element 120 are chosen so
as to be as small as possible while still allowing sufficiently
rapid fluid flow without endangering blood coagulation induced by
blood stasis or low-flow zones. Computational fluid dynamics
methods can be used to appropriately shape the element so as to
minimize low-flow zones and maximize laminar flow. The inside
diameter of the shunt tube is preferably greater than 1 mm and less
than 5 mm, but it will be understood that a wide range of shapes
and diameters can be constructed that will effect the purpose of
the present invention in a variety of patients and flow conditions
within those patients. The shunt tube element 120 is preferably
formed of either metallic or polymeric materials and may be coated
and/or textured as mentioned above. Pyrolitic carbon coating, as is
commonly used in implantable mechanical heart valves, can be used
to increase the degree to which the surface is biologically inert.
Examples of such commercially available materials include On-X
{circle over (R)} Carbon, from Medical Carbon Research Institute,
LLC, of Austin, Tex.
[0020] Also illustrated in FIG. 1 is a valve element 130, which as
explained below is not necessarily included in all embodiments
within the scope of the present invention and can be of a variety
of forms. As illustrated a leaflet 131,132 can be used, either in a
single piece or as a dual leaflet design as illustrated. In the
embodiment shown in FIG. 1, each leaflet 131,132 is a flat plate
that pivots to open and close the orifice of the shunt tube. A
ball-and-socket design can be used as well. Another alternative
design is the duckbill-type valve. The valve element can be formed
using the same range or materials and coatings mentioned above for
the shunt tube,
[0021] From the foregoing, it will be appreciated by those of skill
in the art that the present invention is well adapted to
percutaneous placement via femoral access, however, other
implantation techniques such as surgical techniques using either an
open chest procedure or those using minimally invasive techniques
are also within the scope of the present invention.
[0022] The concepts of allowing pressure to be relieved in one area
of the circulation by shunting to an area of lower pressure as
disclosed herein may take many embodiments, all of which will be
apparent to those of skill in the art upon review of the foregoing
descriptions of the physiology and medicine involved, and the
description of the embodiment of FIG. 1.
[0023] In accordance with the present invention, the device may or
may not include the valve element 130, since in certain patients or
to treat certain conditions a valve would add complexity while not
providing necessary functionality. Similarly, depending upon the
circumstances of use, the valve element 130 may be either passive
(actuated by the force of blood) or active (actuated by some other
portion of the device). In active valve embodiments, the valve
element 130 may include electric or electromagnetic elements that
can be selectively actuated to open and close the valve element 130
or, if the valve element is designed for gradual opening and
closing, move the valve element 130 between a first position and a
second position. In some embodiments, the valve will be chosen and
designed so that it responds only upon certain conditions occurring
within the heart, such as the following: absolute left atrial
pressure, differential atrial pressure, other intra-cardiac
pressures, other cardiovascular pressures, or other physiological
conditions that might correlate to an exacerbated state of
diastolic heart failure, such as blood oxygen saturation or pH. In
such embodiments, response to any given pressure or differential
pressure will imply that a portion of the implanted device is in
fluid communication with the relevant pressure source or sources.
These embodiments will provide robust and reliable functionality by
being mechanical and operating with signal inputs. All shunts,
whether they include a valve or not can be further enhanced by
including a check-valve that will prevent backflow. Those of skill
in the art will appreciate that it is typically desirable to
prevent flow from the right heart to the left heart, and thus one
or more check valves can be appropriately placed. A double-check
valve allows blood pressure above a lower limit but below a higher
limit to actuate the valve, thus in a preferred embodiment,
shunting blood from the left side to the right side only during a
period of diastole.
[0024] Referring now to FIG. 2, another aspect of the devices of
the present invention is that the shunt 100 may or may not be in
fluid communication with a pump 140, such as either a surgically
implanted pump that continuously moves a small amount of blood from
one chamber or area to another, for example from the left ventricle
chamber to the aorta for chronic reduction of LVEDP. Alternatively,
the invention can include a catheter-based pump that continuously
moves a small amount of blood from the LV chamber to the aorta for
acute reduction of LVEDP. In certain preferred embodiments, the
pump and valve will have a heart-synchronized actuated valve to
allow specific regimens of left-to-right shunting to be applied. As
seen in FIG. 2, after the shunt 100 is placed in a septum or other
area, the pump 140 may be placed so as to direct fluid toward the
shunt, the pump may be directly connected to the shunt, juxtaposed
to the shunt, or displaced from the shunt but capable of directing
flow in such a way as to effect more efficient pressure
reduction.
[0025] FIG. 2 shows an implant similar to that of FIG. 1 that is
placed surgically for the chronic reduction of LVEDP. This device
includes a relatively small-sized pump 140, which can be similar to
those used in Left-Ventricular Assist Devices (LVADs). Unlike the
LVAD, however, the disclosed invention does not seek to
significantly "support" the function of the left ventricle by
pumping blood from the LV chamber to the body. Rather, it is
intended only to "offload" the excessive pressure that builds
through the diastolic phase of the cardiac cycle in some CBF
patients. Whereas a normal LVEDP is in the range of 6-12 mmHg,
patients with diastolic dysfunction heart failure (DDHF),
end-diastolic pressure (EDP) in the left atrium (LA) and left
ventricle (LV) can rise considerably above normal levels. Therefore
the present invention encompasses a number of embodiments that are
both capable of being either implanted during a surgical procedure
or using a catheter (percutaneous). The shunt 100 allows blood to
flow in the direction shown by the arrows so long as there is a
lower pressure in the chamber or vessel adjoining the LV. In any
embodiment, the methods and apparatus of the present invention
reduce EDP, and in particular mitigate the most severe consequences
of significantly increased EDP, such as pulmonary edema.
[0026] Thus, in preferred embodiments of the present invention the
shunt is disposed in a wall between the chambers of a patient's
heart, and most preferably, disposed in the atrial septum to permit
blood to flow from the left ventricle when the pressure within the
ventricle exceeds the pressure of the adjoining atrial chamber. In
another particular embodiment, a sophisticated shunt apparatus
implanted in the intra-atrial septum to allow intermittent and
controlled blood flow from the left atrium to the right atrium
(RA), thereby reducing LAEDP. Alternatively, the shunt might have
its origin in locations other than the LA, such as the LV, and
might have its output at locations other than the RA, such as the
light ventricle (RV).
[0027] As explained above, although one class of embodiments of the
present invention is designed to be purely mechanical and will have
certain advantages, the present invention also encompasses
additional embodiments wherein additional features such as internal
signal processing unit 148 and an energy source 150, such as a
battery, are included. In such embodiments, the shunts described
above will include a valve apparatus that responds to conditions
other than those occurring within the heart and/or has internal
signal processing requiring an energy source. A device of this type
responds according to programmed algorithms to all of the
conditions mentioned above. The signal processing ability of
devices in such embodiments enable adaptive approaches as well, in
which the device response to conditions will change over time
according to a pre-programmed adaptation algorithm. Such
embodiments will include additional apparatus, such as a power
source 150, sensors 155 and the like. The provision of implantable,
programmable electrical devices that collect cardiac data and
effect the operation of certain other elements of a device are well
known in the field of cardiac pacing, for one example. In one
particular embodiment, the actively controlled valve of the shunt
as in senses and responds to electrical signals so as to act in
synchronization with the cardiac cycle.
[0028] Either passive or active devices may be linked to an
external indicator 157, such as pendant worn by the patient, that
displays the device status. Such an indicator enables the patient
to notify a physician in the event of an activation of the
implanted device that corresponds to the significantly exacerbated
state heart failure. In this case, the device will be acting to
prevent the occurrence of pulmonary edema during the time that the
patient notifies a physician and then undergoes medical treatment
to reduce the severity of the patient's condition.
[0029] Similarly, any embodiment of the present invention may be
designed so that an external device can be used on occasion to
either mechanically adjust (in the case of passive devices; for
example, by magnetic coupling) and/or to reprogram (in the case of
active devices the functioning of the implanted device.
[0030] The methods mentioned above will prevent from excessive
pressures to build up in the left ventricle and help restore wall
stress in diastole and systole to normal values quickly thus
helping the introduction of pharmacological agents as adjunct
therapy or vice versa. This mode of therapy will be complementary
to the current management of the patients and allow more controlled
stabilization. It can be added as a component of cardiac pacemaker
(dual or biventricular) and derive the power supply from the
pacemaker battery.
[0031] The pressure/flow/volume requirements of the various
embodiments of the present invention will be determined using
methodologies similar to those used to design a Left Ventricular
Assist Device (LVAD) but with certain distinctly different flow
requirements, rather than the intent of supporting systemic
circulation requirements found in a LVAD. Thus, certain shunts made
in accordance with the present invention can use designs and
dimensions that would not be appropriate or adequate for an LVAD.
Patients with heart failure dominated by systolic dysfunction
exhibit contraction abnormalities, whereas those in diastolic
dysfunction exhibit relaxation abnormalities. In most patients
there is a mixed pathophysiology. Normal pulmonary venous pressure
(PVP) necessary for the normal LV to adequately fill and pump is
less than 12 mmHg. Patients with systolic dysfunction have larger
LV volume to maintain SV and may need increased PVP to fill (mixed
systolic diastolic dysfunction). Patients with diastolic
dysfunction need increased PVP for the LV to fill and adequately
pump.
[0032] The hemodynamic performance of the present invention, and
thus the design of the shunt and its actuation, placement etc. will
be determined by a variety of factors, for example, the following
table is in the form of:
TABLE-US-00001 IF ({LAEDP} AND/OR {Mean LA P}) AND/OR ({.DELTA.
LAEDP-RAEDP} AND/OR {.DELTA. Mean LA P-Mean RA P}} THEN
{ACTION}
[0033] In which LAEDP, Mean LA P. RAEDP and Mean RA P refer to
minima, maxima or ranges for the respective pressures (please
specify which in the table), and the AND/OR indicate that a logical
operator or an NA (not applicable) should be entered
TABLE-US-00002 IF AND/ Mean AND/ .DELTA. Atrial AND/ .DELTA. mean
Then Scenario LAEDP OR LA P OR EDP OR atrial P (Action) Ex. Exceeds
Or Exceeds NA NA NA NA Remove sufficient 25 20 blood from the LA to
reduce LA pressure by 5 mmHg
[0034] Thus for example, a chronic device can be a preventive
device where when pressures rise for some reason to dangerous
levels the pump goes into action and helps to lower the pressure in
the left ventricle, thereby preventing the acute development of
dyspnea and pulmonary edema and assures that the LVDP are always at
an optimal level of no more than 15 mmHg.
[0035] In other embodiments and for other indications, the present
invention might move an extra volume of blood from the LV into the
aorta. To do so, the pump 140 must be capable of moving blood from
a chamber exhibiting 20 mmHg in diastole to 70 mmHg in the aorta.
Another possible chamber where blood from the LA (throughout the
cardiac cycle) or LV (only in diastole) can be directed to is the
Right Atrium, and alternatively right ventricle. The benefit of
directing blood from LA to RA is that the pressure differences are
smaller and the blood can be moved in diastole and systole as well.
Filling of the atria (R and L) during the systolic phase of the
cardiac cycle determines the pressure in the atria at the onset of
diastole and the opening of the valves.
[0036] Those of skill in the art will appreciate that there are a
number of techniques for placement and locations for placement of
shunts made in accordance with the present invention. For example,
a surgically implanted passive shunt can be placed between the left
ventricle and the right atrium for chronic reduction of LVEDP.
Alternatively, a surgically implanted passive shunt can be placed
between the left atrium and the right atrium for chronic reduction
of LVEDP. For percutaneous placement, a catheter-based passive
shunt can be inserted from the right atrium trans-septally into the
left atrium for acute reduction of LVEDP. Another catheter
delivered embodiment is a passive shunt that is implanted from the
right atrium trans-septally into the left atrium for chronic
reduction of LVEDP.
[0037] Although the present invention provides new and useful
methods of treatment, the techniques of implanting shunts as
described herein is well known. For one example, in a preferred
embodiment of the present invention, as illustrated in FIGS. 3-5, a
transseptal needle set 160 is advanced toward the wall of the right
atrial septum. Access has been made from the femoral vein with the
system being advanced through the inferior vena cava and into the
right atrium. Devices that allow such access and subsequent
transseptal puncture are available from Cook Incorporated. For
example, the procedure can be carried out using a stainless steel
and obrturator set TSNC-18-71.0 for adults and TSNC-19-56.0 for
pediatric patients. Once transseptal puncture has been achieved, a
guidewire 170 is exchanged for the needle component in the
commercially available device described above and then passed into
the left atrium. The process of securing catheter access to the
left atrium by way of a transseptal puncture is further described
in the standard medical text Braunwald, Heart Disease, (Ch. 6, p.
186) which is incorporated herein by reference. After the
transseptal sheath 165 is positioned in the left atrium, as
described above, the placement of a shunt 100 made in accordance
with the present invention is initiated. The following is a
generalized sequence; the placement procedure will be done
according to the typical methods of interventional cardiology as
are well known to physicians trained in that subspecialty. The
typical supporting apparatus found in the cardiac catheterization
laboratory will be used, such as fluoroscopy for visualization and
hemodynamic and ECG monitoring equipment to assess catheter
position and patient vital signs.
[0038] The dilator and wire will be withdrawn from the sheath that
now extends from the femoral vein access point in the patient's
groin to the left atrium, traversing the femoral vein, the illiac
vein, the inferior vena cava, the right atrium, and the atrial
septum The delivery catheter will be passed through the sheath
while under fluoroscopic visualization. Radiopaque markers are
provided on this catheter as well as the sheath in order to locate
specific points. The delivery catheter is carefully and slowly
advanced so that the most distal portion of the left-atrial
fixation wire is emitted from the distal opening of the catheter
and into the chamber of the left atrium. The fixation wire is
formed from a spring-like material and/or may be super-elastic of
shape memory alloy, so that as it leaves the constraint provided by
the inner lumen of the delivery catheter, it reforms into its fully
formed shape, which may circular or polygonal as previously
disclosed. The assembly of the sheath and the delivery catheter are
then slowly retracted en bloc so as to withdraw the fixation wire
towards the atrial septum. The physician stops this retraction when
it becomes apparent by fluoroscopic visualization as well as by
tactile feedback that the fixation wire has become seated against
the atrial septum. At that point, the sheath alone is retracted,
uncovering the shunt and positioning it within the opening that has
been created within the atrial septum. The sheath is then further
retracted, allowing the right-atrial fixation wire to reform into
its fully formed shape. The entire shunt assembly is then detached
from the delivery catheter system The shunt is controlled within
the delivery catheter by means of long controller wire that has
independent translational control within the catheter lumen. This
attachment is formed by any conventional method, e.g., a solder or
adhesive or the like that will mechanically detach at a prescribed
tension level, that level being exceeded by the physician at this
point in the procedure by firmly retracting the controller
wire.
[0039] Although certain embodiments have been set forth and
described herein, numerous alterations, modifications, and
adaptations of the concepts presented will be immediately apparent
to those of skill in the art, and accordingly will lie within the
scope of the present invention, as defined by the claims appended
hereto.
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