(Circulation. 1997;96:535-541.)
© 1997 American Heart Association, Inc.
Articles |
Noninvasive Measurement of Shortening in the Fiber and Cross-Fiber Directions in the Normal Human Left Ventricle and in Idiopathic Dilated Cardiomyopathy
From the Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Md; Department of Biomedical Engineering (H.A.), Technion IIT, Haifa, Israel; and the University of Antwerp (F.E.R.), Belgium.
Correspondence to Edward P. Shapiro, MD, Division of Cardiology, The Johns Hopkins Bayview Medical Center, 4940 Eastern Ave, Baltimore, MD 21224. E-mail eshapiro{at}welchlink.welch.jhu.edu
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Abstract |
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Background Studies in anesthetized dogs have shown that myocardial fibers shorten
8%. However, in the
endocardium, shortening occurs to a much greater extent at 90° to the
fiber orientation ("cross-fiber shortening") than it does along
the fiber direction. The purpose of this study was to estimate the
extent of fiber and cross-fiber shortening in the normal human left
ventricle and in patients with idiopathic dilated
cardiomyopathy (IDC). Methods and Results Ten normal subjects and nine patients with IDC were imaged with magnetic resonance tissue tagging. Finite strain analysis was used to calculate endocardial and epicardial shortening in the fiber and cross-fiber directions using anatomic fiber angles from representative autopsy specimens as references. Anatomic fiber angles were not different between normal subjects and IDC patients. Epicardial fiber strain was -0.14±0.01 in normal subjects and -0.08±0.01 in IDC patients (P<.0001 versus normal subjects). Epicardial cross-fiber strain was -0.08±0.01 in normal subjects and -0.06±0.01 in IDC patients (P=NS). Endocardial fiber strain was -0.16±0.01 in normal subjects and -0.09±0.01 in IDC patients (P<.0001), and endocardial cross-fiber strain was -0.26±0.01 in normal subjects and -0.15±0.01 in IDC patients (P<.0001). Cross-fiber shortening was greater than fiber shortening at the endocardium in both normal subjects (P<.0001) and IDC patients (P<.05).
Conclusions In normal humans, the direction of
maximal deformation aligns with the fiber direction in the epicardium
but is perpendicular to the fiber direction in the endocardium. When
strain in a coordinate system aligned to the fibers is estimated,
cross-fiber shortening is found to be the dominant shortening strain at
the endocardium. Normal fiber shortening is 15%, and this is
markedly reduced in IDC. The normal transition in fiber orientation
through the wall is not altered in IDC, and cross-fiber shortening is
still the dominant strain at the endocardium, suggesting that
interactions between myocardial layers persist in these patients.
Key Words: magnetic resonance imaging • mechanics • cardiomyopathy • myocardial contraction
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The fibers of the human left ventricle are arranged in a complex fashion, with epicardial fibers directed in a counterclockwise spiral and endocardial fibers in a clockwise spiral from apex to base. Therefore, there is transition in the orientation of fibers through the wall of the left ventricle, with epicardial fibers oriented obliquely, midwall fibers oriented horizontally, and endocardial fibers oriented obliquely in the opposite direction from epicardial fibers.1
This fiber architecture has important functional consequences.
Analysis of canine myocardial shortening with respect to fiber
orientation2 3 has shown that at the epicardium,
shortening is predominantly aligned in the direction of epicardial
fibers. However, at the endocardium, maximal shortening is 90°
from the endocardial fiber direction.3 4 This
"cross-fiber shortening" is thought to be accomplished by the
physical rearrangement of fibers or fiber bundles2 induced
by contraction of layers with different fiber orientation. LeGrice et
al5 suggested that this rearrangement occurs along
cleavage planes that separate sheets of myocytes and that it is
associated with transverse shearing deformation. These rearrangements
and shears allow the endocardium to shorten in two orthogonal
directions, producing extensive thickening in a third direction to
preserve volume. This would explain the marked systolic
endocardial thickening that is essential for normal
ejection.3
The extent of fiber and cross-fiber shortening in the left
ventricle of normal and abnormal human hearts is unclear. Rademakers et
al,3 using MR tagging, and Waldman et al,4
using radiopaque beads, have shown that fiber shortening in
anesthetized dogs is 8%. In humans, studies that used
echocardiography corrected with geometric models
have calculated that fiber shortening is 21% in normal subjects and
18% in subjects with left ventricular
hypertrophy and normal global function.6
Studies that used MR tagging have suggested that fiber shortening is
30% in normal subjects and 21% in patients with left
ventricular hypertrophy.7 Thus,
marked differences in the extent of fiber shortening have been observed
between human and experimental studies.
It is not known how fiber and cross-fiber shortening are affected in idiopathic dilated cardiomyopathy (IDC). Myocardial fiber shortening might be reduced, directly reflecting reduced contractility. Alternatively, dilation of the left ventricle might have effects on fiber orientation, resulting in a more circumferential fiber arrangement. As the variation in fiber orientation through the left ventricular wall diminishes, cross-fiber shortening might be reduced. Finally, because integration of epicardial and endocardial strains may be mediated via connective tissue,8 cross-fiber shortening might be reduced due to alterations in this matrix.9
The aims of the present study were to use MR tissue tagging, a noninvasive method of marking specific segments of myocardial tissue,10 11 to estimate fiber shortening in the normal in vivo human myocardium and to determine if marked cross-fiber shortening occurs at the endocardium. We also sought to determine the extent of fiber shortening and cross-fiber shortening in IDC.
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Methods |
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Study Population
Ten normal volunteers who had no history of cardiac disease or hypertension and nine patients with compensated heart failure (NYHA class II or III) due to IDC were studied (Table 1
). IDC
was diagnosed by clinical evidence of heart failure,
echocardiographic evidence of chamber dilation, and
normal coronary arteries on selective angiography. All patients
had ejection fractions <35%, were in sinus rhythm, had no history of
hypertension, and were treated with digoxin, ACE inhibition, and
diuretics. Informed consent was obtained from all participants.
Approval for this study was obtained from the institutional review
board.
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MRI
Images were acquired with a Resonex RX4000, 0.38-T
resistive magnet using a spin-echo pulse sequence with time to echo of
30 ms and time to repeat of every two RR cycles. Three short-axis
images were acquired, aligned so that the plane of the images was
parallel to the AV groove and spaced 1.5 to 3.0 cm apart to cover the
left ventricle from base to apex. Tags were created by radiofrequency
saturation of thin planes orthogonal to the short axis at end
diastole.10 On each short-axis slice, three
radially spaced tags (transecting the myocardium at six
locations), intersecting at the center of the left ventricle, were
placed at 120° apart (Fig 1). When long-axis images
were being acquired, the imaging and tagging planes used in the
short-axis images were interchanged so that three long-axis images were
obtained 120° apart, each with three transverse tags in the planes
previously used to obtain short-axis images (Fig 2).
Images were acquired at end diastole (defined by the QRS
complex) and at end systole (timed by a Doppler echocardiogram
immediately before the scan).
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Image Analysis
The tag intersection points at the endocardium and
epicardium were digitized, yielding a set of six endocardial and six
epicardial points per short- and long-axis slice, as described by
Rademakers et al.12 The endocardial and epicardial tag
intersection points from the short- and long-axis images were combined
to yield three-dimensional coordinates using an algorithm as described
by Moore et al13 and Azhari et al11 (Fig 3). Thus, from the combined short- and long-axis images,
six tag points at the epicardium and six tag points from the
endocardium across three slices yielded a set of data with 36 points
per time point. The 36 data points were grouped to yield 12 cuboids
(see Fig 3) for each time point.
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Finite Strain Analysis
Finite strain analysis, as originally described by
Waldman et al2 and adapted to MR tagged data by Azhari et
al,11 was applied to the endocardial and epicardial faces
of the cuboids. Each face was divided into four triangles and
transformed into a regional coordinate system. Strain analysis
was applied to each triangle to calculate the circumferential and
longitudinal strains (Fig 3
). Subsequently, the principal strain was
calculated, defined as the magnitude and direction of maximal
shortening. The direction of the principal strain was expressed as an
angle with respect to the circumferential direction. A negative sign
for strain values indicates shortening.
Estimation of Fiber and Cross-Fiber Shortening
Representative anatomic fiber angles were
obtained from autopsy specimens from nine patients who died of
noncardiac causes with normal hearts and nine patients with IDC
confirmed at autopsy. All hearts were fixed overnight in a distended
state by introducing formalin into the cavities at 30 to 40 cm
H2O while the entire heart was immersed in
formalin.3 The age at death for the autopsied
cardiomyopathy patients was 45±7 years, and the
weight of the hearts was 705±156 g. The hearts were sliced along three
equally spaced transverse sections aligned so that the plane of the
sections was parallel to the AV groove,3 in a similar
fashion to the method used for the selection of the short-axis MR
images. Two layers were therefore obtained that measured 1.5 to 2.5 cm
in the long-axis direction, depending on the size of the ventricle.
These two layers were each divided into 6 cuboids by three equally
spaced radial dissection planes that intersected at the center of the
left ventricle, in a similar fashion to the method used to define the
long-axis imaging planes. The first cuboid was defined by the radial
cut from the mid interventricular septum to the anterior
wall, and cuboids 2 to 6 were defined in a clockwise direction around
the short axis of the left ventricle when viewed from apex to base.
Cuboids 7 to 12 were arranged in the same format, though in the second,
more apical short-axis slice. These anatomic cuboids, each
corresponding to an imaged cuboid, were sectioned parallel to the
epicardium. After the outermost 0.5 mm was discarded, the
orientation of the fibers with respect to the short-axis plane was
identified with the use of a x7 magnifier containing a protractor
graticule. Similarly, fiber orientation was obtained 1 mm inward
from the endocardial surface. Fiber angles were expressed as an angle
with respect to the short-axis direction.
The mean fiber angles at the epicardial and endocardial faces for each
of the 12 cuboids for the normal and IDC hearts were then used to
calculate estimated fiber and cross-fiber direction shortening using a
method similar to that described by Waldman et al4 and
adapted for MR tagged data by Rademakers et al3 (Fig 3).
Thickening
Thickening was calculated by use of a three-dimensional
volume-element method as described and validated by Beyar et
al14 and Lima et al.15 The thickness of a
cuboid at a given time point was defined as the volume of the cuboid
divided by the average surface area of the epicardium and
endocardium.
Torsion
Because angular rotation (torsion angle) is directly
proportional to radius and is also affected by long-axis shortening, it
is necessary to take these into account when groups with different left
ventricular cavity sizes are compared. Angular
circumferential-longitudinal shear (shear CL), which is derived from
the torsion angle, takes into account both of these factors. This is
defined as the difference between the systolic position of an
apical tag point and the equivalent tag point on the basal slice as
expressed as an angle of which the vertex is the tag point on the basal
slice (Fig 4); it is calculated according to the formula
used by Buchalter et al16 :
shearCL=tan-1[2rsin(t/2)/h],
where r is the radius, t is the torsion angle,
and h is the distance between the basal and apical
slices.
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Left Ventricular Mass
Images were acquired for quantification of left
ventricular mass during the same session that tagged images
were acquired. Five to six short-axis slices spanning the entire left
ventricle were acquired, and left ventricular mass was
calculated as described by Shapiro et al.17
Statistical Analysis
Statistical analysis compared the differences in strains
between the normal control subjects and the patients with IDC,
expressed as a mean (±SEM, unless otherwise stated) of the regional
endocardial and epicardial strain values. Repeated measures ANCOVA was
used to compare the two groups, accounting for each individual's age,
sex, and body surface area. ANOVA was used to compare strains within
groups.
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Results |
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Anatomic Fiber Angles
No significant differences in fiber angles between normal hearts and hearts with IDC were found at either the epicardium or endocardium (Figs 5
and 6). There were
significant regional differences in fiber angles among the various
segments for the normal hearts (epicardium: P=.01;
endocardium: P<.05) and only at the epicardium for the IDC
hearts (epicardium: P<.05; endocardium:
P=NS).
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To demonstrate the validity of estimating fiber and cross-fiber
shortening with anatomic samples from subjects other than those
undergoing the imaging studies, the variability of fiber angle
measurements as determined by the mean±SD for each individual cuboid
is presented in Table 1. In normal subjects, the variability in
measurements is low, with the SD averaging only 5.8° and measuring
<10° for all cuboids. In IDC, the variability is slightly higher but
still averages only 9°. This low variability among individuals
indicates that a reliable mean fiber angle for a strain reference can
be obtained and that it is possible to estimate fiber shortening and
cross-fiber shortening using as an anatomic reference a group of hearts
from subjects other than those being imaged.
Finite Strain Analysis
In normal subjects, the principal strain was -0.18±0.03 and the
principal strain angle was 75±12° at the epicardium. In IDC
patients, the principal strain at the epicardium was -0.14±0.03
(P<.005; probability values are for normal subjects versus
IDC patients unless otherwise stated) and the principal strain angle
was 54±13° (P<.01). Thus, in normal subjects, maximal
shortening at the epicardium aligns very closely with the anatomic
fiber direction. In IDC, the magnitude of maximal shortening at the
epicardium is reduced and the direction is more oblique than in normal
subjects but still within 20° of the anatomic fiber orientation (Fig 5).
At the endocardium in normal subjects, the principal strain was
-0.31±0.03 and the principal strain angle was 6±9°. In IDC
patients, the principal strain at the endocardium was -0.24±0.03
(P<.005) and the principal strain angle was 16±10°
(P=.08). Thus, the direction of maximal shortening at the
endocardium is 76° and 86° from the endocardial fiber angle in
normal subjects and IDC patients, respectively, indicating that maximal
shortening is oriented at nearly right angles to the anatomic fiber
angles in both these groups (Fig 6).
Estimated Fiber and Cross-Fiber Shortening
Epicardial fiber shortening was -0.14±0.01 and
-0.08±0.01 in normal subjects and IDC patients, respectively
(P<.0001). Endocardial fiber shortening was -0.16±0.01
and -0.09±0.01 in normal subjects and IDC patients, respectively
(P<.0001). Thus, fiber shortening was 15% in normal
subjects and was markedly reduced in IDC. There was a small but
significant difference in fiber shortening between the epicardium and
endocardium in normal subjects (P<.05) and a similar trend
but no significant difference in the IDC patients.
Epicardial cross-fiber shortening was significantly less than epicardial fiber shortening in the normal subjects (P<.0001), although there was no significant difference in the IDC patients (P=NS). Epicardial cross-fiber shortening was -0.08±0.01 in normal subjects and was not significantly different in IDC patients (-0.06±0.01; P=NS). Endocardial cross-fiber shortening was significantly greater than endocardial fiber shortening for both the normal (P<.0001) and IDC groups (P<.05). Endocardial cross-fiber shortening was -0.26±0.01 in normal subjects and -0.15±0.01 in IDC patients (P<.0001).
All strain values, including circumferential shortening, longitudinal
shortening, fiber cross-fiber shear strain, and shear CL are
presented in Tables 2 and 3.
Transmural wall thickening, end-diastolic wall thickness,
and left ventricular mass are presented in Table 4.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study has demonstrated that in normal humans, the direction of maximal deformation aligns with the fiber direction in the epicardium but is perpendicular to the fiber direction in the endocardium. When strain in a coordinate system aligned to the fibers is estimated, cross-fiber shortening is found to be the dominant shortening strain at the endocardium. Fiber shortening in the normal human myocardium is
15%, and this is markedly reduced
in IDC. The normal transition in fiber orientation through the left
ventricular wall is not significantly altered in IDC.
Consequently, the anatomic substrate for endocardial cross-fiber
shortening is preserved so that although cross-fiber shortening is also
reduced in IDC, this is still a dominant endocardial strain.
Cross-Fiber Shortening
Shortening of a layer of myocardium in its cross-fiber
direction is thought to occur by the rearrangement of those fibers in
three-dimensional space.3 4 Because a fiber can generate
force only in the direction of its sarcomere orientation, cross-fiber
shortening must be driven by contraction of other layers in which
fibers are oriented differently. Epicardial fiber shortening, at a
mechanical advantage due to its greater radius and with lateral
tethering by collagen cross bridges between fiber groups, may be able
to force the endocardium to shorten in a direction perpendicular to its
anatomic fibers.3 4 Indeed, an association between the
extent of epicardial fiber shortening and endocardial cross-fiber
shortening has been demonstrated previously.3 Endocardial
fibers also shorten in the fiber direction, though to a lesser extent
than in the cross-fiber direction. The significance of shortening in
two directions is that bundles of fibers must thicken extensively in
the third direction to preserve volume. This has been postulated as a
mechanism producing marked endocardial thickening, essential for normal
ejection.3 Cleavage planes within the
myocardium may provide the anatomic substrate for this
fiber rearrangement, which results in longitudinal-radial
shear.5 Another possible explanation for endocardial
cross-fiber shortening is that it merely represents the coming
together of endocardial trabeculae. However, at the
epicardium, where trabeculae are absent, cross-fiber
shortening is still evident both in the canine heart3 4
and in the human heart, as demonstrated here. This suggests that
endocardial cross-fiber shortening is the result of rearrangement
within the internal structure of the wall.
The present study has shown that the anatomic fiber angles in IDC are not significantly different from those in normal human hearts. Although this has not been demonstrated previously, it is consistent with a previous report18 of human hypertensive cardiomyopathy in which no difference in fiber angles was shown. Thus, the essential anatomic factor necessary for cross-fiber shortening, that is, the transmural transition in fiber orientation, is preserved in these stable patients with IDC. Consequently, endocardial cross-fiber shortening remains a dominant endocardial strain. Whether anatomic fiber angles and endocardial cross-fiber shortening are preserved in all forms of cardiomyopathy, including acute myocarditis, or in patients with a more rapidly progressive course remains to be determined.
Even without a difference in epicardial fiber angle between groups, there was a difference in the angle of epicardial principal strain. The more oblique angle of maximal shortening in ICD patients appears to be due to the preservation of epicardial cross-fiber shortening, which was not significantly reduced despite a 40% reduction in fiber shortening. The reasons for this relative sparing of epicardial cross-fiber shortening are uncertain. As is the case with endocardial cross-fiber shortening, epicardial cross-fiber shortening must be due to shortening at another myocardial layer, presumably the clockwise fibers of the endocardium. We speculate that the preservation of this strain in cardiomyopathy might occur because of a relative increase in endocardial mechanical influence over the epicardium. This increased influence could result from ventricular dilatation, which augments both epicardial and endocardial radii by similar amounts and thereby reduces the ratio of epicardial to endocardial radius. That is, the epicardial and endocardial radii become more similar, and there is a reduction in the usual extent of epicardial dominance. The influence of one layer on the other may thus become more bidirectional.
Fiber Shortening
Fiber shortening in the human left ventricle was found in this
study to be 15%. Although fiber shortening in the epicardium and
the endocardium could not be evaluated in normal subjects before the
development of the methods used here, several previous imaging studies
have evaluated midwall shortening in normal humans. Because midwall
fibers are oriented circumferentially, values of midwall
circumferential shortening may approximate fiber shortening. These
studies have produced different results. Palmon et al,7
using MRI with spatial modulation of magnetization (SPAMM), a tagging
method, reported values of midwall circumferential shortening of 30%,
although a more recent study using the same methods found lesser values
ranging from 15% to 28%.19 This wide range in normal
subjects may relate to differences in global function within the normal
range, which also might explain some of the differences among these
studies, which used relatively small sample sizes. Aurigemma et
al6 used echocardiography to track
midwall shortening, with a geometric correction used for different
epicardial versus endocardial thickening, and found values of 21%.
However, unlike the present work, neither method used data from
three dimensions in the calculation of circumferential shortening.
Therefore, these studies could not take into account both the effect of
differential epicardial versus endocardial thickening and the effect of
the considerable shortening that occurs along the long axis in the
human left ventricle20 (Fig 2) on circumferential
shortening. Through-plane motion due to long-axis shortening results in
alteration of the mass of any short-axis slice as
myocardium that was not present in diastole
moves into the imaging plane in systole.20 The advantages
of using a three-dimensional approach have been clearly
demonstrated.15
Those limitations are not present in studies of transplanted
hearts containing radiopaque beads. Ingels et al21
measured midwall shortening along cords in the circumferential
direction in that model and found cord shortening of 14%, in agreement
with the current study. Finite strain analysis was used to
determine fiber shortening in epicardial and endocardial locations in
canine models by Waldman et al4 using bead placement and
by Rademakers et al3 using MRI tagging, and values of
8% were found. The discrepancy between human data and these canine
studies may be related to the administration of anesthesia
in the canine model; in studies of conscious pigs, similar strain
values to those of normal humans in the present study have been
documented.22
The major abnormality in IDC demonstrated in the present
study is the marked reduction in fiber shortening at both the
epicardium and the endocardium. We demonstrated a small but significant
difference in fiber shortening across the left ventricular
wall in normal subjects (epicardium -0.14±0.01 versus endocardium
-0.16±0.01; P<.05) and a trend in the same direction in
IDC patients. Arts et al23 24 suggested that equal fiber
shortening at the epicardium and endocardium as a consequence of
torsion of the left ventricle results in uniform distribution of muscle
fiber stress, fiber shortening, and contractile work across the left
ventricular wall.25 In that model of left
ventricular mechanics, when torsion is allowed, the
transmural differences in sarcomere shortening and end-systolic
fiber stress are <16% and 18%, respectively. When torsion is
prevented, the transmural differences increase to 32% and 42%. In
both normal subjects and IDC patients, the transmural difference in
fiber shortening was 12% in the present study. Although this
difference is significant in the normal subjects, its magnitude is
small, and these results are therefore consistent with the
hypothesis that there is only minor variation in fiber shortening
across the ventricular wall. An essential component of the
model of Arts et al23 is the transmural transition in
fiber orientations, which produces torsion, which in turn results in
uniform fiber shortening. Because fiber orientations are not altered in
IDC, this probably explains the maintenance of a relatively
uniform transmural fiber shortening in this group.
Potential Limitations
Quantifying Fiber Angles From Autopsy Specimens
To estimate fiber and cross-fiber shortening, we used
anatomic data from autopsy specimens. The extremely low variation in
fiber angles among individuals indicates that it is possible to use a
reference fiber angle from an autopsied population to estimate fiber
and cross-fiber shortening in an individual subject, as we did here.
Error could potentially result from incorrect matching of imaged and
autopsied regions. However, the regional variation in the anatomic
fiber angles is low, so mismatches are unlikely to have affected the
estimates of fiber and cross-fiber shortening values significantly. For
example, even the unlikely error of mismatching functional data by one
whole cuboid (1/6 of the circumference) would result in a maximal
possible error of only 7° in normal subjects and 8° in IDC
patients. A mismatch between basal and apical halves of the LV would
have even less of an effect.
The autopsied cardiomyopathy patients likely had more severe heart failure than our imaged cardiomyopathy population. However, because the fiber angles are the same in normal subjects and those dying of IDC, it is unlikely that our patient population with less severe heart failure has significantly different fiber angles from those measured.
In this study, fiber angles were not modified for any changes that might occur between end systole and end diastole. However, it is known that changes in fiber angles during the cardiac cycle are small,26 so that the error in applying fiber angles measured in diastolic- or systolic-arrested hearts to live hearts is likely to be small. In addition, the postmortem hearts were likely to have arrested in a state somewhere between end diastole and end systole, so the fiber angles measured probably represent an intermediate value.
Cuboid Size
Finite strain analysis assumes regional homogeneity
of deformation and was therefore applied only to deformation of the
epicardial and endocardial faces, in which fibers course in a generally
uniform direction. Analysis of deformation within the
short-axis plane, ie, wall thickening, which occurs in a direction
along which fiber orientation and therefore material properties are
known to vary, was performed by use of simple geometric
methods14 15 rather than finite strain analysis.
However, even within the epicardial and endocardial faces, small
inhomogeneities might occur, and this represents a potential
source of error. The average end-diastolic segment lengths
of the endocardial arc, epicardial arc, and long-axis edge of the
cuboids were 2.6, 3.0, and 1.8 cm for the normal subjects and 3.0, 3.6,
and 2.2 cm for the cardiomyopathy patients. These
are greater than in our previous canine studies of deformation using
MRI3 11 because imaging additional planes adds imaging
time, which is constrained in patients. However, note that
beads2 4 21 or other devices27 28 29 implanted
for strain analysis in previous invasive canine studies have
usually been separated by at least 1 to 2 cm, and in previous human
studies, circumferential bead separation was 4.75 cm.21
Errors introduced by regional inhomogeneities in the present study
are therefore similar to those of prior invasive canine studies and
less than those of prior invasive human studies. The noninvasive nature
of the method and the ability to analyze data from multiple
regions throughout the left ventricle are important advantages of the
present study. Marked improvements in both tag density and imaging
time are now possible30 and will result in a greater
homogeneity and spatial resolution in future work.
Conclusions
Fiber shortening in the normal human myocardium
is 15% and is similar in the epicardium and endocardium. However,
cross-fiber shortening is the dominant strain in the normal human
endocardium and exceeds 25%. In stable patients with IDC, fiber
shortening is markedly reduced. Also, the transmural transition in
anatomic fiber orientations are not significantly altered in these
patients, and as a consequence, although cross-fiber shortening is
reduced, this is still the dominant endocardial strain. This supports
the concept that significant interactions between layers of the human
left ventricle occur during systole in both normal subjects and
patients with IDC. MR tagging is a promising technique with which
regional strains, including fiber shortening and cross-fiber
shortening, can be studied noninvasively in humans.
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Acknowledgments |
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This study was supported by NHLBI grants RO1-HL-46223 (Dr Shapiro) and RO1-HL-43722 (Dr Weiss).
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Footnotes |
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Presented in part at the 66th Scientific Sessions of the American Heart Association, Atlanta, Ga, November 8-11, 1993, and previously published in abstract form (Circulation. 1993;88[pt 2]:I-346).
Received July 29, 1996; revision received January 28, 1997; accepted February 3, 1997.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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