Circulation, Vol 85, 259-268, Copyright © 1992 by American Heart Association
SA Wickline, ED Verdonk, AK Wong, RK Shepard and JG Miller
BACKGROUND. Remodeling of myocardial tissue after infarction may culminate
in the development of either a well-healed scar or a thin, expanded heart
wall segment that predisposes to ventricular aneurysm formation, congestive
heart failure, or ventricular tachycardia. The three-dimensional
architecture of mature human infarct tissue and the mechanisms that
determine it have not been elucidated. We have previously shown that
quantitative ultrasonic backscatter can be used to define the transmural
organization of human myofibers in the normal ventricular wall by measuring
the dependence of backscatter on the angle of insonification, or ultrasonic
anisotropy. We propose that measurement of ultrasonic anisotropy of
backscatter may permit quantitative characterization of the transmural
architecture of tissue from areas of myocardial infarction and facilitate
identification of fundamental mechanisms of remodeling of the ventricular
wall. METHODS AND RESULTS. We measured integrated backscatter in 33
transmural sections from 12 cylindrical biopsy specimens (1.4-cm diameter)
sampled from central regions of mature infarction in six explanted fixed
human hearts. Tissue samples were insonified in two-degree steps around
their entire circumference at successive transmural levels with a 5-MHz
broad- band piezoelectric transducer. Backscatter radio frequency data were
gated from the center of each specimen, and spectral analysis was performed
on the gated radio frequency for the computation of integrated backscatter.
Histological morphometric analysis was performed on each specimen for
determination of the predominant fiber orientation and the percentage of
tissue infarcted at consecutive transmural levels. The average percentage
of tissue infarcted for all transmural levels was 49 +/- 3% (range,
13-80%). Histological attributes varied from patchy fibrosis to extensive
confluent zones of scar tissue. The angle-averaged integrated backscatter
for all transmural levels in infarct tissue was approximately 5 dB greater
than that previously measured in normal tissue in our laboratory (-48.3 +/-
0.5 versus -53.4 +/- 0.4 dB, infarct versus normal). Marked anisotropy of
backscatter was observed in tissue from areas of infarction and was
characterized by a sinusoid-like dependence on the angle of insonification
at each transmural level. Insonification perpendicular to infarct fibers
yielded values for integrated backscatter 14.8 +/- 0.5 dB greater than
those for insonification parallel to these fibers. Juxtaposition of the
sinusoid-like anisotropy functions from all consecutive transmural levels
demonstrated a progressive shift in the orientation of scar tissue elements
from epicardial to endocardial levels of 14.6 +/- 1.5 degrees/mm of tissue.
The transmural shift in fiber orientation per millimeter of tissue from the
area of infarction exceeded that previously measured for normal tissue (9.2
+/- 0.7 degrees/mm) by 59%. This marked augmentation in angular shift per
millimeter of tissue results from a generalized structural rearrangement
(or reorientation) of fibers across the entire ventricular wall in the
infarct zone that we hypothesize is determined in part by dynamic
mechanical forces, imposed by the surrounding functional normal tissue,
that tether the "infarcted" tissue. CONCLUSIONS. Myocardial tissue from
areas of myocardial infarction manifests substantial anisotropy of
ultrasonic scattering that may be useful for quantitative characterization
of the alignment and overall three-dimensional anatomic organization of
mature infarct scars.
ARTICLES
Structural remodeling of human myocardial tissue after infarction. Quantification with ultrasonic backscatter
Cardiovascular Division, Washington University School of Medicine, St. Louis, MO 63110.
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