Download Myocardial Mural Thickness During the Cardiac Cycle

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Cardiac contractility modulation wikipedia , lookup

Electrocardiography wikipedia , lookup

Heart failure wikipedia , lookup

Coronary artery disease wikipedia , lookup

Cardiac surgery wikipedia , lookup

Hypertrophic cardiomyopathy wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Transcript
Myocardial Mural Thickness During
the Cardiac Cycle
By Eric O. Feigl, M.D., and Donald L. Fry, M.D.
Downloaded from http://circres.ahajournals.org/ by guest on April 30, 2017
•
An understanding of the relationship between forces and velocities of contraction in
muscle fibers to the pressures and flows generated by the intact myocardium requires
detailed information such as fiber orientation,
wall curvature, sequence of contraction, and
wall thickness. It was the purpose of this
study to measure instantaneous myocardial
thickness throughout the cardiac cycle, and,
when possible, relate it to the simultaneous
tangential strain occurring on the surface of
the heart.
Methods
A transducer has been devised to measure the
change in thickness of the myocardial wall during
the cardiac cycle, and is illustrated in figure 1. A
slender stainless steel shaft, A, is fitted with a harpoon-like toggle end piece, B. The shaft with the
toggle folded flat against it can be inserted
through the myocardium. When the shaft is
pushed through the heart wall, the toggle piece
unfolds inside the heart, forming a catch so that
the shaft cannot be withdrawn. The shaft moves
through a small base plate, C, which has a guiding
sleeve that keeps the shaft aligned. The toggle
piece is held against the inside of the heart by a
light compression spring which works between the
base plate and an adjustable stop, D. The to-andfro motions of the shaft with respect to the base
plate are sensed by the flexure of a brass shim, E,
which has one end fixed to the base plate and
the other to the stop on the shaft. Two etched foil
strain gauges are mounted on the brass shim and
form two arms of a resistance bridge. The changes
in the bridge resistance which result from motions
of the shaft are sensed and suitably amplified with
a standard carrier amplifier. The transducer is
attached to the epicardium with shallow sutures
threaded through the holes in the base plate. At
the end of the experiment the instrument must be
cut out of the heart muscle.
From the Section of Clinical Biophysics, Cardiology
Branch, National Heart Institute, U. S. Public Health
Service.
Received for publication November 29, 1963.
Circulation Research, Volume XIV, June 1964
The transducer was calibrated following each
run with a small test stand, utilizing a micrometer
to move the shaft known distances. The instrument was essentially linear through the ranges encountered. A static calibration curve is shown on
the left of figure 2. The dynamic amplitude vs.
frequency response of the transducer is shown
on the right of figure 2.
Large dogs were anesthetized with chloralose
(60 mgAg) and urethane (600 mg/kg) after
morphine (2 mg/kg) preanesthetic. The left aspect of the heart was exposed with a sternal splitting incision and partial resection of four to six left
ribs. Aortic arch pressure was recorded through
a catheter inserted via the left subclavian artery.
Left ventricular pressure was recorded with a
cannula through an apical myocardial puncture.
Pressures were measured with Statham P23d manometers. Instantaneous flow was measured at the
root of the aorta just above the valves with a 400
cycles/sec gated sine wave electromagnetic flowmeter. Recording was done on a Sanborn 350
oscillograph.
FIGURE 1
Myocardial wall thickness transducer. See text for
description of its operation.
541
542
FEIGL, FRY
The thickness gauge was inserted through the
myocardium of the left ventricle midway between apex and base, either to the left or right of
the anterior papillary muscle, as verified postmortem.
Changes in the size of the left ventricle were
estimated by continuously measuring the length of
an arc of the epicardial surface. Frequently two arc
lengths were recorded, one arc in the longitudinal
direction, that is from base to apex, and the other
at right angles to this in the transverse direction.
The arc lengths were measured with electrical
i
1
Static calibration of
- thickness gauge
i
i
>
20
30
Dynamic characteristics of
thickness gauge
105-
us 100
o
y 95fDownloaded from http://circres.ahajournals.org/ by guest on April 30, 2017
i
2
4
6
CHANGE IN THICKNESS mm
1
2
i
5
10
FREQUENCY -CPS
FIGURE 2
Static calibration and dynamic amplitude vs. frequency response curves for the thickness
transducer.
Myocardial Mural Thickness and Strain
Dog
no.
Body
weight
Minimum
diastolic
thickness
Thickness
beginning
of ejection
TABLE 1
Maximum
systolic
thickness
Ejection
thickness
strain
Ejection
transverse
arc strain
Ejection
longitudinal
arc strain
+.053
+.063
+.164
+.225
+ .110
+.088
+.130
+ .066
+.038
+ .113
+.1049
-.057
-.013
-.009
+ .156
+ .076
+.154
+ .194
+.123
+.183
+.185
+.107
+.144
+.176
+ .1498
Control
kg
I
2
3
4
5
6
7
8
9
10
Mean
28.2
32.7
25.9
24.5
31.4
24.1
22.7
29.5
18.2
15.9
25.31
mm
mm
8.97
9.40
7.98
7.24
8.05
7.90
8.47
8.35
7.50
9.92
8.378
9.41
10.72
8.78
7.87
8.88
8.44
8.89
10.60
8.62
11.02
9.323
mm
9.91
11.40
10.22
9.64
9.86
9.18
10.04
11.30
8.95
12.26
10.276
-.038
-.055
-.085
-.036
-.080
-.007
-.008
-.035
-.072
-.044
-.0376
-.0460
-.066
-.046
+ .020
During norepinephrine
1
2
3
4
5
6
7
8
9
10
Mean
28.2
32.7
25.9
24.5
31.4
24.1
22.7
29.5
18.2
15.9
25.31
8.72
9.19
7.98
7.97
8.54
7.40
8.23
8.29
6.14
9.79
8.225
9.22
11.77
9.34
10.78
9.58
8.32
9.50
11.43
7.82
11.48
9.924
10.66
12.66
10.78
12.87
10.76
9.84
11.26
12.65
8.95
13.50
11.393
-.017
-.076
-.127
+.028
-.104
-.021
-.020
-.031
-.071
-.123
-.0533
-.0468
Circulation Research, Volume XIV, June 1964
MYOCARDIAL MURAL THICKNESS
543
LEFT VENT. PRESSURE mmHg
150 —
0 AORTIC PRESSURE mmHg
80AORTIC
ROOT
FLOW
Downloaded from http://circres.ahajournals.org/ by guest on April 30, 2017
10.0-
9.0-,
8.0TRANSVERSE ARC LENGTH mm
16.25LONGITUDINAL
21.0
ARC LENGTH mm
20.520.0I sec
•
FIGURE 3
Simultaneous records of pressures, flow, myocardial wall thickness, and two perpendicular arc
lengths on the epicardial surface. Vertical bars on the thickness record indicate ejection period
as judged from the flow record.
calipers sewn to the surface of the heart. The
caliper has been described in detail previously.1
An effort was made to place the calipers close to
the point where the thickness gauge was inserted,
but this was not always possible since it was
necessary to avoid the coronary vessels on the surface of the heart.
After thickness and surface strain determinaCirculalion Research, Volume XIV, June 1964
tions were made in a control state an intravenous
infusion of norepinephrine (approximately 0.001
mg/kg per minute) was given to raise the arterial
pressure 10 to 20 mm Hg and the measurements
were repeated.
Strains were calculated with respect to the
initial dimension at the beginning of ejection. That
is, the value at the beginning of ejection was sub-
544
FEIGL, FRY
tracted from the value at the end of ejection and
the resulting difference divided by the value at
the beginning of ejection. Thus a positive strain
indicates an increase in size during ejection, a
negative strain a decrease. The ejection period
was determined from the aortic root flow record.
Results
Downloaded from http://circres.ahajournals.org/ by guest on April 30, 2017
A representative record of mural thickness
is shown in figure 3. The change in thickness
of the heart wall during the cardiac cycle has
a characteristic pattern. A sharp increase in
thickness at the beginning of systole during
the "isovolumic" phase was regularly observed. With the onset of ejection a somewhat
slower increase in thickness was observed.
Thickness became fairly constant in the later
portion of ejection and often remained so for
a brief period after the aortic valves had
closed. The wall became thinner during diastole, usually thinning in a smooth manner.
Successful determinations were made in ten
animals. The data are summarized in table 1.
The table lists the dogs with their weights
and is divided into two similar parts: control
and norepinephrine. The minimum diastolic
and maximum systolic wall thicknesses during
a cardiac cycle are given in millimeters. Also
the strains during the ejection period are given for thickness, as well as longitudinal and
transverse arcs. Under control conditions the
average increase in wall thickness from diastole to the beginning of ejection in ten
animals was + 0.113. The average control
thickness strain during ejection was -f- 0.105.
The average of seven transverse surface
strains during the same ejection period was
— 0.038. The average of six longitudinal strains
during ejection was — 0.046.
With a norepinephrine infusion the change
in thickness during ejection changed to an
average strain of + 0.150 in the same animals.
The average transverse arc strain was — 0.053
in seven animals with norepinephrine. The
average longitudinal arc strain in six animals
was — 0.047 with norepinephrine.
Discussion
The toggle piece in the transducer used was
held against the endocardium by a light com-
pression spring. The turgor of the myocardium
is less during diastole than systole which
means that the toggle could indent the muscle
more during diastole than during systole when
it became stiffer. This effect would tend to
exaggerate the change in thickness observed
between diastole and systole. It was not possible to determine the magnitude of this error,
but it was estimated to be small since special
care was used to keep the spring tension as
light as possible. The change in turgor of the
myocardium during the ejection phase of systole is probably not very great so that the
measurements made in this period and the
strains calculated would be less subject to this
type of error.
Since muscle is predominately composed of
water it would be expected that little volume
change would accompany contraction. The
volume change that skeletal muscle undergoes
during contraction has been shown to be extremely small, less than one hundredth of one
per cent.2 It is unlikely that the changes in
thickness observed were influenced by
changes in volume of the cardiac muscle.
If muscle tissue is incompressible, then the
sum of infinitesimal strains in three mutually
perpendicular directions at a point will be
zero. However, when strains are estimated in
a curved object such as the heart and finite
dimensions and finite strains are measured,
this is only approximately true. For a given
stroke volume, the endocardial surface must
undergo a greater strain than the epicardial
surface. Since the change in thickness represents the strain integrated across the entire
wall, the strain estimated from the change in
thickness will be greater than the sum of the
tangential strains on the epicardial surface.
Although the data manifest considerable scatter, inspection of table 1 shows that the sum
of the transverse and longitudinal epicardial
strains with ejection was on the average somewhat smaller than the mean radial strain computed from change in thickness. These comparisons lend support to the values observed
and indicate that the thickness measurements
were probably of the correct order of magnitude.
Circulation Research, Volume XIV, June 1964
MYOCARDIAL MURAL THICKNESS
Downloaded from http://circres.ahajournals.org/ by guest on April 30, 2017
It was not possible with this transducer to
measure thickness changes of the ventricular
wall where the ventricle has a short radius of
curvature, as at the apex or close to the aortic
ring. It can only be assumed that these measurements, made midway between apex and
base, are representative of the left ventricle
generally.
The average of ten dogs showed an increase
in wall thickness of over 10% between diastole
and the beginning of ejection and a further
increase of 10% during ejection. These values
increased by about half again when norepinephrine was given. When tension (force per
unit area) is to be calculated for the heart
wall the changes in thickness during the cardiac cycle should be kept in mind. Moreover,
myocardial force gauges which are sutured to
the outer surface of the heart register forces
which may be altered in a complex manner
by changes in thickness.
545
ness increased an additional 10% during the
ejection period of systole. These average values increased to 20% and 15% respectively with
the administration of norepinephrine (approximately 0.001 mg/kg per minute).
Transverse and longitudinal epicardial arc
strains were compared with thickness strain of
the myocardium. Assuming the myocardium is
incompressible, reasonable agreement was
found in the three strains, which lends support to the measurements that were made.
It is concluded that changes in the thickness
of the myocardial wall during the cardiac
cycle may be important in some considerations
of the heart's performance.
Acknowledgment
We thank Mr. Raymond P. Kelly for expert help
in designing and fabricating the transducer used in
this study. We also thank Mr. Joseph M. Pearce for
his careful technical assistance.
Summary
References
The instantaneous and continuous thickness
of the left ventricular wall was measured in
ten dogs with a specially designed transducer.
The thickness change during the "isovolumic"
phase of systole was 11%. The average thick-
1. MALLOS, A. J.: An electrical caliper for continuous measurement of relative displacement.
J. Appl. Physiol. 17: 131, 1962.
Circulation Research, Volume XIV, June 1964
2. ABBOTT, B. C ,
AND BASKIN, R. J.:
Volume
changes in frog muscle during contraction.
J. Physiol. 161: 379, 1962.
Myocardial Mural Thickness During the Cardiac Cycle
ERIC O. FEIGL and DONALD L. FRY
Downloaded from http://circres.ahajournals.org/ by guest on April 30, 2017
Circ Res. 1964;14:541-545
doi: 10.1161/01.RES.14.6.541
Circulation Research is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1964 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7330. Online ISSN: 1524-4571
The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://circres.ahajournals.org/content/14/6/541
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in
Circulation Research can be obtained via RightsLink, a service of the Copyright Clearance Center, not the
Editorial Office. Once the online version of the published article for which permission is being requested is
located, click Request Permissions in the middle column of the Web page under Services. Further information
about this process is available in the Permissions and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Circulation Research is online at:
http://circres.ahajournals.org//subscriptions/