 |
Claims  |
|
|
That which is claimed is:
1. A closed-heart method for treating ventricular tachycardia in a
myocardial infarct patient afflicted with ventricular tachycardia, said
method comprising:
(a) defining the boundaries of a thin layer of spared myocardial tissue
positioned between the myocardial infarct scar tissue and the inner
surface of the myocardium (the endocardium) of said patient; and then
(b) ablating said thin layer of spared myocardial tissue by a closed-heart
procedure with an ablation catheter.
2. A method according to claim 1, wherein said defining step comprises the
step of defining a thin layer having a thickness of up to about 5
millimeters.
3. A method according to claim 1, wherein said defining step comprises the
step of defining a thin layer having a thickness of from about 25 to 2
millimeters.
4. A method according to claim 1, wherein said defining step comprises the
step of defining a thin layer having an endocardial surface area of at
least 15 square centimeters.
5. A method according to claim 1, wherein said defining step comprises the
step of defining a thin layer having an endocardial surface area of from
about 20 to 40 square centimeters.
6. A method according to claim 1, wherein said defining step is carried out
in the absence of ventricular tachycardia.
7. A method according to claim 1, wherein said defining step is carried out
by detecting said thin layer of spared myocardial tissue by
echocardiography.
8. A method according to claim 1, wherein said defining step is carried out
by detecting said infarct overlying said thin layer of spared myocardial
tissue by echocardiography.
9. A method according to claim 1, wherein said defining step is carried out
by visualization of endocardial fibrosis beneath said thin layer of spared
myocardial tissue.
10. A method according to claim 1, wherein said defining step is carried
out by electrically stimulating the endocardium to detect an increased
pacing threshold.
11. A method according to claim 1, wherein said defining step is carried
out with a catheter mounted echocardiographic ultrasound crystal sensor
inserted into the interior of the heart of said patient.
12. A method according to claim 1, wherein said defining step is carried
out with an echocardiographic ultrasound crystal sensor positioned in the
esophagus of said patient.
13. A method according to claim 1, wherein said ablating step comprises
destroying all of said thin layer of spared myocardial tissue.
14. A method according to claim 1, wherein said ablating step comprises the
step of electrically separating a portion of said thin layer sufficient in
size to combat ventricular tachycardia from the remainder of the
endocardium.
15. A method according to claim 1, wherein said ablating step comprises the
step of creating at least one elongate lesion in said thin layer extending
from the endocardium to said myocardial infarct scar tissue, wherein said
at least one elongate lesion divides said thin layer into a plurality of
electrically separated portions, and wherein each of said portions is
incapable of originating ventricular tachycardia.
16. A method according to claim 15, wherein said at least one elongate
lesion comprises a plurality of elongate lesions.
17. A method according to claim 1, wherein said ablating step is followed
by the step of verifying that said thin layer of spared myocardial tissue
is no longer capable of originating a ventricular tachycardia.
18. A method according to claim 17, wherein said verifying step comprises a
programmed pacing technique to induce ventricular tachycardia.
19. A closed-heart method for treating ventricular tachycardia in a
myocardial infarct patient afflicted with ventricular tachycardia, said
method comprising:
(a) defining the boundaries of a thin layer of spared myocardial tissue
positioned between the myocardial infarct scar tissue and the inner
surface of the myocardium (the endocardium) of said patient, said thin
layer having a thickness up to about five millimeters and an endocardial
surface area of at least 15 square centimeters; and then
(b) ablating said thin layer of spared myocardial tissue by creating at
least one elongate lesion in said thin layer extending from the
endocardium to said myocardial infarct scar tissue in a closed-heart
procedure with an ablation catheter, wherein said at least one elongate
lesion is configured to reduce any portion of said thin layer in
electrical contact with the remainder of the endocardium to a size, in
surface area, sufficient to combat ventricular tachycardia in said
patient.
20. A method according to claim 19, wherein said ablating step comprises
the step of electrically separating from the remainder of the endocardium
a portion of said thin layer sufficient in size, in surface area to combat
ventricular tachycardia.
21. A method according to claim 19, wherein said electrically separating
step comprises the step of creating a continuous lesion extending from the
endocardium to said myocardial infarct scar tissue around said thin layer
of spared myocardial tissue, said continuous lesion encircling said thin
layer to electrically separate said thin layer from adjacent myocardial
tissue.
22. A method according to claim 19, wherein said ablating step comprises
the step of creating at least one elongate lesion in said thin layer
extending from the endocardium to said myocardial infarct scar tissue,
wherein said at least one elongate lesion divides said thin layer into a
plurality of electrically separated portions, and wherein each of said
portions is reduced to a size, in surface area, sufficient to combat
ventricular tachycardia.
23. A method according to claim 19, wherein said at least one elongate
lesion comprises a plurality of elongate lesions.
24. A method for prognosing the likelihood of ventricular tachycardia
occuring in a myocardial infarct patient not previously diagnosed as
afflicted with ventricular tachycardia, said method comprising detecting
the boundaries of a thin layer of spared myocardial tissue positioned
between the myocardial infarct scar tissue and the inner surface of the
myocardium (the endocardium) in said patient.
25. A method according to claim 24, wherein said method is a closed-heart
method.
26. A method according to claim 24, wherein said detecting step is carried
out by:
(a) determining if a thin layer of spared tissue exists between the infarct
and the endocardium, and then
(b) creating a map of the locations of the thin layer identified in said
determining step to define the thin layer areas, and
(c) evaluating the dimensions of said thin layer areas to determine if the
contiguous portions of said thin layer areas are of sufficient size to
support reentrant pathways.
27. A method according to claim 24, wherein said detecting step comprises
the step of detecting a thin layer having a thickness of up to about 5
millimeters.
28. A method according to claim 24, wherein said detecting step comprises
the step of detecting a thin layer having a thickness of from about 0.25
to 2 millimeters.
29. A method according to claim 24, wherein said detecting step comprises
the step of detecting a thin layer having an endocardial surface area of
at least 15 square centimeters.
30. A method according to claim 24, wherein said detecting step comprises
the step of detecting a thin layer having an endocardial surface area of
from about 20 to 40 square centimeters.
31. An apparatus for the ablation treatment of ventricular tachycardia,
comprising:
an intraventricular catheter;
detecting means for detecting the boundaries of a thin layer of spared
endocardial tissue connected to said intraventricular catheter;
ablation means for ablating said thin layer of spared endocardial tissue
connected to said intraventricular catheter; and
analyzing means operatively associated with said detecting means for
prognosing the likelihood of ventricular tachycardia arising from said
thin layer.
32. An apparatus according to claim 31, wherein said analyzing means
comprises a software program running in a computer.
33. A closed-heart method for treating ventricular tachycardia in a
myocardial infarct patient afflicted with ventricular tachycardia, said
method comprising:
(a) defining a thin layer of spared myocardial tissue positioned between
the myocardial infarct scar tissue and the inner surface of the myocardium
(the endocardium) of said patient; and then
(b) ablating said thin layer of spaced myocardial tissue by a closed-heart
procedure with an ablation catheter;
wherein said ablating step comprises the step of creating a continuous
lesion extending from the endocardium to said myocardial infarct scar
tissue around said thin layer of spared myocardial tissue, said continuous
lesion encircling said thin layer to electrically separate said thin layer
from adjacent myocardial tissue.
34. A method according to claim 33, wherein said defining step is carried
out in the absence of ventricular tachycardia.
35. A method according to claim 33, wherein said defining step is carried
out by detecting said thin layer of spared myocardial tissue by
echocardiography.
36. A method according to claim 33, wherein said defining step is carried
out by detecting said infarct overlying said thin layer of spared
myocardial tissue by echocardiography.
37. A method according to claim 33, wherein said defining step is carried
out by visualization of endocardial fibrosis beneath said thin layer of
spared myocardial tissue.
38. A method according to claim 33, wherein said defining step is carried
out by electrically stimulating the endocardium to detect an increased
pacing threshold. |
|
 |
|
 |
Claims |
|
|
|
Description |
|
|
FIELD OF THE INVENTION
This invention relates to methods for the ablation of cardiac tissue for
the treatment of ventricular tachycardia and to diagnostic methods for
detecting conditions which indicate a high risk of ventricular
tachycardia.
BACKGROUND OF THE INVENTION
Ventricular tachycardia is a disease of the heart in which the heart's
normal rhythmic contraction is altered, thus affecting heart function. The
condition is often described as a heart beat which is too fast, although
the disease is far more complex. Ventricular tachycardia occurs most often
in patients following a myocardial infarction. A myocardial infarction,
commonly referred to as a heart attack, is a loss of blood flow to a
region of the heart causing the myocardial (muscle) tissue in that region
to die and be replaced by an area of scar tissue known as a myocardial
infarct. In most cases, this occurs in the left ventricle.
Ventricular tachycardia ("VT") may be initiated and sustained by a
re-entrant mechanism, termed a "circus" movement. The mechanism of
re-entry, as it is currently understood, is discussed in M. Josephson and
H. Wellens, Tachycardias: Mechanisms, Diagnosis, Treatment, Chap. 14
(1984)(Lea & Febiger). Most cases of sudden cardiac death that have
occurred during cardiac monitoring have begun as VT that degenerated into
ventricular fibrillation.
While VT can be halted after it begins by pacing or cardioversion, it is
preferable to prevent the arrhythmia from arising. Drug therapy has been
used, but is successful in only 30 to 50 percent of patients and has
undesirable side effects. Endocardial resection, a surgical procedure
involving removing the tissue in the ventricle thought to be the source of
the VT, has been reported to eradicate VT in up to 90 percent of patients,
but it suffers from a 5 to 10 percent incidence of perioperative
mortality. For a discussion of surgical procedures, see T. Ferguson and J.
Cox, Surgical Therapy for Cardiac Arrhythmias, in Nonpharmacological
Therapy of Tachyarrhythmias (G. Breithardt et al. eds. 1987).
As an alternative to surgery, the technique most often attempted is
ablation. Typically, programmed premature pacing is performed from a
catheter electrode in the right or left ventricular cavity. During
programmed premature pacing, a stimulus, usually of twice diastolic
threshold, is repeatedly given prematurely until either VT is induced or
the tissue is too refractory to be excited. The ECG is examined during
induced VT and compared to the ECG showing spontaneous bouts of VT. If the
ECG is similar, it is assumed that the patient's clinical VT is being
induced. A mapping catheter in the left ventricular cavity is used to
record from numerous sites sequentially to determine the activation
sequence along the left ventricular endocardium during the induced VT. The
site from which activation appears to originate during the induced VT is
identified and assumed to be a portion of the reentrant pathway. The
techniques of pace mapping and entrainment may then be used in an attempt
to confirm or refine the localization of the region rising to VT. The
region is then ablated. Unfortunately, this technique is usually
unsuccessful unless repeated many times. For example, it has been reported
by Downar et al. that for a similar technique (the electrodes were located
on an endocardial balloon instead of a catheter), anywhere from 10 to 42
shocks through different electrodes were required to prevent the
reinduction of VT. It is assumed that failures occur because ablation is
not performed at the correct site or does not create a lesion deep enough
within the ventricular wall to reach the reentrant pathway.
It is extremely desireable to prognose the likelihood of a myocardial
infarct patient being susceptible to ventricular tachycardia. U.S. Pat.
No. 4,680,708 to M. Cain and B. Sobel suggests a method and apparatus for
analyzing electrocardiogram signals to prognose ventricular tachycardia,
but the early detection of myocardial infarct patients susceptible to
ventricular tachycardia remains a problem.
In view of the foregoing, an object of the present invention is to provide
a technique which is effective in combatting VT, does not require the
administration of drugs, and does not require open-heart surgery.
A further object of the present invention is to provide a means for
prognosing the likelihood of ventricular tachycardia occuring in a
myocardial infarct patient not previously diagnosed as having ventricular
tachycardia.
SUMMARY OF THE INVENTION
The present invention is based on the concept that a thin layer of viable
myocardial tissue adjacent to the endocardium in a myocardial infarct
patient is capable of supporting multiple re-entrant pathways, any one of
which can give rise to ventricular tachycardia.
In view of the foregoing finding, a first aspect of the present invention
is a closed-heart method for treating ventricular tachycardia in a
myocardial infarct patient afflicted with ventricular tachycardia. The
method comprises, first, defining a thin layer of spared myocardial tissue
positioned between the myocardial infarct scar tissue and the inner
surface of the myocardium (the endocardium) of the patient, and then
ablating the thin layer of spared myocardial tissue by a closed-heart
procedure with an ablation catheter.
In a particular embodiment of the foregoing, the ablating step is carried
out by creating at least one elongate lesion in said thin layer extending
from the endocardium to the myocardial infarct scar tissue in a
closed-heart procedure with an ablation catheter. The at least one
elongate lesion is configured to reduce the size, in surface area, of any
portion of the thin layer in electrical contact with the remainder of the
endocardium sufficient to combat ventricular tachycardia in said patient.
This may be carried out by electrically separating from the remainder of
the endocardium a portion of the thin layer which has a size, in surface
area, sufficient to combat ventricular tachycardia (e.g., by creating a
continuous elongate lesion around the thin layer of spared myocardial
tissue, the continuous lesion encircling the thin layer to electrically
separate the thin layer from adjacent myocardial tissue), or by creating
at least one (or a plurality) of elongate lesions in the thin layer,
wherein the at least one elongate lesion divides the the layer into a
plurality of electrically separated portions, with the capability of each
portion for originating ventricular tachycardia being reduced sufficiently
to combat ventricular tachycardia in the patient.
Another aspect of the present invention is an apparatus for the ablation
treatment of ventricular tachycardia. The apparatus comprises an
intraventricular catheter, a detecting means for detecting a thin layer of
spared endocardial tissue connected to the intraventricular catheter, an
ablation means for ablating the thin layer of spared endocardial tissue
connected to the intraventricular catheter; and an analyzing means
operatively associated with the detecting means for prognosing the
likelihood of ventricular tachycardia arising from the thin layer.
Another aspect of the present invention is a method for prognosing the
likelihood of ventricular tachycardia occuring in a myocardial infarct
patient not previously diagnosed as afflicted with ventricular
tachycardia. The method comprises detecting a thin layer of spared
myocardial tissue positioned between the myocardial infarct scar tissue
and the inner surface of the myocardium (the endocardium) in the patient.
Previous work in the diagnosis and treatment of ventricular tachycardia has
always looked for functional or electrical characteristics of tissue
rather than a specific anatomic structure. The present invention, in
contrast, is based on the finding that a specific macroscopic anatomical
structure gives rise to ventricular tachycardia.
BRIEF DESCRIPTION OF THE DRAWINGS
FIG. 1 is a side view of a human heart, with portions cut away to reveal
the internal chambers and myocardial walls.
FIGS. 2A, 2B, 2C illustrate typical cross-sectional slices from control
(FIG. 2A), subacute ventricular tachycardia (FIG. 2B), and chronic
ventricular tachycardia (FIG. 2C) groups.
FIGS. 3A-3F schematically illustrates various ablation patterns on the
internal surface of the heart which may be employed in carrying out the
present invention.
FIG. 4 schematically illustrates an apparatus useful for carrying out the
ablation method of the present invention.
FIGS. 5-6 illustrate the use of an apparatus as given in FIG. 4.
FIGS. 7A-G shows the initiation of sustained ventricular tachycardia
settling into a monomorphic figure of 8 reentry pattern. The activation
times and isochronal maps of the last beat of the S1 train (Panel A) are
shown as well as the first 5 beats of VT (Panels B-F) induced after a 20
mA S2 stimulus at an S1S2 interval of 210 ms as recorded by a plaque of
121 bipolar electrodes over the infarct in the left ventricle. The S1S1
interval of the pacing train is 300 ms. The long axis of the spared
myocardial fibers is represented by the double headed arrow at the top of
the figure. Each number gives the activation time in ms at an electrode
site. The isochronal interval is 20 ms. In panel A time zero is the
beginning of the S1 stimulus. In Panels B-F time zero is the beginning of
the S2 stimulus. In panel B, the first beat after S2 stimulation, arrows
indicate that the activation fronts conduct around both sides of a line of
block (reepresented by the heavy black bar in this and subsequent
figures). The hatched line (in this and subsequent figures) represents a
frame line between panels in which reentry is believed to occur. In panel
C, the adjoining solid and hatched lines indicate block between beats one
and two and reentry between beats two and three respectively. Panel 2
shows the monomorphic ventricular tachycardia as recorded by the surface
leads I, II and III. Closed arrow indicates S2.
FIGS. 8A-E shows the initiation of sustained monomorphic ventricular
tachycardia with a figure of 8 reentry pattern in a second animal in which
the S1 was delivered from the right ventricular free wall. The activation
times and isochronal maps of the last beat of the 300 ms S1 train (Panel
A) as well as those of the first 3 beats of ventricular tachycardia
(Panels B-D) induced by a 30 mA S2 stimulus at an S1S2 interval of 230 ms
are shown. In panel B, the activation pattern of the first beat post S2
stimulation is compatible with figure of 8 reentry. The initial activation
sequence is directed back toward the S1 stimulation site in the direction
opposite the S1 activation sequence. Figure of 8 reentry is also seen in
the subsequent beats of ventricular tachycardia (Panels C and D). Panel E
shows the lead II rhythm strip of ventricular tachycardia induced. Open
arrow indicates the first S1 and closed arrow indicates S2. The long axis
of the spared myocardial fibers is represented by the double headed arrow
at the top of the figure.
FIGS. 9A-E shows the initiation of sustained monomorphic ventricular
tachycardia with a figure of 8 reentry pattern in which the S1 was
delivered from the left ventricular free wall in the same animal as for
FIG. 8. The activation times and isochronal maps, of the last beat of the
300 ms S1 train (Panel A) as well as those of the first 3 beats of
ventricular tachycardia (Panels B-D) induced by a 30 mA S2 stimulus at an
S1S2 interval of 230 ms, are shown. In panel B, the activation pattern of
the first beat post S2 stimulation is compatible with figure of 8 reentry
and once again the initial activation is generally back toward the S1
stimulation site in the direction opposite the S1 activation sequence.
Figure of 8 reentry is also seen in subsequent beats (Panels C and D).
Panel E shows the lead II rhythm strip of ventricular tachycardia induced.
Open arrow indicates the first S1 and closed arrow indicates S2.
DETAILED DESCRIPTION OF THE INVENTION
The basic anatomy of the human heart 10 is illustrated in FIG. 1. Its walls
are composed primarily of myocardial (muscle) tissue. The muscle tissue
walls of the heart are referred to as the myocardium 11. The inner surface
of the myocardium, which is in contact with the blood in the heart
chambers, is the endocardium 12,12'. The heart is longitudinally divided
into left and right halves. Each half has an upper chamber called an
atrium 13,14, and a lower chamber called a ventricle 15,16. Between the
atrium and the ventricle of each half is an atrioventricular (AV) valve 17
which is a one way valve allowing blood flow only from the atrium into the
ventricle. The right and left ventricles are separated by the
interventricular septum 18.
The circulatory system is comprised of two separate systems, pulmonary and
systematic circulation. In the pulmonary circuit blood is pumped by the
right ventricle 15 into the pulmonary artery which then splits into a
right pulmonary artery 20 and a left pulmonary artery 21 allowing to flow
through the lungs and then into the pulmonary veins 22,23,24,25 which flow
into the left atrium 14. The oxygen rich blood from the pulmonary circuit
is pumped by the left ventricle into the systemic circuit via the aorta.
After passing throughout the body, the blood returns to the right atrium
via the inferior vena cava and the superior vena cava.
The thickness of the walls of the chambers of the hearts vary in relation
to the amount of pumping work they perform. The atria 13, 14 are of little
importance in pumping the blood except under high demand conditions, such
as exercise, and are thin walled (2-3 millimeters). The right ventricle 15
only pumps blood through the relatively short pulmonary circuit and is
significantly more thin walled than the left ventricle 16 which must
maintain the pressure within the systemic circuit (8-12 millimeters).
FIG. 2 illustrates typical cross-sectional slices of ventricles from
patients with myocardial infarction but no ventricular tachycardia
(control) (FIG. 2A), patients with subacute myocardial infarction with
ventricular tachycardia (FIG. 2B), and patients with chronic myocardial
infarction with ventricular tachycardia (FIG. 2C) groups. The subacute
group had predominantly large solid myocardial infarcts 30 with ribbon
spared subendocardium 31. The chronic ventricular tachycardia group has
predominantly large patchy myocardial infarcts 32 with irregular spared
subendocardium. The control group had smaller hearts and smaller more
randomly distributed patchy myocardial infarcts 34 with little ribbon
spared subendocardium 35. Black represents solid myocardial infarct, and
stippling represents patchy myocardial infarct. Slices are seen from the
basal aspect. These data are known. See D. Bolick et al., Circulation 74,
1266, 1273 (1986).
The thin layer referred to herein is a layer of surviving myocardial tissue
located between the surface of the endocardium 12,12' and the myocardial
infarct scar tissue. The thin layer may be in the right or left ventricle,
but more typically the left ventricle. A layer of fibrosis may be
positioned beneath the thin layer, as explained below. While the precise
dimensions of the thin layer will vary from patient to patient, with some
variability due to the variability of the infarct in the epicardial to
endocardial dimension, the thin layer will generally have a thickness of
up to about 5 millimeters, and will generally have an endocardial surface
area of at least 15 square centimeters. Typically, the thin layer will
have a thickness of from about 0.25 to 2 millimeters, and will have an
endocardial surface area of from about 20 to 40 square centimeters.
The present invention is directed to both diagnostic and treatment methods
for ventricular tachycardia in a patient afflicted with a myocardial
infarct. The treatment method of the present invention involves first,
defining a thin layer of spared myocardial tissue positioned between the
myocardial infarct scar tissue and the inner surface of the myocardium
(the endocardium) of the patient, and then ablating the thin layer of
spared myocardial tissue. The diagnostic method provides a means for
examining myocardial infarct patients to determine their risk of
developing ventricular tachycardia by detecting the presence of a thin
layer of spared myocardial tissue positioned between the myocardial
infarct scar tissue and the inner surface of the myocardium (the
endocardium).
Reentrant pathways causing VT may arise from numerous sites within the thin
layer of spared tissue between the infarct and the endocardium, the first
or defining step involves identifying the presence and location of this
thin layer instead of inducing and mapping the activation sequence during
a particular incidence of induced VT as was done previously. Thus, the
subject on which the defining step is performed need not have VT induced
prior to the procedure, and need not be in VT during the defining step.
The thin layer can be defined by any one or a combination of several
techniques, including (1) analyzing recordings during regular rhythm from
electrodes on a catheter; (2) pacing from an electrode on the catheter and
analyzing the pacing threshold as well as recordings of the pacing
stimulus and the ensuing activation sequence from other electrodes on the
same catheter; (3) direct visualization of the thin layer of spared
myocardial tissue by an imaging technique such as
echocardiography/ultrasound which can differentiate healthy myocardial
tissue from infarcted tissue; (4) detecting by echocardiography the
infarct itself overlying the thin layer of spared myocardial tissue (e.g.,
by detecting altered heart wall motion overlying the infarct or by
detecting altered backscatter from the infarct); (5) visualization of
endocardial fibrosis beneath the thin layer of spared myocardial tissue
(i.e., between the thin layer of spared myocardial tissue and the
ventricular cavity); and (6) electrically stimulating the endocardium to
detect an increased pacing threshold (due to the presence of endocardial
fibrosis overlying the thin layer of spared myocardial tissue).
Any suitable apparatus may be employed to carry out the defining step, such
as a catheter mounted echocardiographic ultrasound crystal sensor inserted
into the interior of the heart of said patient, an echocardiographic
ultrasound crystal sensor positioned in the esophagus of the patient, or
echocardiographyic ultrasound crystal sensor applied to the chest wall by
contact to the skin. The imaging device need not be on a catheter (is in
the case of an esophageal echocardiograph), though preferably the mapping
is performed with a catheter mounted sensing device. Particularly suitable
is an echocardiagraphic/ultrasound crystal sensor mounted on a catheter
which is inserted into the interior of the heart of the patient. This same
catheter can also carry the ablation device as discussed below. Suitable
detection devices are known, examples of which are disclosed in U.S. Pat.
No. 5,000,185 and in PCT Application Number WO 91/02488. (Applicants
intend that all U.S. Patent references cited herein be incorporated herein
by reference). An ultrasonic technique for mapping myocardial tissue with
an external sensor is discussed in B. Barzilai et al., J. Am. Soc. Echo.
1, 179-186 (1988)(showing altered backscatter from myocardial infarct).
Once the thin layer of spared myocardium is identified, it can be ablated
by a variety of methods. Three such methods of the present invention,
along with prior art methods, are schematically illustrated in FIG. 3. The
endocardial surface is schematically illustrated in FIG. 3A, the prior art
surgical resection technique is illustrated in FIG. 3B, and prior art
catheter ablation techniques are schematically illustrated in FIG. 3C. In
the embodiment of the invention illustrated in FIG. 3D, ablation is
accomplished by creating a continuous lesion 41 extending from the
endocardium to the myocardial infarct scar tissue around the thin layer of
spared myocardial tissue. This continuous lesion encircling the thin layer
electrically isolates the thin layer from adjacent myocardial tissue so
that any arrhythmias arising in the thin layer are not able to propagate
into the rest of the heart. In the embodiment of the invention illustrated
in FIG. 3E, ablation is accomplished by creating at least one, or as
illustrated a plurality of, elongate lesions 42 in the thin layer, with
each lesion extending from the endocardium to the myocardial infarct scar
tissue. The elongate lesion(s) are patterned to divide the thin layer into
a plurality of electrically separated portions each, of which is
substantially incapable of originating ventricular tachycardia. In the
embodiment of the invention illustrated in FIG. 3F, ablation is
accomplished by destroying all of the thin layer of spared myocardial
tissue with a large lesion 43.
A variety of devices are known and available for performing the ablation
step. A direct current ablation electrode such as that disclosed in U.S.
Pat. No. 4,896,671 or a laser ablation catheter such as that disclosed in
U.S. Pat. No. 4,985,028 may be used. More preferably, a radio frequency
(RF) ablation catheter as disclosed in U.S. Pat. No. 4,945,912 or a
microwave ablation catheter such as that discussed in J. Langberg et al.,
Pace 14, 2105 (December, 1991) is used. Another approach is to ablate the
thin layer with ultrasound at high energy, as discussed in greater detail
below.
As noted above, both the detecting means such as an
echocardiagraphic/ultrasound crystal sensor and an ablation means such as
a laser unit may advantageously be located on the same catheter. Examples
of such catheter devices are disclosed in U.S. Pat. No. 5,000,185, U.S.
Pat. No. 4,936,281 and in PCT Application Number WO 91/02488. A schematic
diagram of such a catheter device using and ultrasound sensing means and a
laser ablation means is shown in FIG. 4. The system 50 includes a catheter
probe assembly 51 including a distal subassembly 52 inserted within a
guide catheter 53. The proximal end of the guide catheter 53 is coupled to
a conventional side arm connector 54. The distal subassembly 52 is coupled
to a suitable motor means 55 which provides the drive to maneuver the
distal subassembly 52. The ultrasonic imaging components within the distal
subassembly 52 are electrically connected with an electroacoustic
transducer and an ultrasound transceiver 56 via suitable electrical
contact brushes 57. To perform detection the ultrasonic imaging components
within the distal subassembly are activated and the received signals are
processed by the ultrasound transceiver 56. The signals are further
processed by algorithms performed by the computer 58 to generate an image
of the tissue structures reflecting the ultrasonic energy toward the
distal subassembly 52. The ablating is performed by a laser means. A laser
driver 60 provides a source of laser radiation which passes via the
contact brushes 57 to a dual function electrical/optical connector 61
which couples the ultrasonic imaging components and laser optical
components within the distal subassembly 52 to the ultrasound transceiver
56 and the laser driver 60. The computer 58 also functions to allow the
operator to control the laser driver to perform ablation of tissue where
desired.
A software program running in the computer 58, which computer is
operatively associated with the detecting means, provides a means for
prognosing the likelihood of ventricular tachycardia arising from said
thin layer. In a typical embodiment of this method, the detecting step
includes determining if a thin layer of spared tissue exists between the
infarct scar tissue and the endocardium, then creating an anatomical map
of the locations of the thin layer identified to define the thin layer
areas, and then evaluating the dimensions of the thin layer areas to
determine if the contiguous portions of these areas are of sufficient size
to support reentrant pathways.
Another option in an apparatus of the present invention is, as noted above,
to use ultrasound energy at higher power levels to ablate the thin layer
of tissue. An intraventricular catheter for accomplishing this method
would have two sets of ultrasound crystal connected thereto: one set
configured for detecting the thin layer, and another set configured for
ablation of the thin layer.
FIGS. 5-6 illustrate the use of a catheter of FIG. 4 in a method of the
present invention. The catheter 51 is first introduced into the
circulatory system, preferably through a vessel in the leg, and advanced
into the heart 10. In the typical case of a patient suffering from VT
following a myocardial infarction, the infarct scar tissue is located in
the left ventricle 16, either within the outer walls of the ventricle or
within the interventricular septum 18. In such a patient, the catheter is
advanced into the left ventricle 16, for example by advancing the catheter
into the femoral artery and then through the aorta 26 into the left
ventricle 16. The detecting means is then activated and the catheter is
manipulated substantially throughout the left ventricle 16 to locate any
areas of thin layers of surviving tissue between the endocardium 12 and
the infarct scar tissue. Preferably, this information is generated for
substantially the entire area affected and then the catheter is withdrawn.
In the treatment of the present invention, each thin layer area located is
rendered substantially incapable of supporting VT by the ablating step.
The ablating step may be performed for all the thin layer areas found
after the mapping is completed or, more preferably, is performed on each
contiguous thin layer area once the area is defined. The portions of
tissue to be ablated depends upon the embodiment of the present invention
utilized as was discussed previously.
The ablating step is optionally followed by the step of verifying that the
thin layer of spared myocardial tissue is no longer capable of originating
a ventricular tachycardia. This verifying step can be accomplished using a
programmed pacing technique to induce ventricular tachycardia. Such
techniques are discussed in M. Josephson and H. Wellens, Tachycardias:
Mechanisms, Diagnosis, Treatment, Chap. 14, (1984).
As noted above, the present invention further provides a method for
prognosing the likelihood of ventricular tachycardia occuring in a
myocardial infarct patient not previously diagnosed as afflicted with
ventricular tachycardia. The method comprises detecting a thin layer of
spared myocardial tissue positioned between the myocardial infarct scar
tissue and the inner surface of the myocardium (the endocardium) in the
patient. The thin layer to be detected is described in detail above. The
procedure is advantageously carried out by closed-heart procedures, as
discussed in detail above. In a typical embodiment of this method, the
detecting step includes determining if a thin layer of spared tissue
exists between the infarct scar tissue and the endocardium, then creating
an anatomical map of the locations of the thin layer identified to define
the thin layer areas, and then evaluating the dimensions of the thin layer
areas to determine if the contiguous portions of these areas are of
sufficient size to support reentrant pathways.
The present invention is explained further in the following Example. This
Example is illustrative of the present invention, and is not to be
construed as limiting thereof.
EXAMPLE 1
High Current Stimuli to the Spared Epicardium of a Large Infarct Induce
Ventricular Tachycardia
This study was carried out to test the hypothesis that a high current
premature stimulus during the vulnerable period over the surviving
epicardium of a four day old infarct in a canine model will induce
sustained VT rather than ventricular fibrillation. As explained in detail
below, it was found that a large S2 over a nontransmural infarct induced
VT if the spared myocardium was thin.
MATERIALS AND METHODS
Surgical preparation. In twelve mongrel dogs, anesthesia was induced using
intravenous thiopental sodium, 20 mg/kg, and maintained using a continuous
infusion of thiopental sodium at a maintenance rate of approximately 0.8
mg/kg/min. Succinylcholine, 1 mg/kg, was also given at the time of
anesthesia induction. The animals were intubated with a cuffed
endotracheal tube and ventilated with room air and oxygen through a
Harvard respirator (Harvard Apparatus Co. South Natick, MA). A femoral
arterial line and two intravenous lines were inserted using sterile
techniques. Systemic arterial pressure was continuously displayed.
Arterial blood samples were drawn every 30-60 min for determination of pH,
PO2, PCO2, base excess, bicarbonate, Na.sup.+, K.sup.+, and Ca.sup.++
content. Ringer's lactate was continuously infused via a peripheral
intravenous line. This was supplemented with sodium bicarbonate, potassium
chloride, and calcium chloride as indicated to maintain pH and
electrolytes within normal values. Electrocardiographic leads were applied
for continuous ECG monitoring. Body temperature was maintained with a
thermal mattress. With sterile surgical techniques the heart was exposed
through a left thoracotomy at the fourth intercostal space; the
pericardium was opened, and the left anterior descending coronary (LAD)
artery was dissected free at the tip of the left atrial appendage. A noose
occluder was placed around the left anterior descending artery and it was
occluded by the Harris two state procedure (A. Harris and A Rojas, Exp.
Med. Surg. 1, 105 (1943)). In order to ensure sparing of the epicardium in
the entire infarct zone, partial occlusion was maintained for 30 min,
followed by complete occlusion for 90 min prior to reperfusion. Five
minutes before initiation of partial occlusion and again before the
termination of complete occlusion the animals were pre-treated with bolus
injections of intravenous lidocaine (2 mg/kg). A second of lidocaine (1
mg/kg) was administered ten minutes later. The chest was closed in layers,
evacuated under negative pressure and the animal was allowed to recover.
Four days after LAD occlusion, anesthesia was induced with intravenous
pentobarbital (30-35 mg/kg body weight) and maintained with a continuous
infusion of pentobarbital at a rate of approximately 0.05 mg/kg per min.
Succinylcholine (1 mg/kg) was also given intravenously at the time of
anesthesia induction. Supplemental doses of 0.25 of 0.5 mg/kg of
succinylcholine were given hourly as needed to maintain muscle relaxation.
The animals were ventilated, hemodynamically monitored and maintained as
described above. A median sternotomy was performed, and the heart was
suspended in a pericardial cradle. The recording apparatus consisted of
121 bipolar Ag-AgCl epicardial electrodes (see F. Witkowski and P.
Penkoske, Am. J. Physiol. 254, H804 (1988)) arranged in 11 columns and 11
rows mounted in a 4.times.4 cm plaque. Each epicardial electrode was 1 mm
in diameter. There was a 2 mm intraelectrode distance between each member
of the bipolar pair and an inter-electrode distance of 4 mm. This plaque
also contained a centrally located stimulating electrode. The plaque of
epicardial recording electrodes was sutured over the infarcted anterior
surface of the left ventricle. Four solid stainless steel wires (American
Wire Gauge #30, Cooner Wire Co. Chatsworth, CA) that were insulated except
at the tip were positioned for S1 p | | |
