U.S. patent application number 11/215710 was filed with the patent office on 2006-01-12 for ischemia detection.
Invention is credited to Shannon D. Nelson, Todd J. Sheldon, Robert W. Stadler, Lee Stylos.
Application Number | 20060009811 11/215710 |
Document ID | / |
Family ID | 25482753 |
Filed Date | 2006-01-12 |
United States Patent
Application |
20060009811 |
Kind Code |
A1 |
Sheldon; Todd J. ; et
al. |
January 12, 2006 |
Ischemia detection
Abstract
Techniques for detection and treatment of myocardial ischemia
are described that monitor both the electrical and dynamic
mechanical activity of the heart to detect and verify the
occurrence of myocardial ischemia in a more reliable manner. The
occurrence of myocardial ischemia can be detected by monitoring
changes in an electrical signal such as an ECG or EGM, and changes
in dynamic mechanical activity of the heart. Dynamic mechanical
activity can be represented, for example, by a heart acceleration
signal or pressure signal. The electrical signal can be obtained
from a set of implanted or external electrodes. The heart
acceleration signal can be obtained from an accelerometer or
pressure sensor deployed within or near the heart. The techniques
correlate contractility changes detected by an accelerometer or
pressure sensor with changes in the ST electrogram segment detected
by the electrodes to increase the reliability of ischemia
detection.
Inventors: |
Sheldon; Todd J.; (North
Oaks, MN) ; Stylos; Lee; (Stillwater, MN) ;
Nelson; Shannon D.; (Minneapolis, MN) ; Stadler;
Robert W.; (Shoreview, MN) |
Correspondence
Address: |
MEDTRONIC, INC.
710 MEDTRONIC PARKWAY NE
MS-LC340
MINNEAPOLIS
MN
55432-5604
US
|
Family ID: |
25482753 |
Appl. No.: |
11/215710 |
Filed: |
August 30, 2005 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
09945179 |
Aug 30, 2001 |
6937899 |
|
|
11215710 |
Aug 30, 2005 |
|
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|
Current U.S.
Class: |
607/17 ; 600/513;
607/3 |
Current CPC
Class: |
A61B 5/4839 20130101;
A61B 5/6869 20130101; A61N 1/368 20130101; A61B 5/349 20210101;
A61B 2562/028 20130101; A61N 1/36542 20130101; A61B 5/7203
20130101; A61B 5/341 20210101; A61B 5/1107 20130101; A61B 2562/222
20130101 |
Class at
Publication: |
607/017 ;
600/513; 607/003 |
International
Class: |
A61N 1/365 20060101
A61N001/365; A61B 5/04 20060101 A61B005/04 |
Claims
1. A system for detecting myocardial ischemia, the system
comprising: means for generating a first signal indicative of
contractile activity of a heart; means for obtaining a second
signal indicative of electrical activity of the heart; and means
for detecting myocardial ischemia based on both the first signal
and the second signal.
2. A system according to claim 1, further comprising means for
controlling, subsequent to when myocardial ischemia is detected,
delivering a therapy to alleviate effects of the ischemia within
the heart.
3. A system according to claim 1, wherein the therapy includes at
least one of a drug delivery therapy, an electrical stimulation
therapy, a combination of the drug delivery therapy and the
electrical stimulation therapy.
4. A system according to claim 1, wherein the means for generating
the first signal includes an implanted accelerometer and the first
signal comprises a heart acceleration signal.
5. A system according to claim 4, wherein the accelerometer
mechanically couples to a distal portion of a lead adapted to be
implantable one of within and on an exterior portion of the
heart.
6. A system according to claim 1, wherein the means for obtaining
the second signal indicative of electrical activity of the heart
includes a subcutaneous electrode array (SEA).
7. A system according to claim 6, wherein the system further
comprises a subcutaneous ischemia monitoring circuit means disposed
within a substantially hermetic housing in electrical communication
with said SEA.
8. A system according to claim 1, wherein the means for obtaining
the second signal indicative of electrical activity of the heart
includes at least one endocardial electrode disposed within a
chamber or vasculature of the heart.
9. A system according to claim 1, wherein the means for obtaining
the second signal indicative of electrical activity of the heart
includes at least one externally mounted electrode adapted to be
coupled to a portion of epidermis of a subject.
10. A computer-readable medium containing instructions to produce a
technical effect via at least one computer processor, comprising:
obtaining a first signal indicative of dynamic mechanical activity
of a heart; obtaining a second signal indicative of electrical
activity of the heart; and detecting a relative degree of an
episode of myocardial ischemia based at least in part on both the
first signal and the second signal.
11. A computer computer-readable medium according to claim 10,
wherein the first signal is derived from one of an implanted
pressure transducer, an accelerometer, a velocity sensing
apparatus.
12. A computer-readable medium according to claim 10, wherein the
first signal relates to one of a right ventricular contractile
activity and a left ventricular contractile activity.
13. A computer-readable medium according to claim 12, wherein the
right ventricular contractile activity is provided from an
endocardial location.
14. A computer-readable medium according to claim 12, wherein the
left ventricular contractile activity is provided from one of an
epicardial location, a pericardial location, a location within a
portion of a great vein or coronary sinus.
15. A computer-readable medium according to claim 12, wherein the
relative degree of the episode of myocardial ischemia is determined
along at least a plurality of axes of one of said first signal and
said second signal.
16. A computer-readable medium according to claim 11, wherein the
accelerometer mechanically couples to a distal portion of a lead
adapted to be implantable one of: within a chamber of the heart, on
an exterior portion of the heart, within a portion of vasculature
of the heart.
17. A computer-readable medium according to claim 10, wherein
obtaining the second signal indicative of electrical activity of
the heart includes a signal derived from a subcutaneous electrode
array (SEA).
18. A computer-readable medium according to claim 17, further
comprising a subcutaneous ischemia monitoring circuit means
disposed within a substantially hermetic housing in electrical
communication with said SEA.
19. A computer-readable medium according to claim 10, wherein
obtaining the second signal indicative of electrical activity of
the heart includes at least one endocardial electrode disposed
within a chamber or a portion of vasculature of the heart.
20. A computer-readable medium according to claim 10, wherein
obtaining the second signal indicative of electrical activity of
the heart includes at least one externally mounted electrode
adapted to be coupled to a portion of epidermis of a subject.
Description
CROSS REFERENCE TO RELATED APPLICATION
[0001] This patent document relates to co-pending application filed
30 Aug. 2001 having serial number 09/945,179 issued 30 Aug. 2005 as
U.S. Pat. No. 6,937,899. This patent document relates to co-pending
application filed 30 Aug. No. 6,937,899; entitled, "Ischemia
Detection," the entire contents of which are hereby incorporated by
reference herein.
FIELD
[0002] The invention relates to cardiac health and, more
particularly, to techniques for detection of myocardial
ischemia.
BACKGROUND
[0003] Myocardial ischemia, a leading cause of mortality, involves
oxygen starvation of the myocardium. Myocardial ischemia can lead
to myocardial infarction if left untreated. Early detection of
myocardial ischemia provides the opportunity for a wide range of
effective therapies such as surgical revascularization, neural
stimulation, and drug delivery to reduce cardiac workload or
improve cardiac circulation. Unfortunately, many episodes of
myocardial ischemia do not cause excessive pain or other noticeable
warning signs, and often go undetected.
[0004] An electrocardiogram (ECG) or electrogram (EGM) presents a
PQRST waveform sequence that characterizes the cyclical cardiac
activity of a patient. The T-wave can be used to identify an
ischemic condition. U.S. Pat. No. 6,016,443 to Ekwall et al., for
example, describes an implantable ischemia detector that employs a
repolarization sensor and a patient workload sensor to identify
ischemic episodes. The repolarization sensor detects T-wave
amplitude or duration to identify increased heart rate. The
workload sensor detects patient activity such as exercise by
monitoring body movement, muscle sounds, fluid pressure waves, or
metabolic changes. When the T-wave indicates an increased heart
rate, without a corresponding increase in workload, the detector
identifies an ischemic condition.
[0005] The ST segment, also associated with the repolarization of
the ventricles, is typically close in amplitude to the baseline,
i.e., isoelectric amplitude, of the signal sensed between
consecutive PQRST sequences. During episodes of myocardial
ischemia, the ST segment amplitude deviates from the baseline.
Accordingly, deviation in the ST segment is often used to identify
an occurrence of myocardial ischemia.
[0006] U.S. Pat. No. 6,021,350 to Mathson, for example, describes
an implantable heart stimulator having an ischemia detector that
indicates an ischemic condition based on elevation of the
ST-segment above a baseline. Alternatively, the ischemia detector
may rely on a measure of heart activity or patient workload. The
stimulator controls the rate of stimulation based on the detection
of ischemia using either of the alternative detection modes.
[0007] Unfortunately, the use of the ST segment as an indicator of
ischemia can be unreliable. The ST segment may deviate from the
baseline due to other factors, causing false indications of
myocardial ischemia. For example, the ST segment may deviate from
the baseline due to changes in the overall PQRST complex, possibly
caused by axis shifts, electrical noise, cardiac pacing stimuli,
drugs and high sinus or tachycardia rates that distort the PQRST
complex. Consequently, the reliability of the ST segment as an
indicator of myocardial ischemia can be uncertain.
[0008] U.S. Pat. No. 6,128,526 to Stadler et al. describes an
ischemia detector that observes variation in the ST segment to
identify an ischemic condition. To improve reliability, the
detector is designed to filter out ST segment variations caused by
factors other than ischemia, such as axis shift, electrical noise,
cardiac pacing, and distortion in the overall PQRST complex.
[0009] Efforts to verify the reliability of the ST segment have
generally proven complicated. Accordingly, there continues to be a
need for a simplified system capable of automatically and reliably
detecting myocardial ischemia.
SUMMARY
[0010] The invention is directed to techniques for more reliable
detection and treatment of myocardial ischemia. In particular, the
invention correlates electrical activity and dynamic mechanical
activity of a heart to detect and verify the occurrence of
myocardial ischemia in a more reliable manner.
[0011] The electrical activity may be represented by the ST
segment. The dynamic mechanical activity may be represented by a
heart acceleration or pressure signal. Heart acceleration or
pressure provides an indication of heart contractility. The term
"contractility" generally refers to the ability of the heart to
contract, and may indicate a degree of contraction. Heart
contractility typically decreases during ischemic episodes.
[0012] Accordingly, the invention determines whether a change in
the ST segment is accompanied by a corresponding change in the
contractility of the heart. Correlation of changes in the
contractility of the heart with changes in the ST segment provides
a more reliable indication of ischemia, reducing the incidence of
false indications due to ST segment changes that are unrelated to
ischemic conditions.
[0013] Changes in the ST segment can be detected from an ECG, EGM,
or subcutaneous electrode array (SEA). Changes in the dynamic
mechanical activity of the heart can be obtained from an
accelerometer or pressure transducer. The accelerometer produces an
acceleration signal indicative of heart wall acceleration within a
chamber of the heart. The pressure transducer produces a pressure
signal indicative of right ventricular, left ventricular, or
arterial pressure, depending upon the location of the pressure
transducer.
[0014] For the ST segment, the electrical signal can be obtained
from a set of implanted or external electrodes. For dynamic heart
activity, an accelerometric signal can be obtained from an
accelerometer deployed within or near the heart. The accelerometer
transduces heart contractions into one or more accelerometric
signals. The pressure signal can be obtained from a pressure
transducer deployed within the heart or vasculature. Alternately,
the pressure sensor could be positioned around a blood vessel.
[0015] The accelerometer can be disposed at the distal tip of an
implanted lead that is deployed within a chamber of the heart. The
pressure transducer can be realized by a cardiac pressure lead. A
signal processing circuit can be used to detect drops in
contractility during myocardial ischemia by comparing the
accelerometric or pressure signal to a criterion such as a
predetermined threshold.
[0016] The invention correlates contractility changes derived from
signals generated by a lead tip accelerometer or cardiac pressure
lead with changes in the ST segment to increase the specificity of
ischemia detection. In particular, the utilization of a lead tip
accelerometer or pressure lead in conjunction with electrical
detection permits differentiation between ST segment changes
accompanied by changes in cardiac contractility and ST segment
changes without significant changes in cardiac contractility.
Changes in cardiac contractility derived from the accelerometer or
pressure lead provide another indication of ischemic conditions,
and confirm the indication provided by the ST segment.
[0017] In one embodiment, the invention provides a method for
detecting myocardial ischemia, the method comprising obtaining a
first signal indicative of dynamic mechanical activity of a heart,
obtaining a second signal indicative of electrical activity of the
heart, and detecting myocardial ischemia based on both the first
signal and the second signal. The invention also may provide
computer-readable media carrying instructions for performing the
method.
[0018] In another embodiment, the invention provides a system for
detecting myocardial ischemia, the system comprising a first sensor
that generates a first signal indicative of dynamic mechanical
activity of a heart, a second sensor that obtains a second signal
indicative of electrical activity of the heart, and a processor
that detects myocardial ischemia based on both the first signal and
the second signal.
[0019] In an added embodiment, the invention provides a method for
detecting myocardial ischemia, the method comprising obtaining a
first signal indicative of contractile activity of a heart,
obtaining a second signal indicative of electrical activity of the
heart, and detecting myocardial ischemia based on both the first
signal and the second signal. The invention also may provide
computer-readable media carrying instructions for performing the
method.
[0020] In a further embodiment, the invention provides a system for
detecting myocardial ischemia, the system comprising means for
generating a first signal indicative of contractile activity of a
heart, means for obtaining a second signal indicative of electrical
activity of the heart, and means for detecting myocardial ischemia
based on both the first signal and the second signal.
[0021] The invention is capable of providing a number of
advantages. For example, correlation of changes in heart
contractility with changes in the ST segment provide a more
reliable indication of an ischemic event. In this manner, the
invention is useful in increasing the specificity of ischemia
detection, generally avoiding false indication of ischemic events
due to axis shifts, electrical noise, cardiac pacing stimuli, high
sinus or tachycardia rates, or other factors that undermine the
effectiveness of a purely electrical detection technique. Also, the
invention is capable of improving sensitivity to ischemic episodes
by allowing the detection of ischemia when either the mechanical or
the electrical signals are indicative of ischemia.
[0022] In addition, the invention can be useful in quantifying a
degree of ischemic tissue according to a degree of cardiac
contractility and a degree of change in the ST segment. Moreover,
the combination of electrical and mechanical monitoring of heart
activity can aid in determining the location of ischemic tissue. In
particular, both the electrical and mechanical signals can be
monitored along multiple axes. The electrical signal may include
multiple electrical signals obtained from different lead sets,
whereas an accelerometer may be sensitive along two and perhaps
three axes. Likewise, multiple accelerometers or pressure sensors
can be used to achieve sensitivity along multiple axes.
[0023] The above summary of the invention is not intended to
describe every embodiment of the invention. The details of one or
more embodiments of the invention are set forth in the accompanying
drawings and the description below. Other features, objects, and
advantages of the invention will be apparent from the description
and drawings, and from the claims.
BRIEF DESCRIPTION OF DRAWINGS
[0024] FIG. 1 is a diagram illustrating an exemplary implantable
medical device in association with a heart.
[0025] FIG. 2 is a diagram illustrating another exemplary
implantable medical device in association with a heart.
[0026] FIG. 3 is a side view illustrating an implantable lead
suitable for incorporation of a lead-tip accelerometer.
[0027] FIG. 4 is a cross-sectional side view of the lead shown in
FIG. 3.
[0028] FIG. 5 is a block diagram illustrating a system for
detection of ischemia.
[0029] FIGS. 6A, 6B, and 6C are graphs illustrating the
relationship between electrical activity and heart acceleration
within a canine heart.
[0030] FIGS. 7A, 7B, and 7C are graphs illustrating the
relationship between electrical activity and heart acceleration
within a canine heart during an episode of ischemia.
[0031] FIG. 8 is another graph illustrating changes in heart
acceleration in the presence of ischemia.
[0032] FIG. 9 is a flow diagram illustrating a process for ischemia
detection.
[0033] FIG. 10 is a flow diagram illustrating another process for
ischemia detection.
[0034] FIG. 11 is a flow diagram illustrating a process for
ischemia detection in greater detail.
DETAILED DESCRIPTION
[0035] FIG. 1 is a diagram illustrating an implantable medical
device (IMD) 10 in association with a heart 34. IMD 10 may be
configured for both monitoring and therapy of heart 34. For
example, IMD 10 may include a pulse generator to deliver electrical
stimulation to heart 34 for use in cardioversion or defibrillation.
In accordance with the invention, IMD 10 obtains a signal
indicative of dynamic mechanical activity of heart 34, and an
electrical signal indicative of electrical activity of the
heart.
[0036] Using both signals, i.e., the electrical signal and the
signal indicative of dynamic mechanical activity, IMD 10 detects
the existence of myocardial ischemia within heart 34. When both
signals reveal ischemic conditions, IMD 10 indicates an ischemic
episode. The signal indicative of dynamic mechanical activity
corroborates the electrical signal.
[0037] If ischemia is detected, IMD 10 can be configured to deliver
appropriate therapy to alleviate its effects. The therapy may
include drug delivery, electrical stimulation, or both. In
addition, according to some embodiments, IMD 10 may determine the
location of ischemic tissue and the severity of the ischemic
condition, providing more specific information that may be useful
in selection of treatment.
[0038] IMD 10 may be generally flat and thin to permit subcutaneous
implantation within a human body, e.g., within upper thoracic
regions or the lower abdominal region. IMD 10 may include a
hermetically sealed housing 14 having a connector block assembly 12
that receives the proximal ends of one or more cardiac leads for
connection to circuitry enclosed within housing 14. In the example
of FIG. 1, connector block assembly 12 receives a ventricular
endocardial lead 28.
[0039] In some embodiments of the invention, ventricular
endocardial lead 28, or other leads, may include an accelerometer
to obtain a heart acceleration signal or a pressure transducer to
obtain a pressure signal. In other embodiments, a pressure signal
can be obtained from outside a blood vessel, e.g., with the use of
implantable blood vessel cuffs as described in U.S. Pat. Nos.
6,010,477 and 6,077,277 to Miesel et al.
[0040] Also, multiple accelerometers or pressure sensors can be
used to achieve sensitivity along multiple axes. For instance, if a
coronary artery providing oxygen to the left side of the heart is
occluded, there may be a decrease in accelerometer--or pressure
sensor-indicated contractility from a left-sided lead, but not
necessarily from a lead in the right ventricle. This may be
particularly the case for an accelerometer lead placed on the right
ventricular free wall, which is not mechanically coupled to the
left ventricle, as well as a lead placed on the ventricular septum.
Accordingly, multiple sensors may be desirable for enhanced
sensitivity.
[0041] An accelerometer will be generally described herein for
purposes of illustration. Ventricular endocardial lead 28 may be,
for example, a bipolar, two wire lead equipped to sense electrical
signals. An accelerometer can be incorporated adjacent a distal tip
30 of lead 28, and thereby deployed within heart 34. As will be
described, housing 14 may enclose circuitry for use in analyzing
the heart acceleration signal produced by the accelerometer, and
electrical signals such as ECGs or EGMs obtained by IMD 10 to
detect ischemia within heart 34.
[0042] To facilitate detection of electrical activity within heart
34, IMD 10 may include a plurality of EGM sense electrodes 16, 18,
20, 22, 24, 26. EGM sense electrodes 16, 18, 20, 22, 24, 26 may be
arranged substantially as described in U.S. Pat. No. 6,128,526, to
Stadler et al., entitled "METHOD FOR ISCHEMIA DETECTION AND
APPARATUS USING SAME," the entire content of which is incorporated
herein by reference. For example, electrodes 16, 18, 20, 22, 24, 26
may form a plurality of sense electrode pairs that are integrated
with the exterior of housing 12 of IMD 10.
[0043] The sense electrode pairs can be used to obtain electrical
signals along one or more sensing axes to formulate one or more EGM
signals. The EGM signal obtained via sense electrodes 16, 18, 20,
22, 24, 26, together with the heart acceleration signal provided by
an accelerometer or pressure transducer, can be used to detect
ischemia, as well as the degree of ischemia and the location of
ischemic tissue within heart 34. The accelerometer provides an
indication of the dynamic mechanical activity of the heart, which
either reinforces or negates an indication of ischemia derived from
a change in the electrical signal.
[0044] As an advantage, in addition to identification of ischemia,
the heart acceleration signal can be used to measure other events
in different frequency ranges. For example, the heart acceleration
signal may be monitored from 0 to 0.5 Hz for the patient's posture
or orientation, from 1 to 5 Hz for the patient's activity, e.g.,
exercise, and from 5 to 100 Hz for the patient's heart
acceleration. The frequency range for analysis of heart
acceleration is the range useful in identification of ischemia.
Thus, the accelerometer may serve multiple purposes. For example,
by analyzing the pertinent frequency bands, the accelerometer may
be used to detect patient activity, patent orientation, and heart
acceleration.
[0045] As further shown in FIG. 1, a programmer/output device 44
with an antenna 46 can be provided for wireless communication with
IMD 10. IMD 10 may include a telemetry circuit that transmits radio
frequency messages, which may include indications of ischemia and
other information to device 44. IMD 10 also may receive programming
information via the telemetry circuit for modification of
operational parameters within the IMD.
[0046] Device 44 also may include a display for graphic or textual
presentation of information transmitted by IMD 10, as well as a
visible or audible annunciator that provides an indication of the
detection of ischemia within heart 34. IMD 10 also may be equipped
with an alarm for notification of the patient in the event ischemia
is detected. Also, device 44 may include a user input device, such
as a keypad, by which a physician may modify operational parameters
for use in programming IMD 10 for diagnosis or treatment.
[0047] FIG. 2 is a diagram illustrating another IMD 48 in
association with a human heart 34. In particular, IMD 48 may be
configured to provide electrical stimuli to heart 34 for
defibrillation. IMD 48 may generally conform to the defibrillation
system described in the above-referenced U.S. Pat. No. 6,128,526.
In the example of FIG. 2, IMD 48 includes an outer housing 54 that
functions as an electrode, along with a set of electrodes 52, 56,
58 provided at various locations on the housing or connector block
50.
[0048] IMD 48 may include leads 60, 62 for deployment of
defibrillation coil electrodes 64, 70 within two chambers of heart
34. Leads 60, 62 may include additional electrodes, such as
electrodes 66, 68, 72, 74, for sensing of electrical activity
within heart 34. Electrodes 66, 68, 72, 74 may form electrode pairs
with respective electrodes 52, 56, 58 on IMD 48. As in the example
of FIG. 1, an accelerometer can be mounted in one of leads 60, 62
to obtain a heart acceleration signal for use in detecting
ischemia. In some embodiments, the heart acceleration signal may be
derived from left-sided leads deployed via the coronary sinus.
Also, a pressure sensor may be used in lieu of the accelerometer in
some embodiments.
[0049] FIG. 3 is a side view illustrating an implantable lead 76
equipped with a lead-tip accelerometer. Lead 76 may be configured
for use as a diagnostic lead, therapeutic lead, or both, and may be
incorporated with a variety of IMDs including those shown in FIGS.
1 and 2. For example, lead 76 may carry sense electrodes,
stimulation electrodes, or both. As shown in FIG. 3, lead 76 may
include a distal tip 78, a first section 80, and a second section
82. First and section sections 80, 82 include outer walls 81, 83,
respectively, formed of nonconductive, biocompatible material.
[0050] One or more sense or stimulation electrodes may be formed
along the longitudinal extent of outer walls 81, 83. Distal tip 78
may include an electrode 84, as well as a number of stabilizing
tines (not shown in FIG. 3) for securing distal tip member 78 in
cardiac tissue upon deployment. In addition, lead 76 may include
electrical conductors which may be coupled to electrode 84 and an
accelerometer assembly mounted within second section 82.
[0051] FIG. 4 is a cross-sectional side view of lead 76 shown in
FIG. 3. FIG. 4 shows first section 80, second section 82, distal
tip 78, electrode 84. Stabilizing tines or other anchoring
structure may be added to distal tip 78, if desired. In the example
of FIG. 4, lead 76 includes an accelerometer assembly 88 mounted
within second section 82 adjacent distal tip 78. Accelerometer
assembly 88 forms a capsule, and includes an accelerometer that may
be fabricated using microelectromechanical systems (MEMS)
technology, providing high tolerance and very small size.
Advantageously, accelerometer assembly 88 may be used in a bipolar
lead system, reducing accelerometer assembly size and increasing
reliability.
[0052] Lead 76 also includes conductors in the form of first and
second conductive coiled conductors 90, 92, which are arranged
coaxially along the length of the lead. Coiled conductors 90, 92
may be coupled to distal electrode 84 and accelerometer assembly 88
to carry electrical current to and from the electrode and
accelerometer assembly to a proximal end of the lead, which may be
coupled to an IMD. For example, inner coiled conductor 90 may be
coupled to interior components of accelerometer assembly 88 via a
feedthrough assembly 86. Outer coiled conductor 92 may be coupled
to the exterior housing of accelerometer assembly 88, which is
electrically conductive and may be formed from titanium, and to
electrode 84. The accelerometer signal may be produced between
conductors 90, 92 via an internal accelerometer connection and the
exterior housing connecting, respectively. The signal from
electrode 84 may be produced between conductor 92 and an electrode
on the IMD housing or "can." Distal tip 78, first section 80, and
second section 82 are crimped together at crimp points indicated
generally by reference numerals 94, 96, 98. An adhesive material 99
fills the void within feedthrough assembly 86.
[0053] The heart acceleration signal varies as a function of the
contractile force of heart 34. The contractile force is transduced
by accelerometer assembly 88 to produce an electrical heart
acceleration signal that represents the contractility of the heart
and, more generally, the dynamic mechanical activity of the heart.
The contractile force of heart 34 physically deforms the
accelerometer in assembly 88 to change its electrical properties,
and modulate the current passing through the accelerometer. Again,
an indication of heart contractility can be obtained alternatively
using a pressure transducer.
[0054] Accelerometer assembly 88 can make use of conventional
accelerometer technology and may take the form of a piezoelectric,
piezoresistive, capacitive, inductive, or magnetic sensor that
produces a change in an electrical property with changes in
accelerometric force within heart 34. The changes in the electrical
property, e.g., resistance, capacitance, inductance, and the like,
in turn produces changes in the electrical signal produced by
accelerometer assembly 88.
[0055] In the example of FIG. 4, accelerometer assembly 88 is
mounted at the tip or distal end of lead 76. Accelerometer assembly
88 could be mounted elsewhere within lead 76, however, provided it
can be properly positioned and oriented to detect accelerometric
force produced by the contractile activity of heart 34. In some
embodiments, accelerometer assembly 88 may be formed to have either
one, two, or three detection axes. In other words, accelerometer
assembly 88 may be configured to detect accelerometric force
extending in multiple directions as a result of the contractile
force generated by different walls within heart 34.
[0056] In this case, accelerometer assembly 88 may be equipped with
a multi-axis accelerometer or multiple accelerometers oriented
orthogonally in relation to the respective axes, as well as
multiple conductors for obtaining the heart acceleration signal as
output from each respective accelerometer. As one example,
accelerometer assembly 88 could include a single conductor line
that carries current to multiple accelerometers, and two or more
additional conductor lines that return current from each of the
accelerometers to provide separate heart acceleration signal
outputs for the different axes. Alternatively, each accelerometer
may be coupled to the same conductor lines, and produce signals
that are time-multiplexed to distinguish the output of each
accelerometer.
[0057] Detection of heart acceleration along multiple axes may be
useful in determining the location of ischemic tissue. If the heart
acceleration signal along one axis is "normal," i.e., not
indicative of ischemia, whereas the heart acceleration signal along
another axis indicates a possible episode of ischemia, the location
of the ischemic tissue can be determined according to the
orientation of the axis along which the pertinent accelerometer is
aligned.
[0058] In this manner, the ischemic condition can be treated, by
intervention of a physician or in an automated manner, and targeted
to an appropriate region of heart 34. For example, based on the
location of the ischemic tissue, electrical stimulation can be
delivered to a selected stimulation electrode best suited for
treatment of the affected location.
[0059] In addition, the amplitude, frequency, or pulse width of
stimulating current can be controlled according to the affected
location to achieve an optimum therapeutic effect. As a further
alternative, determination of the location of ischemic tissue can
be used to choose other types of therapy such as drug delivery, as
well as types, dosages and durations of drug delivery. Also, the
location information can be compared to location information
recorded in the past to determine whether the ischemia is occurring
in a new location or a location of prior ischemic episodes.
[0060] FIG. 5 is a block diagram illustrating a system 100 for
detection of ischemia. As shown in FIG. 5, system 100 may include a
lead selector circuit 102 that selects one or more lead pairs 104,
a signal processor circuit 106, an accelerometer 108, a processor
110, memory 112, a therapy control circuit 112, a therapy delivery
system 114, and a telemetry device 116 with an antenna 118. Lead
selector circuit 102 may be controlled by processor 110, and select
lead pairs for acquisition of electrical signals oriented along
multiple detection axes relative to heart 34.
[0061] Processor 110 may take the form of a microprocessor,
microcontroller, digital signal processor (DSP) or other
programmable logic device. The electrical signals obtained via the
lead pairs can be used to formulate an ECG or EGM for analysis of
the PQRST complex and, in particular, the ST segment. Changes in
the ST segment can be an indicator of ischemia. Analysis of the
dynamic mechanical activity of the heart in combination with
changes in the ST segment, according to the invention, can provide
a more reliable indication of ischemia.
[0062] Signal processor circuit 106 receives the output of lead
selector circuit 102 and a heart acceleration signal from an
accelerometer 108, which may be deployed in a lead tip as described
with reference to FIGS. 3 and 4. In other embodiments, signal
processor circuit 106 may receive a pressure signal from a pressure
transducer. The output of lead selector circuit 102 may be three
electrode pair signals, such as RV coil-can, RV ring-can, and SVC
coil-can. In some embodiments, as discussed above, accelerometer
108 may produce multiple heart acceleration signals oriented along
similar detection axes. Signal processor circuit 106 may include a
number of sense amplifiers that amplify the ECG or EGM signals, as
well as the heart acceleration signal.
[0063] In addition, signal processor circuit 106 may include
sampling and comparator circuitry for analysis of the electrical
signals and heart acceleration signals relative to criteria such as
average, peak-to-peak, or total amplitude thresholds.
Alternatively, processor 110 may digitally sample the signals
amplified by signal processor circuit 106 and perform a
software-based analysis of the digital signals. Thus, signal
processor circuit 106 may include an analog-to-digital converter
that converts the analog signals produced by lead selector circuit
102 and accelerometer 108 into digital samples for analysis by
processor 110. Processor 110 may provide the necessary control and
clock signals for operation of signal processor circuit 106.
[0064] A memory 112 is provided for storage of digital samples
produced by signal processor circuit 106 and intermediate data
stored and retrieved by processor 110. For example, signal
processor circuit 106 may include a number of buffers that hold
digital samples for storage in memory. Although not illustrated in
FIG. 5 for simplicity, processor 110, memory 112, and signal
processor 106 may communicate via a common data and instruction
bus, as is well known in the art. The digital samples may be
parameterized, in signal processor circuit 106 or processor 110, to
produce values for comparison to a predetermined threshold. Again,
the comparison may take place within discrete circuitry provided by
signal processor circuit 106 or via code executed by processor 110.
The code may include instructions carried by a computer-readable
medium accessible by processor 110, such as memory 112 or other
fixed or removable media devices associated with an external
programmer/output device communicatively coupled to the processor
via telemetry device 116.
[0065] ECG, EGM, SEA or other electrical signals produced by lead
selector circuit 102 can be processed and parameterized to
represent a variety of different values useful in the comparison.
In one embodiment, the electrical signals may be processed to
produce an amplitude value, such as an average, peak-to-peak, or
total amplitude, for the ST segment of the PQRST complex. The ST
segment is typically close in amplitude to the baseline of the ECG
or EGM signal sensed between consecutive PQRST sequences. During
episodes of myocardial ischemia, however, the ST segment amplitude
may increase or decrease substantially. Thus, by comparing the
amplitude of the ST segment to an amplitude threshold, processor
110 can identify a potential episode of ischemia.
[0066] In addition, processor 110 may be configured to detect a
location of the ischemic condition based on which one of the lead
pairs produces an ST segment excursion above the amplitude
threshold. In some embodiments, the location may be correlated with
one of several acceleration signals obtained from accelerometer 108
for different sensing axes.
[0067] An average amplitude may be obtained and represented in a
number of ways such as by computing the average of a series of
samples over the period of time coincident with the ST segment. A
peak-to-peak amplitude for each signal can be obtained by detection
of maxima and minima of the ST segment and detection of maxima and
minima of a heart acceleration signal over a duration of time that
generally coincides with the ST segment. A total amplitude for each
signal can be obtained by integrating the ST segment and
integrating the acceleration signal over a duration of time that
generally coincides with the ST segment. Also, because the change
in the ST segment may be elevated or depressed during an ischemic
episode, the ST segment parameter may rely on the absolute value of
the change in the ST segment.
[0068] Because the use of the ST segment as an indicator of
ischemia can be unreliable, processor 110 (and/or signal processor
circuit 106) is also configured to analyze the heart acceleration
signal produced by accelerometer 108. In particular, processor 110
compares a parameterized value representative of the heart
acceleration signal, such as an average amplitude or integrated
amplitude, at a time substantially coincident with the ST segment
to a pertinent threshold. In this manner, system 100 is capable of
correlating the ST segment and the heart acceleration signal for
more reliable detection of ischemia.
[0069] By verifying whether the heart acceleration signal (or
alternatively a pressure signal) also indicates ischemia, processor
110 is able to disregard deviations in the ST segments due to
conditions other than ischemia, e.g., due to changes in the overall
PQRST complex caused by axis shifts, electrical noise, cardiac
pacing stimuli, drugs, and high sinus or tachycardia rates that
distort the PQRST complex. Consequently, system 100 is capable of
reducing the number of false indications of ischemia, and
increasing the reliability of the ST segment as an indicator of
myocardial ischemia.
[0070] Based on deviation of the ST segment and the heart
acceleration signal relative to the pertinent thresholds, processor
110 also may quantify the severity of the ischemic condition. If
the ST segment and the heart acceleration signal both satisfy the
pertinent thresholds, processor 110 indicates an ischemic event,
and may be programmed to effect therapeutic action. For example,
processor 110 may generate a therapy control signal that causes a
therapy control circuit 112 to request delivery of therapy from a
therapy delivery system 114. Therapy delivery system 114 may take,
for example, the form of a drug delivery system or electrical
stimulation system such as a cardioversion or defibrillation
circuit.
[0071] Processor 110 also may indicate to therapy control circuit
112 the location of the ischemic tissue and the severity of the
ischemic condition based on the accelerometer signal. Accordingly,
therapy control circuit 112 may be configured to control therapy
delivery system 114 based on the indications provided by processor
110. For example, therapy control circuit 112 may select the type
of therapy, e.g., drug delivery and/or electrical stimulation, the
dosage, amplitude, and duration of the therapy, as well as the
location for delivery of the therapy, based on the indications of
location and severity provided by processor 110.
[0072] Processor 110 also may control a telemetry device 116 to
communicate an indication of the ischemic condition to an external
device via antenna 118. Thus, the indication may be a wireless,
radio frequency message that indicates an ischemic condition and,
in some embodiments, the location of the ischemic tissue and the
severity of the ischemic condition. In addition, the IMD itself may
have an audible alarm that notifies the patient when an ischemic
episode is occurring.
[0073] The external device, which may be a programmer/output
device, advises a physician or other attendant of the ischemic
condition, e.g., via a display or a visible or audible alarm. Also,
the ischemic events may be stored in memory in the external device,
or within the IMD, for review by a physician. The components of
system 100, with the exception of accelerometer 108 and leads 104,
may be housed in a common housing such as those shown in FIGS. 1
and 2. Alternatively, portions of system 100 may be housed
separately. For example, therapy delivery system 114 could be
provided in a separate housing, particularly where the therapy
delivery system includes drug delivery capabilities. In this case,
therapy control circuit 112 may interact with therapy delivery
system 114 via an electrical cable or wireless link.
[0074] FIGS. 6A, 6B, and 6C are graphs illustrating an example
relationship between electrical activity and heart acceleration
within a canine heart. In particular, FIG. 6A shows an ECG signal,
including the R-wave peak, ST segment and T-wave over a period of
time. FIG. 6B shows the output of a pressure sensor positioned
within the left ventricle, e.g., in a lead deployed within the
ventricle, over the same period of time. FIG. 6C shows the output
of an accelerometer positioned within the right ventricle, e.g., at
the tip of a lead deployed within the ventricle, also over the same
period of time.
[0075] The heart acceleration signal is characterized by a section
120 that generally coincides in time with the ST segment of the ECG
signal. Similarly, the pressure signal has a section 121 that
coincides with the ST segment. In this example, sections 120, 121
are characterized by a momentary positive excursion followed by a
negative excursion, which correspond to the contractile forces of
the left ventricle. The increase in pressure is due to the pressure
developed during contraction. The pressure drops during relaxation.
For the acceleration signal, the increase is due to the heart's
acceleration or vibration during contraction, with the acceleration
signal occurring during the same time as the maximum slope of the
pressure signal (DP/DT). A second acceleration signal, typically of
a lower amplitude than the first acceleration signal and
corresponding to the maximum negative DP/DT, also can be seen. The
waveforms may vary significantly, however, depending on the
location of the lead, the accelerometer sensitivity axis, and other
factors.
[0076] FIGS. 6A and 6C also illustrate example amplitude thresholds
T1 and T2. The thresholds may be used in analysis of the ST segment
amplitude and heart acceleration signal amplitude, respectively. A
similar threshold can be used for the pressure signal. The
thresholds may reflect an average amplitude over the duration of
the ST segment or a peak-to-peak amplitude. As an alternative,
total amplitudes obtained, e.g., by integration of the heart
acceleration signal, could be used for comparison to total
amplitude thresholds. In the example of FIGS. 6A-6C, thresholds T1
and T2 represent peak-to-peak amplitude thresholds for comparison
to the maxima and minima of the ST segment and heart acceleration
signal, respectively.
[0077] FIGS. 7A, 7B, and 7C are graphs illustrating an example
relationship between electrical activity and heart acceleration
within a canine heart during an episode of ischemia. As shown in
FIG. 7A, the ST segment of an ECG or EGM signal may show a
significant increase when the heart tissue becomes ischemic. In
comparison to FIG. 6A, for example, the amplitude of the ST segment
in FIG. 7A is markedly increased, and exceeds the threshold T1,
which may be specified by a physician for identification of
ischemic conditions. In FIG. 7B, the amplitude of the pressure
signal is decreased relative to that shown in FIG. 6B.
[0078] As shown in FIG. 7C, the heart acceleration signal also
shows the effects of ischemia. Specifically, in a case of ischemia,
the section 120 of the heart acceleration signal that coincides
with the ST segment is markedly decreased in amplitude relative to
FIG. 6C. In this example, section 120 has a peak-to-peak amplitude
that is less than the threshold T2. Thus, when the amplitude of the
ST segment exceeds threshold T1 and the amplitude of the heart
acceleration signal drops below threshold T2, an episode of
ischemia can be more reliably indicated in accordance with the
invention.
[0079] Again, the amplitudes of the ST segment and heart
acceleration signal, as well as the thresholds T1 and T2, may be
peak-to-peak, average, or total amplitudes, or any other parameter
deemed reliable in detection of ischemia. The basic technique
simply involves analysis of both the ST segment and the heart
acceleration signal in a correlative manner to reduce the
possibility that changes in the ST segment are due to factors other
than ischemia. This enables a reduction in the number of false
indications.
[0080] FIG. 8 is another graph illustrating changes in heart
acceleration in the presence of ischemia. In particular, FIG. 8
illustrates changes in the heart acceleration signal 122 during an
experiment in which ischemia is induced in a canine heart. The left
axis of the graph shows the accelerometer peak-to-peak signal,
measured in gravitational gs. The bottom axis shows the progression
of time. The right axis shows an ischemia parameter 124. The
ischemia parameter 124 can be derived from, for example, an
electrical signal such as the ST segment of an ECG or EGM signal.
In particular, ischemia parameter 124 may represent the ST segment
change as a percentage of the R-wave amplitude.
[0081] As shown in FIG. 8, following a dobutamine infusion 123, the
heart acceleration signal 122 peaks sharply, as the dobutamine
induces a forceful contraction in the heart. Later, the heart is
subjected to balloon occlusion to intentionally limit the flow of
blood, and thereby induce ischemia. At that time, the ischemia
parameter peaks sharply, as indicated by reference numeral 125,
whereas the heart acceleration signal 122 drops noticeably, as
indicated by reference numeral 128. When the balloon occlusion is
again applied, as indicated by reference numeral 126, the heart
acceleration signal 122 again drops while the ischemia parameter
peaks. The vertical dashed lines in FIG. 8 denote the duration of
the dobutamine infusion, first balloon occlusion, and second
balloon occlusion.
[0082] FIG. 9 is a flow diagram illustrating a process for ischemia
detection. In general, the process may include obtaining an
electrical signal such as an ECG or EGM signal (130) and applying a
first criterion to the signal (132). For example, the first
criterion may be an amplitude threshold that is compared to an
amplitude parameter of the electrical signal, such as an average,
peak-to-peak or total amplitude of the ST segment of the electrical
signal. If the first criterion is not satisfied, the process
returns to evaluation of the electrical signal (130).
[0083] If the first criterion is satisfied (134), the technique
involves obtaining an accelerometer signal, i.e., a heart
acceleration signal (136), and applying a second criterion to the
accelerometer signal (138). The second criterion, like the first
criterion, may be an amplitude threshold that is compared to an
amplitude parameter of the heart acceleration signal, such as an
average, peak-to-peak, or total amplitude in a region that
temporally coincides with the ST segment of the electrical
signal.
[0084] If the second criterion is not satisfied, the process
returns to evaluation of the electrical signal (130). If the second
criterion is satisfied (140), however, the process indicates an
ischemic episode (142). In some embodiments, the process may
respond to an indication of ischemia by delivering therapy to the
patient (144). For example, the process may involve drug delivery
or electrical stimulation. The drug delivery and electrical
stimulation may be delivered by an implantable medical device,
including one that is integrated with ischemia detection circuitry.
Alternatively, drug delivery and electrical stimulation may be
administered to the patient externally.
[0085] FIG. 10 is a flow diagram illustrating another process for
ischemia detection. The process of FIG. 10 is similar to that of
FIG. 9, but illustrates the acquisition of multiple electrical
signals for different axes to facilitate determination of the
location of ischemic tissue. In particular, the process may involve
obtaining multiple ECG signals (144), applying a first criterion to
the signals (146), and determining whether the criterion is
satisfied for any of the signals (148). If so, the process
identifies the electrical signals that satisfy the criterion (150),
and then obtains the accelerometer signal (152).
[0086] Upon application of a second criterion to the accelerometer
signal (154), and satisfaction of that criterion (156), the process
indicates an episode of ischemia along with an indication of the
location of ischemic tissue based on which of the electrical
signals satisfied the first criterion (158), i.e., which of the
electrical signals showed a change in the ST segment indicative of
ischemia. On this basis, the process may further involve delivery
of therapy (160) and, in some embodiments, delivery of therapy to a
particular location within the heart, or in a form selected for a
particular location.
[0087] Determination of the location of ischemic tissue within the
heart also can be aided by obtaining multiple heart acceleration
signals along multiple axes. Like the electrical signals, the heart
acceleration signals may indicate ischemia along one axis but not
necessarily the others, enabling isolation of more specific region
of ischemia within the heart. As with the electrical signals, this
may aid in selection of the type, level, and focus of the therapy
delivered to the patient.
[0088] FIG. 11 is a flow diagram illustrating a process for
ischemia detection in greater detail. As shown in FIG. 11, the
process may involve analysis of an electrical signal such as an ECG
or EGM signal to identify the ST segment (162). The ST segment may
be parameterized (164), e.g., as a peak-to-peak amplitude, average
amplitude, or total amplitude, and compared to an amplitude
threshold T1 (166). If the ST segment amplitude exceeds the
threshold T1, there is a potential ischemic condition.
[0089] To more reliably confirm the ischemia, the process involves
obtaining an accelerometer signal (168), parameterizing the
accelerometer signal (170), and comparing it to an amplitude
threshold T2 (172). If the accelerometer signal amplitude drops
below the threshold T2 (172), a contractility change is confirmed
in addition to the increase in the ST segment, providing a more
reliable indication of ischemia. On this basis, the process
indicates an ischemic condition (174) and may use the indication as
the basis for delivery of therapy (176) to the patient.
[0090] Amplitude thresholds are described herein for purposes of
example, and are not to be read as limiting of the invention as
broadly claimed. Other signal parameters may be appropriate for
evaluation in identifying ischemia. Also, it is noted that
exceeding a given threshold may refer to a change that results in
an increase above or below a certain level, for example, as
described with reference to the graphs of FIGS. 6, 7, and 8.
Specifically, in some cases, ischemia may be indicated by an
increase in the ST segment amplitude and a decrease in the heart
acceleration signal at the time of the ST segment. Also, in some
embodiments, the electrical and acceleration signals could be
combined into a single parameterized value that is compared to a
single threshold value to determine whether an ischemic episode is
indicated.
[0091] The use of a signal indicative of dynamic mechanical heart
activity to confirm an episode of ischemia indicated by the ST
segment of an electrical signal can provide a number of advantages
including more reliable indication of ischemia, avoidance of false
indications and unnecessary administration of treatment. In
addition, the heart acceleration signal may be useful, alone or in
combination with the electrical signal, in more reliably
quantifying the contractile function of the heart, and hence the
degree of ischemia, providing a standard for the type or amount of
therapy delivered to the patient.
[0092] In addition, a multi-dimensional heart acceleration signal,
alone or in combination with the electrical signal, can be used to
better identify the location of ischemic tissue. In effect, the use
of a multi-axial accelerometer in a lead tip can detect axis shift
due to postural changes and add sensitivity to the ischemia
detection. The multi-axial accelerometer signals can be combined in
a logical OR fashion to increase sensitivity to ischemia, or
combined in a logical AND fashion to increase specificity, i.e., in
terms of the location of the ischemic tissue. In addition, relative
changes in the orthogonal accelerometer signals can be used to more
narrowly identify the location of ischemic tissue.
[0093] Various embodiments of the invention have been described.
Alternative embodiments are conceivable. Rather than an
accelerometer, for example, other sensors such as the pressure
transducer described herein may be employed to obtain a signal
indicative of cardiac contractility. Additionally, the maximum
value of the first derivative of the pressure signal, often called
the maximum DP/DT, can be used to assess the cardiac contractility
and be used a signal indicative of ischemia. In particular, a blood
pressure or velocity transducer may provide a signal useful in
deriving a measure of cardiac contractility. These and other
embodiments are within the scope of the following claims.
* * * * *