U.S. patent application number 13/914437 was filed with the patent office on 2014-04-03 for heart wall tension reduction apparatus and method.
The applicant listed for this patent is Edwards Lifesciences. Invention is credited to Todd J. Mortier, Cyril J. Schweich, JR., Robert M. Vidlund.
Application Number | 20140094647 13/914437 |
Document ID | / |
Family ID | 43357196 |
Filed Date | 2014-04-03 |
United States Patent
Application |
20140094647 |
Kind Code |
A1 |
Schweich, JR.; Cyril J. ; et
al. |
April 3, 2014 |
HEART WALL TENSION REDUCTION APPARATUS AND METHOD
Abstract
Devices and methods for treatment of a failing heart by reducing
the heart wall stress. The device can be one which reduces wall
stress throughout the cardiac cycle or only a portion of the
cardiac cycle.
Inventors: |
Schweich, JR.; Cyril J.;
(St. Paul, MN) ; Vidlund; Robert M.; (Maplewood,
MN) ; Mortier; Todd J.; (Minneapolis, MN) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
Edwards Lifesciences |
Irvine |
CA |
US |
|
|
Family ID: |
43357196 |
Appl. No.: |
13/914437 |
Filed: |
June 10, 2013 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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13609585 |
Sep 11, 2012 |
8460173 |
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13914437 |
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12832507 |
Jul 8, 2010 |
8267852 |
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13609585 |
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10127731 |
Apr 23, 2002 |
7883539 |
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12832507 |
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09843078 |
Apr 27, 2001 |
6402680 |
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10127731 |
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09522068 |
Mar 9, 2000 |
6264602 |
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09843078 |
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09124321 |
Jul 29, 1998 |
6077214 |
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09522068 |
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09985361 |
Nov 2, 2001 |
6589160 |
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10127731 |
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09697597 |
Oct 27, 2000 |
6332864 |
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09985361 |
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09492777 |
Jan 28, 2000 |
6162168 |
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09697597 |
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08778277 |
Jan 2, 1997 |
6050936 |
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09492777 |
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Current U.S.
Class: |
600/37 |
Current CPC
Class: |
A61F 2/2481 20130101;
A61B 2017/048 20130101; A61B 2017/00243 20130101; A61B 17/00234
20130101; A61B 2017/0404 20130101; A61B 2017/0496 20130101; A61B
17/1227 20130101 |
Class at
Publication: |
600/37 |
International
Class: |
A61F 2/24 20060101
A61F002/24 |
Claims
1. A method for improving the function of a heart, the method
comprising: positioning a passive device relative to an external
heart wall, the device including a wrap and at least one elongated
band secured to the wrap, wherein the wrap has sufficient length to
encircle a portion of the heart, and wherein the band extends in a
direction substantially perpendicular to the length of the wrap;
encircling a portion of the heart with the wrap of the device;
securing the device to an epicardial surface of the heart; and
exerting a force on the external heart wall with the device during
a portion of a cardiac cycle.
2. The method of claim 1, wherein the band includes a plurality of
bands.
3. The method of claim 2, wherein the plurality of bands are
secured to one another.
4. The method of claim 1, wherein the device includes a
predetermined size adapted to not encompass an apex of the heart,
and wherein encircling a portion of the heart with the wrap of the
device comprises leaving the apex of the heart uncovered by the
wrap.
5. The method of claim 1, wherein exerting a force on the external
heart wall comprises altering a geometric configuration of the
heart.
6. The method of claim 5, wherein the geometric configuration is a
shape of a heart chamber.
7. The method of claim 6, wherein the heart chamber is a left
ventricle of the heart.
8. The method of claim 1, wherein encircling a portion of the heart
with the device comprises fully encircling the heart.
9. The method of claim 1, wherein the wrap is substantially
elastic.
10. The method of claim 1, wherein the wrap is substantially
inelastic.
11. A device for improving the function of a heart, the device
comprising: a wrap having sufficient length to encircle at least a
portion of the heart but not encompass an apex of the heart; and a
plurality of bands disposed along the length of the wrap, wherein
each of the bands extends transversely to the length of the wrap,
and wherein the device is a passive device.
12. The device of claim 11, wherein the plurality of bands are
configured to be secured to one another.
13. The device of claim 11, wherein the wrap is configured to
completely encircle the heart.
14. The device of claim 11, wherein each of the plurality of bands
is substantially rigid.
15. The method of claim 11, wherein the wrap is substantially
elastic.
16. The method of claim 11, wherein the wrap is substantially
inelastic.
Description
RELATED APPLICATIONS
[0001] This application is a continuation of U.S. application Ser.
No. 13/609,585, entitled Heart Wall Tension Reduction Apparatus and
Method, filed Sep. 11, 2012, which is a divisional of U.S.
application Ser. No. 12/832,507, entitled Heart Wall Tension
Reduction Apparatus and Method, filed Jul. 8, 2010, now U.S. Pat.
No. 8,267,852, which is a continuation of U.S. application Ser. No.
10/127,731 ("the '731 application") of Cyril J. Schweich Jr. et
al., entitled Heart Wall Tension Reduction Apparatus and Method,
filed on Apr. 23, 2002, now U.S. Pat. No. 7,883,539, which is a
continuation-in-part of U.S. application Ser. No. 09/985,361,
entitled Heart Wall Tension Reduction Apparatus and Method, filed
Nov. 2, 2001, now U.S. Pat. No. 6,589,160, which is a continuation
of U.S. application Ser. No. 09/697,597, filed Oct. 27, 2000, now
U.S. Pat. No. 6,332,864, which is a continuation of application
Ser. No. 09/492,777, filed Jan. 28, 2000, now U.S. Pat. No.
6,162,168, which is a continuation of application Ser. No.
08/778,277, filed Jan. 2, 1997, now U.S. Pat. No. 6,050,936.
[0002] The '731 application also is a continuation-in-part of U.S.
application Ser. No. 09/843,078 of Todd J. Mortier et al. for
Stress Reduction Apparatus and Method, filed Apr. 27, 2001, now
U.S. Pat. No. 6,402,680, which is a continuation of application
Ser. No. 09/522,068, filed Mar. 9, 2000, now U.S. Pat. No.
6,264,602, which is a continuation of application Ser. No.
09/124,321, filed Jul. 29, 1998, now U.S. Pat. No. 6,077,214. The
entirety of each of the above applications is incorporated herein
by reference.
FIELD OF THE INVENTION
[0003] The present invention pertains to the field of apparatus for
treatment of a failing heart. In particular, the apparatus of the
present invention is directed toward reducing the wall stress in
the failing heart.
BACKGROUND OF THE INVENTION
[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.
[0005] 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 slight ventricular
dilation and muscle 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.
[0006] 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 filling 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.
[0007] Prior art treatments for heart failure fall into three
generally categories. The first being pharmacological. for example,
diuretics. The second being assist systems, for example, pumps.
Finally, surgical treatments have been experimented with, which are
described in more detail below.
[0008] With respect to pharmacological treatments, diuretics have
been used to reduce the workload of the heart by reducing blood
volume and preload. 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 which 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 like 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.
[0009] Assist devices include mechanical pumps and electrical
stimulators. 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. Electrical stimulation such as bi-ventricular pacing have
been investigated for the treatment of patients with dilated
cardiomyopathy.
[0010] 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.
SUMMARY OF THE INVENTION
[0011] The present invention pertains to a non-pharmacological,
passive apparatus for the treatment of a failing heart. The device
is configured to reduce the tension in the heart wall. It is
believed to reverse, stop or slow the disease process of a failing
heart as it reduces the energy consumption of the failing heart,
decrease in isovolumetric contraction, increases sarcomere
shortening during contraction and an increase in isotonic
shortening in turn increases stroke volume. In embodiments, the
device reduces wall tension during diastole (preload) and
systole.
[0012] In an embodiment, the apparatus includes a compression
member for drawing at least two walls of a heart chamber toward
each other to reduce the radius or area of the heart chamber in at
least one cross sectional plane. In one embodiment of the
apparatus, a frame is provided for supporting the compression
member.
[0013] Yet another embodiment of the invention includes a clamp
having two ends biased toward one another for drawing at least two
walls of a heart chamber toward each other. The clamp includes at
least two ends having atraumatic anchoring member disposed thereon
for engagement with the heart or chamber wall.
[0014] The present invention also pertains to a device and method
for reducing mechanical heart wall muscle stress. Heart muscle
stress is a stimulus for the initiation and progressive enlargement
of the left ventricle in heart failure. Reduction of heart wall
stress with the devices and methods disclosed herein is anticipated
to substantially slow, stop or reverse the heart failure disease
process. Although the primary focus of the discussion of the
devices and methods of the present invention herein relates to
heart failure and the left ventricle, these devices and method
could be used to reduce stress in the heart's other chambers .
[0015] The devices and methods of the present invention can reduce
heart wall stress throughout the cardiac cycle including end
diastole and end systole. Alternatively, they can be used to reduce
wall stress during the portions of the cardiac cycle not including
end systole. Those devices which operate throughout the cardiac
cycle are referred to herein as "full cycle splints". Those devices
which do not operate to reduce wall stress during end stage systole
are referred to as "restrictive devices". Restrictive devices
include both "restrictive splints" which alter the geometric shape
of the left ventricle, and "wraps" which merely limit the magnitude
of the expansion of the left ventricle during diastolic filling
without a substantial shape change.
[0016] While it is desirable to reduce wall stress for the
treatment of heart failure, to slow or reverse the disease process
and to increase heart wall muscle shortening and pumping
efficiency, it is also desirable to maintain or improve stroke
volume and allow for variable preload.
[0017] Improving muscle shortening both total length change and
extent at end systole, is particularly important in symptomatic
heart failure wherein the heart has decreased left ventricle
function and has enlarged. Full cycle splinting can be used to
obtain a substantial increase in muscle shortening. Improved
shortening will lead to an increase in pump function, and
chronically may result in muscle strengthening and reversal of the
disease because of increased pumping efficiency. The increase in
shortening should be balanced against a reduction in chamber
volume.
[0018] In asymptomatic, early stage heart failure, it may be
possible to use only a restrictive device or method as elevated
wall stress is considered to be an initiator of muscle damage and
chamber enlargement. Restrictive devices and methods acting during
diastole will reduce the maximum wall stress experienced during end
diastole and early systole. It should be understood that
restrictive devices and methods can be used in combination with
full cycle splinting to more precisely control or manipulate stress
reduction throughout the cardiac cycle. control or manipulate
stress reduction throughout the cardiac cycle.
BRIEF DESCRIPTION OF THE DRAWINGS
[0019] FIG. 1 is a vertical side view of a heart including a
transventricular splint and band splint;
[0020] FIG. 2 is a horizontal cross section of the heart, splint
and band splint of FIG. 1;
[0021] FIG. 3 is a graph showing the relationship between stress
and strain for the sarcomeres of the left ventricle for a normal
and failing heart throughout the cardiac cycle;
[0022] FIG. 4 is an idealized horizontal cross section of a left
ventricle splinted to form two lobes;
[0023] FIG. 5 is an idealized horizontal cross sectional left
ventricle splinted to for three lobes;
[0024] FIG. 6 is a vertical view of a heart including two
transventricular splints and two bands splints;
[0025] FIG. 7 is a cross sectional view of the heart, a band splint
and a splint of FIG. 6;
[0026] FIG. 8 is a vertical view of a heart including a
transventricular splint and a partial band splint;
[0027] FIG. 9 is a horizontal cross sectional view of the heart,
splint and band splint of FIG. 8;
[0028] FIG. 10 is a horizontal cross section of a heart including a
splint having full cycle and restrictive elements at the beginning
of diastolic filling;
[0029] FIG. 11 is a view of the splint of FIG. 10 at end
diastole;
[0030] FIG. 12 is a vertical view of the heart in phantom line
including a band splint;
[0031] FIG. 13 is an alternate embodiment of the bank splint of
FIG. 12;
[0032] FIG. 14 is an alternate embodiment of the bank splint of
FIG. 12;
[0033] FIG. 15 is an alternate embodiment of the bank splint of
FIG. 12;
[0034] FIG. 16 is a vertical view of a heart including a partial
circumferential strap;
[0035] FIG. 17 is a horizontal cross sectional view of the heart
and strap of FIG. 16;
[0036] FIG. 18 is a vertical view of a heart in phantom line
including a single element wrap including longitudinal axis
securing points;
[0037] FIG. 19 is an alternate embodiment of the wrap of FIG.
18;
[0038] FIG. 20 is an alternate embodiment of the wrap of FIG.
18;
[0039] FIG. 21 is an alternate embodiment of the wrap of FIG.
18;
[0040] FIG. 22 is a vertical view of the heart including a mesh
wrap;
[0041] FIG. 23 is a cross sectional view of a patient's torso and
heart showing a band splint anchored to the patient's ribs;
[0042] FIG. 24 is a partial vertical view of the heart and band
splint of FIG. 23;
[0043] FIG. 25 is a partial vertical view of a failing heart;
[0044] FIG. 26 is a cross sectional view of the heart of FIG.
25;
[0045] FIG. 27 is a vertical view of the heart for decreasing the
horizontal radius of the ventricles and increasing their vertical
length;
[0046] FIG. 28 is an exaggerated vertical view of the heart of FIG.
25 elongated by the device of FIG. 27;
[0047] FIG. 29 is a view of the cross section of FIG. 26 showing
the decrease in radius of the ventricles;
[0048] FIG. 30 is a horizontal cross sectional view of the left and
right ventricles including reinforcement loops;
[0049] FIG. 31 is an alternate embodiment of the reinforcing loops
of FIG. 30;
[0050] FIG. 32 shows a vertical view of the heart including the
reinforcement loops of FIG. 31 and a rigid shape changing
member;
[0051] FIG. 33 is a transverse cross-section of the left and right
ventricles of a human heart showing the placement of an external
compression frame structure in accordance with the present
invention;
[0052] FIG. 34 is a transverse cross-section of the left and right
ventricles of a human heart showing a clamp in accordance with the
present invention;
[0053] FIG. 35 is a idealized cylindrical model of a left ventricle
of a human heart;
[0054] FIG. 36 is a splinted model of the left ventricle of FIG.
35;
[0055] FIG. 37 is a transverse cross-sectional view of FIG. 36
showing various modeling parameters;
[0056] FIG. 38 is a transverse cross-section of the splinted left
ventricle of FIG. 36 showing a hypothetical force distribution;
and
[0057] FIG. 39 is a second transverse cross-sectional view of the
model left ventricle of FIG. 36 showing a hypothetical force
distribution.
DESCRIPTION OF THE EMBODIMENTS
[0058] The present invention is directed at reducing wall stress in
a failing heart. Diastolic wall stress is considered to be an
initiator of muscle damage and chamber enlargement. For this
reason, it is desirable to reduce diastolic wall stress to prevent
the progression of the disease. The significant impact of stress
occurs at all stages and functional levels of heart failure,
however, independent of the original causes. For example, in
asymptomatic early stages of heart failure, mechanical stress can
lead to symptomatic heart failure marked by an enlarged heart with
decreased left ventricle function. As the heart enlarges,
mechanical stress on the heart wall increases proportionally to the
increasing radius of the heart in accordance with LaPlace's Law. It
can thus be appreciated that as stress increases in symptomatic
heart failure, those factors that contributed to increasing stress
also increase. Thus, the progression of the disease accelerates to
late stage heart failure, end stage heart failure and death unless
the disease is treated.
[0059] Three parameters influence mechanical stress on the muscle.
These are: (1) muscle mass, i.e., as reflected by the thickness of
the muscle; (2) pressure in the chamber which is a function of the
resistance to blood flow of the patient's vasculature and the
volume of blood within the patient; and (3) chamber geometry. The
present invention pertains to devices and methods for directly and
passively changing chamber geometry to lower wall stress. In
addition to treatment of heart failure, the devices and methods of
the present invention also lend themselves to application in the
case of a decrease in cardiac function caused by, for example,
acute myocardial infarction.
[0060] The devices disclosed herein for changing chamber geometry
are referred to as "splints". In addition to splints, wraps which
can be placed around the heart can limit muscle stress without the
chamber shape change. When a wrap is used, wall stress is merely
transferred to the wrap, while the generally globular shape of the
heart is maintained. A wrap could be used in conjunction with a
splint to modulate heart wall stress reduction at various stages of
the cardiac cycle.
[0061] The present invention includes a number of splint
embodiments. Splints and wraps can be classified by where in the
cardiac cycle they engage the heart wall, i.e., mechanically limit
the size of the left ventricle in the case of wraps and change the
geometry of the ventricle in the case of splints. If a splint or
wrap only begins to engage during diastolic filling, the splint can
be termed a "restrictive splint". If the splint or wrap is engaged
throughout the cardiac cycle, both during diastolic filling and
systolic contraction and ejection, the splint can be termed a "full
cycle splint". The wrap will generally be a restrictive device
which begins to engage during diastolic filling to increase the
elastance (reduces compliance) of the chamber. If a wrap is made
from elastic material it may engage full cycle, but the force
required to elongate the wrap will increase as diastolic filling
progresses, preload strain will be reduced without an improvement
in systolic contraction.
[0062] FIG. 1 is a view of a heart A in a normal, generally
vertical orientation. A wrap 11 surrounds heart A and a
transventricular splint 12 extends through the heart and includes
an anchor or anchor pad 13 disposed on opposite sides of the heart.
FIG. 2 is a horizontal cross sectional view of heart A taken
through wrap 11 and splint 12. Splint 12 includes a tension member
15 extending through left ventricle B. Anchor pads 13 are disposed
at each end of tension member 15. Right ventricle C is to the left
of left ventricle B.
[0063] In FIG. 1, wrap 11 and splint 12 are shown engaged with
heart A. In FIG. 2, heart A is shown spaced from wrap 11 except at
anchor pads 13. In FIG. 2, heart A is thus at a point in the
cardiac cycle where the muscles are shortening during systole, or
have yet to stretch sufficiently during diastolic expansion to
reach wrap 11. Accordingly, wrap 11 can be considered a restrictive
device as it does not engage the heart full cycle. Although wrap 11
is in contact with heart A at pads 13, only the splint is providing
a compressive force to change the shape of the heart and limiting
the stress of the heart in FIG. 2.
[0064] If heart A, as shown in FIG. 2 is at end systole,
transventricular splint 12 is a full cycle device as the cross
section of left ventricle B does not have the generally circular
unsplinted shape. Alternately, wrap 11 could be secured to heart A
by sutures or other means than splint 12, in which case wrap 11
would be merely a restrictive device. It should be noted that
unless wrap 11 extends vertically along heart A a sufficient
amount, as heart A expands and engages wrap 11, the portion of left
ventricle B disposed above or below wrap 11 could expand
substantially further than that portion of the left ventricle wall
restrained by wrap 11. In such a case, left ventricle B could have
a bi-lobed shape in a vertical cross section. As such, the wrap 11
would not be merely limiting the size of the left ventricle, but
rather inducing a shape change in the left ventricle. In such a
case, the element 11 would not be a wrap, but rather a splint which
could be referred to as a "band splint".
[0065] Each of the splints, wraps and other devices disclosed in
this application preferably do not substantially deform during the
cardiac cycle such that the magnitude of the resistance to the
expansion or contraction of the heart provided by these devices is
reduced by substantial deflection. It is, however, contemplated
that devices which deflect or elongate elastically under load are
within the scope of the present invention, though not preferred.
The materials from which each device are formed must be
biocompatible and are preferably configured to be substantially
atraumatic.
[0066] The distinction between restrictive devices, such as
restrictive splints and wraps, and full cycle splints and wraps,
can be better understood by reference to FIG. 3. FIG. 3 is a plot
of sarcomere, i.e., heart wall muscle, stress in (g/cm.sup.2)
versus strain throughout a normal cardiac cycle N, and a failing
heart cardiac cycle F. The cardiac cycles or loops shown on FIG. 3
are bounded by the normal contractility curve N.sub.c and failing
heart contractility curve F.sub.c above and to the left, and the
diastolic filling curve 12 toward the bottom and right.
Contractility is a measure of muscle stress at an attainable
systolic stress at a given elongation or strain. It can be
appreciated that the muscle contractility N.sub.c of normal muscle
tissue is greater than the contractility F.sub.c of the muscle
tissue of a failing heart. The diastolic filling curve 12 is a plot
of the stress in the muscle tissue at a given elongation or strain
when the muscle is at rest.
[0067] An arbitrary beginning of the normal cardiac cycle N can be
chosen at end diastole 14, where the left ventricle is full, the
aortic valve is closed. Just after end diastole 14, systole begins,
the sarcomere muscles become active and the mitral valve closes,
increasing muscle stress without substantially shortening
(sometimes referred to as "isovolumic contraction"). Stress
increases until the aortic valve opens at 16. Isotonic shortening
begins and stress decreases and the muscles shorten until end
systole 18, where the blood has been ejected from the left
ventricle and the aortic valve closes. After end systole 18,
diastole begins, the muscles relax without elongating until
diastolic filling begins when the mitral valve opens at 20. The
muscles then elongate while the mitral valve remains open during
diastolic filling until end diastole 14. The total muscle
shortening and lengthening during the normal cycle N is
N.sub.s.
[0068] An analogous cycle F also occurs in a failing heart. As the
left ventricle has dilated, in accordance with LaPlace's Law, the
larger radius of a dilated left ventricle causes stress to increase
at a given blood pressure. Consequently, a failing heart must
compensate to maintain the blood pressure. The compensation for the
increased stress is reflected in the shift to the right of failing
heart cardiac cycle F relative to the normal cycle N. The stress,
at end diastole 22 is elevated over the stress at end diastole 14
of the normal heart. A similar increase can be seen for the point
at which the aortic valve opens 24, end systole 26 and the
beginning of diastolic filling 28 relative to the analogous points
for the normal cycle N. Muscle shortening and elongation F.sub.s
throughout the cycle is also reduced in view of the relative
steepening of the diastolic curve 12 to the right and the flatter
contractility curve F.sub.c relative to the normal contractility
N.sub.c.
[0069] By reference to the heart cycle stress strain graph of FIG.
3, the effect on mechanical muscle stress and strain caused by the
use of the devices and methods of the present invention can be
illustrated. Restrictive devices begin to engage during diastolic
filling, which in the case of a failing heart occurs along
diastolic filling curve 12 between point 28 and 22. Restrictive
devices do not engage at end systole 26. Thus, the acute effect of
placement of a restrictive device is to reduce muscle stress at end
diastole relative to the stress at point 22, and shift the line
22-24 to the left reducing muscle shortening and elongation
F.sub.s. Acutely, the cardiac cycle will still operate between the
failing heart contractility curve F.sub.c and the diastolic filling
curve 12. If chronic muscle contractility increases such that the
muscle contractility curve F.sub.c shifts back toward the normal
heart contractility curve N.sub.c as a consequence of the stress
reduction, the stress/strain curve F of the cardiac cycle will
shift to the left reducing mechanical stress still further.
[0070] The effect on the stress/strain relationship of a full cycle
splint will acutely shift the entire stress/strain curve F for the
cycle to the left. That is, stress is reduced at both end diastole
22 and end systole 26. Muscle shortening and elongation F.sub.s
will increase acutely. If, as in the case of a restrictive splint,
muscle contractility F.sub.c improves, the entire cardiac cycle
curve F will shift further to the left reducing mechanical stress
still further.
[0071] The type and magnitude of shape change are important factors
in determining the effectiveness of splinting. There are several
types of lower stress cardiac geometries that can be created from
an enlarged globular left ventricular chamber typically associate
with heart failure. They include lobed, disc-like, narrowed
elongate, and multiple vertically stacked bulbs.
[0072] FIG. 4 shows an idealized horizontal cross section of a left
ventricle 30 subdivided into two symmetrical lobes 32 and 34 having
an arc passing through an angle .theta.>.pi., and a radius R
lobes 32 and 34 can be formed using a splint, such as
transventricular splint 12 shown in FIGS. 1 and 2. Lobes 32 and 34
are joined at points 36 and 38. Points 36 and 38 are separated by a
distance l.
[0073] FIG. 5 is an idealized horizontal cross section of a left
ventricle 40 subdivided into three generally equal sized lobes 42,
44 and 46. Each lobe has an equal radius and has an arc passing
through an angle less than .pi.. Adjacent ends of the lobes 48, 50
and 52 are separated by a distance l. A plurality of
transventricular splints such as splint 12 as shown in FIGS. 1 and
2 could be extended between adjacent ends 48, 50 and 52 to form
lobes 42, 44 and 46.
[0074] For a restrictive splint, the horizontal cross sections 30
and 40 will have a generally circular shape, i.e., a non-splinted
shape at end systole. As diastolic filling proceeds, the radius of
the circular shape will continue to increase until the splint
engages. At the point the splint engages, the lobed shape will
begin to form. In the case of the two lobe splinting of FIG. 4, the
radius will continue to increase as diastolic filling proceeds. In
the case of the three or more lobed shape, such as the three lobed
configuration of FIG. 5, radius R will decrease as diastolic
filling proceeds. The radius will continue to decrease unless or
until the pressure in the heart causes tile heart to expand such
that the arc of the lobe passes through an angle .theta. greater
than .pi..
[0075] In the case of a full cycle splint, at end systole, the
splint will already be engaged. Thus, for a full cycle splint at
end systole, the horizontal cross section of the chamber will not
have the normal generally circular shape. Rather, at end systole,
the horizontal cross sections 30 and 40 will have a lobed shape
such as shown in FIGS. 4 and 5. Subsequent shape change during
diastolic filling for a full cycle splint will be similar to that
described with respect to restrictive splints.
[0076] In view of LaPlace's Law which states that stress is
directly proportional to radius of curvature, it can be appreciated
that whether the radius is increasing or decreasing during
diastolic filling, will have an impact on heart pumping
performance. Where R is increasing during diastolic filling, wall
stress will increase more rapidly than where R is decreasing. The
number of lobes that are created can significantly influence the
level of end diastolic muscle stress reduction achieved through
splinting. Eventually adding additional lobes forms a configuration
which approaches a behavior similar to a wrap. If a wrap is
substantially inelastic, or of sufficient size, a wrap will only
engage the heart wall at some stage of diastolic filling. If the
wrap is substantially inelastic, as pressure increases in the
chamber during diastolic filling, stress in the heart wall muscle
will increase until the wrap fully engages and substantially all
additional muscle elongating load created by increased chamber
pressure will be shifted to the wrap. No further elongation of the
chamber muscles disposed in a horizontal cross section through the
wrap and the chamber will occur. Thus, inelastic wraps will halt
additional preload muscle strain (end diastolic muscle
stretch).
[0077] The type of shape change illustrated in FIGS. 4 and 5 is of
substantial significance for restrictive splints. It is undesirable
in the case of restrictive splints, to excessively limit preload
muscle strain. The Frank-Starling Curve demonstrates the dependence
and need for variable preload muscle strain on overall heart
pumping performance. During a person's normal activities, their
body may need increased blood perfusion, for example, during
exertion. In response to increased blood perfusion through a
person's tissue, the heart will compensate for the additional
demand by increasing stroke volume and/or heart rate. When stroke
volume is increased, the patient's normal preload strain is also
increased. That is, the lines 14-16 and 22-24 of the normal and
failing hearts, respectively, will shift to the right. An inelastic
wrap will, at engagement, substantially stop this shift. In the
case of the bi-lobed shape change of FIG. 4 or a multiple lobed
change having a small number of lobes of FIG. 5, significant stress
reduction can be achieved while allowing for variable preload
strain. If the number of lobes is increased substantially, however,
variable preload will decrease as the multi-lobed configuration
approaches the performance of an inelastic wrap.
[0078] The magnitude of shape change in the case of full cycle
splinting becomes very important as full cycle splinting generally
reduces chamber volume more than restrictive splinting. Although as
with restrictive devices, the type of shape change is also
important to allow for variable preload strain. Both restrictive
device and full cycle splints reduce chamber volume as they reduce
the cross sectional area of the chamber during the cardiac cycle.
The magnitude of the shape change can vary from very slight at end
diastole, such that chamber volume is only slightly reduced from
the unsplinted end diastolic volume, to an extreme reduction in
volume, for example, complete bifurcation by transventricular
splint. The magnitude of the shape change, for example, as measured
by the ratio of splint length to nonsplinted ventricular diameter,
is preferably modulated to reduce muscle stress while not overly
reducing chamber volume. For full cycle splint, the reduction of
chamber volume is compensated for by increased contractile
shortening, which in turn leads to an increased ejection fraction,
i.e., the ratio of the stroke volume to chamber volume. For given
stress/volume and stress/shortening relationships, there will be a
theoretical optimum maximal stroke volume. Clinically, 20% to 30%
stress reduction is expected to be attainable through full cycle
bi-lobe splinting. See U.S. Pat. No. 5,961,440 and the discussion
further herein for calculation of stress reduction for idealized
bi-lobe splinting.
[0079] When using the full cycle and restrictive devices described
herein, caution should be .exercised to limit the pressure on the
coronary vasculature. In the case of transventricular splints,
valve structure, electrical pathways and coronary vasculature
should be avoided.
[0080] FIG. 6 is a vertical view of a heart A similar to that shown
in FIG. 1. Rather than having a single band splint surrounding
heart A, there are two band splints 51 affixed to the heart by two
transventricular splints 52. Splints 52 include oppositely disposed
anchors or anchor pads 53. FIG. 7 is a horizontal cross sectional
view of heart A of FIG. 6, wraps 51 and splint 52. Splints 52
include a tension member 54 disposed through left ventricle B. Pads
53 are disposed on the opposite ends of tension members 54. Right
ventricle C is shown to the left of left ventricle B.
[0081] Splints 52 can be restrictive or full cycle splints. Band
Splints 51 are shown as restrictive band splints as in FIG. 6,
heart A is shown engaged with the band splints 51, whereas in FIG.
7, heart A has contracted to move away from band splints 51. Wraps
51 and splints 52 should be made from biocompatible materials. Band
splints 51 are preferably made from a pliable fabric or other
material which resists elongation under normal operating loads.
Band splints 51 can, however, be made from an elastic material
which elongates during the cardiac cycle. Tension members 54 also
preferably resist elongation under normal operating loads. Tension
members 54 can, however, be made from an elastic material which
elongates during the cardiac cycle.
[0082] FIG. 8 is a vertical view of heart A, partial wrap 61 and
transventricular splint 62. Transventricular splint 62 includes
anchor pads 63. FIG. 9 is a horizontal cross sectional view of
heart A, partial band splint 61 and splint 62. Splint 62 is
essentially similar to wrap or band splint 12 shown in FIGS. 1 and
2. Partial band splint 61 is also essentially similar to wrap or
band splint 11 shown in FIGS. 1 and 2 except that band splint 61
only surrounds a portion of heart A. This portion is shown in FIGS.
8 and 9 to the left including a portion of left ventricle B.
[0083] FIG. 10 is a horizontal cross sectional view of left
ventricle B and right ventricle C of heart A taken at a similar
elevation as that shown in FIG. 2. A splint 70 is shown disposed on
heart A. Splint 70 includes a frame having two heart engaging
anchors or pads 72 disposed at its opposite ends. A third heart
engaging pad 73 is disposed along frame 70 approximately midway
between pads 72.
[0084] Pads 72 are shown engaged with heart A to change the shape
of ventricle B in FIG. 10. Pads 73 are not engaged with heart A in
FIG. 10. FIG. 11 is the same horizontal cross sectional view as
FIG. 10 except that heart A has to contact pad 73 to create a
further shape change of left ventricle B.
[0085] Frame 70 is preferably rigid enough that pads 72 could be
disposed on the heart for full cycle splinting and sufficiently
adjustable that pads 72 could be spaced further apart for
restrictive splinting. Pad 73 accomplishes restrictive splinting.
Frame 71, pads 72 and 73 of splint 70 are made of a biocompatible
material. Pads 72 and 73 are preferably substantially
atraumatic.
[0086] FIG. 12 is a vertical view of heart A shown in phantom line.
Shown disposed about the ventricles of heart A is a basket-like
band splint 100. Band splint 100 includes a horizontal encircling
band 101 around an upper region of the ventricles and four bands
102 which extend downward toward the apex of heart A. It can be
appreciated that bands 102 can act as splints to form four lobes in
heart A in a horizontal plane. Depending on the placement of bands
102 around heart A, lobes could be created only in the left
ventricle or in the left ventricle and/or other chambers of the
heart. Band 102 is joined at the apex. Band 101 and band 102 can be
made from a webbing, fabric or other biocompatible material.
[0087] If band splint 100 substantially elongated elastically under
normal operating loads, it could be friction fit to heart A and act
full cycle, limiting muscle stress at end diastole as well end
systole. Band splint 100 could be sutured into place or otherwise
held on heart A and act as a restrictive device. If band 101 were
securely fastened to heart A, bands 102 could limit the vertical
elongation of heart A during diastolic filling.
[0088] FIG. 13 is an alternate embodiment 110 of the band splint of
FIG. 12. Band splint 110 includes a horizontally heart encircling
band 111 and four bands 113 extending downward from band 111. Bands
113, however, unlike bands 102 of band splint 100 do not extend to
the apex of heart A, but rather to a second horizontally heart
encircling band 112.
[0089] Band splint 110 could be made of the same materials as band
splint 100. Band splint 110 can also be used in a manner similar to
band splint 100 except that band splint 110 would limit the
vertical elongation of the ventricles less than band splint
100.
[0090] FIG. 14 is yet another alternate embodiment 120 of the wrap
of FIG. 12. Band splint 120 closely resembles alternate embodiment
110 of FIG. 13, except that rather than having four vertically
extending web members, band splint 120 includes two substantially
rigid members 123 interconnecting two horizontally encircling web
members 121 and 122.
[0091] FIG. 15 is yet another alternate embodiment 130 of the band
splint of FIG. 12. Like the wrap of FIG. 12, band splint 130
includes a horizontally encircling member 131 and four downwardly
extending members 132. At a location proximate of the apex of heart
A, members 132 are joined by a ring 133. Members 132 extend through
ring 133. Ring 133 can be used to adjust the length of members 132
between band 131 and ring 133. Ring 133 can be formed from metallic
material and crimped inwardly to fix its position along members
132. Other means of holding ring 133 in position would be readily
apparent to those skilled in the art.
[0092] FIG. 16 is a vertical view of heart A including a partial
band splint 140 secured around a substantial portion of left
ventricle B. Band splint 140 includes a vertically elongating
anchor member 141 which sutures 142 can encircle to anchor member
141 to heart A. A band 143 extends generally horizontally from
anchor member 141 to an opposite anchor 141.
[0093] The length of band 143 can be seen in its entirety in FIG.
17 which is a horizontal cross sectional view of heart A through
band 143, left ventricle B and right ventricle C. In FIG. 16, heart
A is shown engaged with band 143, however, In FIG. 17, band 143 is
shown spaced from heart A. Thus, in this configuration, wrap 140
would be acting as a restrictive device. If band splint 140 were
made from a material that substantially deforms elastically under
normal loads, band splint 140 could also be secured sufficiently
snuggly to heart A to act as a full cycle device. Preferably.
however, band 143 of band splint 140 is formed from a webbing or
substantially inelastic fabric.
[0094] FIG. 18 is a vertical view of heart A including a wrap 160.
Wrap 160 can include a single thread or line 161 encircling the
heart several times. After line 161 encircles heart A, line 161 can
be threaded through a bar 162, including a plurality of eyelets 163
spaced along its length in pairs. Bar 162 is preferably rigid
enough to substantially maintain the distance between eyelets 163
under normal operating loads.
[0095] When line 161 is placed in heart A, one end of line 161 can
be tied to bar 162 at 164. Line 161 can then encircle the heart and
be drawn through eyelet 162 adjacent the beginning of line 161 at
164. Line 161 can then be drawn through one eyelet 163 of a lower
pair of eyelets to encircle the heart again. This process continues
until line 161 is tied to an eyelet 163 at 165. It can be
appreciated that wrap 160 could be used as a restrictive or full
cycle device depending on the diameter of loop formed by line
161.
[0096] FIG. 19 is an alternate embodiment 170 of the wrap of FIG.
18. Wrap 170, however, includes two vertically extending bars 172
having eyelets 173 through which line 171 is threaded. Line 171 can
be tied to one of the bars 172 at 174 and 175.
[0097] FIG. 20 is a vertical view of heart A including yet another
embodiment 180 of the wrap of FIG. 18. Wrap 180 includes a line 181
encircling heart A a plurality of times. Rather than having a
single vertically extending bar 162 to position line 180 on heart
A, wrap 180 includes a plurality of horizontal bars 182 including a
pair of eyelets 183. One end of line 181 is tied to an upper bar
182 at 184 and the opposite end of line 181 is tied to a lower bar
182 at 185. Between 184 and 185, line 181 is threaded through
eyelets 182 to form the heart encircling pattern shown in FIG.
20.
[0098] FIG. 21 is a vertical view of heart A including yet another
alternate embodiment 190 of the wrap of FIG. 18. Wrap 190 closely
resembles 180 of FIG. 20. Line 181 has, however, been threaded
through eyelets 183 of bars 182 in a pattern which unlike that of
FIG. 20, bars 182 are disposed at various selected locations around
the circumference of heart A.
[0099] FIG. 22 is a vertical view of heart A including a wrap 200.
Wrap 200 is substantially similar to wrap 11 of FIGS. 1 and 2,
except that wrap 200 extends vertically a greater distance than
wrap 11. Wrap 200 is not shown with a transventricular splint. It
can be appreciated that wrap 200 could be used as restrictive or
full cycle device.
[0100] FIG. 23 is a horizontal cross section of a human torso
including heart A, left ventricle B, right ventricle C, lungs E and
ribs G. A wrap 210 is shown partially encircling heart A. Opposite
ends of wrap 210 are anchored at 211 to ribs G. At 211, wrap 210
can be anchored to ribs G by bone screw, knot or other means of
fastening. It can be appreciated that band splint 210 could be used
as a restrictive or full cycle device.
[0101] FIG. 25 is a vertical view of heart A having a horizontal
width W.sub.1. FIG. 26 is an idealized horizontal cross sectional
view of heart A of FIG. 25. Heart A includes left ventricle B and
right ventricle C. Left ventricle B has a radius R.sub.1.
[0102] FIG. 27 is a view of a device 220. Device 220 includes a
horizontally encircling band 222 which can be affixed to heart A by
sutures, other attachment means or friction fit. Extending from
band 222 is a substantially rigid elongate member 224. Member 224
extends to the apex of heart A. Pin 226 extends into left ventricle
B of the apex. An anchor or pad 228 is disposed within left
ventricle B to anchor the apex of heart A to elongate member 224.
Elongate member 224 can be made of sufficient length such that
heart A is vertically elongate full cycle, or alternately not at
end diastole.
[0103] FIG. 28 is a vertical view of an elongate heart A having a
horizontal width W.sub.2 less than W.sub.1. FIG. 29 is a horizontal
cross section of the heart A of FIG. 28 including left ventricle B
and right ventricle C. In FIG. 29, the radius R.sub.2 of left
ventricle B is less than R.sub.1 of FIG. 26. Assuming that the
hearts of FIGS. 25 and 28 are at the same point in the cardiac
cycle, it can be appreciated that the wall stress in heart A is
less in FIG. 29 as R.sub.2 is shorter R.
[0104] If elongate bar 224 is sized such that device 220 does not
engage at end diastole, but rather anchor pad 228 first engages
during systolic contraction, device 220 can fall into a third class
of device neither full cycle nor restrictive. Such a device would
reduce wall stress during a portion of systolic contraction
including end systole, but not reduce wall stress during end
diastole, thus maintaining maximum preload.
[0105] Band 222 of device 220 is preferably formed from a web
material or other fabric. Band 220 is preferably does not elongate
substantially during diastolic filling. Members 224, 226 and 228
are formed from materials which remain substantially rigid under
the influences of the forces encountered during the cardiac
cycle.
[0106] FIG. 30 is a horizontal cross sectional view of heart A
including left ventricle B and right ventricle C. A device 260
including a thread or line 261 is disposed transventricularly and
transmyocardially through heart A. A portion of line 261 is
disposed outside of heart A. Opposite ends of line 261 are
connected at 262. Those portions of line 261 outside heart A form
loops 263. The size of loops 263 are exaggerated for purposes of
illustration. It is assumed that heart A in the process of
diastolic filling in FIG. 30, and loops 263 are sufficiently small,
eventually heart A will engage loops 263. In such a configuration,
device 260 is used as a restrictive device. Loops 263 could be
sized, however, such that they engage full cycle.
[0107] Line 261 is preferably made from atraumatic biocompatible
material. The diameter of line 261 is preferably sufficiently great
that cutting of heart A does not occur during diastolic
filling.
[0108] FIG. 31 is a horizontal cross sectional view of heart A
including left ventricle B and right ventricle C and an alternate
embodiment 270 of the device of FIG. 30. Device 270 includes a line
271 which does not extend transventricularly but extends through
the myocardium of heart A to form four loops 273.
[0109] Device 270 can be formed from material similar to that used
to form device 260. Additionally, device 270 can be made to
function as a restrictive device or full cycle device in a manner
similar to that of device 260.
[0110] Line 261 and line 267 could be disposed within a tube to
avoid cheese cutting of the myocardium. The tube may be highly
flexible, yet durable enough to prevent the line from cheese
cutting through the myocardium of the heart. Devices 260 and 270
could extend through the septum or right ventricle to avoid forming
lobes in right ventricle C.
[0111] FIG. 32 is a vertical view of heart A including three
devices 270 disposed at three spaced elevations. An elongate
generally rigid bar 274 is disposed through loops 273 to distribute
the load on heart A from loops 273 across a larger area than lines
271 can alone.
[0112] It should be understood that although devices disclosed
herein are described in relation to the left ventricle of a human
heart, these devices could also be used to reduce the radius or
cross-sectional area of the other chambers of a human heart in
transverse or vertical directions, or at an angle between the
transverse and vertical.
[0113] FIG. 33 shows a transverse cross-section of a left ventricle
10' and a right ventricle 12' of a human heart 14'. FIG. 33 also
shows an embodiment of the present invention deployed with respect
to left ventricle 10' of human heart 14'. Here a compression frame
structure 300 is engaged with heart 14' at atraumatic anchor pads
310. A compression member 312 having an atraumatic surface 314
presses against a wall of left ventricle 10' to reduce the radius
or cross-sectional area thereof.
[0114] FIG. 34 is a transverse cross-sectional view of human heart
14' showing yet another embodiment of the present invention. In
this case a clamp 400 having atraumatic anchor pads 410 biased
toward each other is shown disposed on a wall of left ventricle
10'. Here the radius or cross-sectional area of left ventricle 10'
is reduced by clamping off the portion of the wall between pads
410. Pads 410 can be biased toward each other and/or can be held
together by a locking device.
[0115] Each of the various embodiments of the present invention can
be made from materials which can remain implanted in the human body
indefinitely. Such biocompatible materials are well-known to those
skilled in the art of clinical medical devices.
[0116] In use, the various embodiments of the present invention are
placed in or adjacent the human heart to reduce the radius or
cross-section area of at least one chamber of the heart. This is
done to reduce wall stress or tension in the heart or chamber wall
to slow, stop or reverse failure of the heart.
[0117] To discuss further the stress reduction associated with
splinting, FIG. 35 is a view of a cylinder or idealized heart
chamber 48' which is used to illustrate the reduction of wall
stress in a heart chamber as a result of deployment of the splint
in accordance with the present invention. The model used herein and
the calculations related to this model are, intended merely to
illustrate the mechanism by which wall stress is reduced In the
heart chamber. No effort is made herein to quantify the actual
reduction which would be realized in any particular in vivo
application.
[0118] FIG. 36 is a view of the idealized heart chamber 48' of FIG.
35 wherein the chamber has been splinted along its length L such
that a "figure eight" cross-section has been formed along the
length thereof. It should be noted that the perimeter of the
circular transverse cross-section of the chamber in FIG. 35 is
equal to the perimeter of the figure eight transverse cross-section
of FIG. 36. For purposes of this model, opposite lobes of the
figure in cross-section are assumed to be minor images.
[0119] FIG. 37 shows various parameters of the figure eight
cross-section of the splinted idealized heart chamber of FIG. 36.
Where l is the length of the splint between opposite walls of the
chamber, R.sub.2 is the radius of each lobe, .theta. is the angle
between the two radii of one lobe which extends to opposite ends of
the portion of the splint within chamber 48' and h is the height of
the triangle formed by the two radii and the portion of the splint
within the chamber 48' (R.sub.1 is the radius of the cylinder of
FIG. 35). These various parameters are related as follows:
h=R.sub.2 COS(.theta./2)
l=2R.sub.2 SIN(.theta./2)
R.sub.2=R.sub.1n/(2.pi.-.theta.)
[0120] From these relationships, the area of the figure eight
cross-section can be calculated by:
A.sub.2=2.pi. (R.sub.2).sup.2 (l-.theta./2.pi.)+h1
[0121] Where chamber 48' is unsplinted as shown in FIG. 35,
A.sub.1, the original cross-sectional area of the cylinder, is
equal to A.sub.2 where .theta.=180.degree., h=O and l=2R.sub.2.
Volume equals A.sub.2 times length L and circumferential wall
tension equals pressure within the chamber times R.sub.2 times the
length L of the chamber.
[0122] Thus, for example, with an original cylindrical radius of
four centimeters and a pressure within the chamber of 140 mm of
mercury, the wall tension T in the walls of the cylinder is 104.4
newtons. When a 3.84 cm splint is placed as shown in FIGS. 36 and
37 such that l=3.84 cm, the wall tension T is 77.33 newtons.
[0123] FIGS. 38 and 39 show a hypothetical distribution of wall
tension T and pressure P for the figure eight cross-section. As
.theta. goes from 180.degree. to 0.degree., tension T.sub..theta.
in the splint goes from 0 to a 2T load where the chamber walls
carry a T load.
[0124] Numerous characteristics and advantages of the invention
covered by this document have been set forth in the foregoing
description. It will be understood, however, that this disclosure
is, in many respects, only illustrative. Changes may be made in
details, particularly in matters of shape, size and ordering of
steps without exceeding the scope of the invention. The invention's
scope is defined in the language of the claims.
* * * * *