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1 Department of Oral Biology, Ohio State University, Columbus 43210; 2 Center for Anesthesiology Research, Cleveland Clinic Foundation, Cleveland, Ohio 44195; and 3 Division of Cardiology, Department of Pediatrics, University of Washington, Seattle, Washington 98195
The goal of this study was to test
the hypothesis that the relative amounts of the cardiac myosin heavy
chain (MHC) isoforms MHC-
and MHC-
change during development and
transition to heart failure in the human myocardium. The relative
amounts of MHC-
and MHC-
in ventricular and atrial samples from
fetal (gestational days 47-110) and nonfailing and
failing adult hearts were determined. The majority of the fetal right
and left ventricular samples contained small relative amounts of
MHC-
(mean < 5% of total MHC). There was a small significant
decrease in the level of MHC-
in the ventricles between 7 and 12 wk
of gestation. Fetal atria expressed predominantly MHC-
(mean > 95%), with MHC-
being detected in most samples. The majority of
adult nonfailing right and left ventricular samples had detectable
levels of MHC-
ranging from 1 to 10%. Failing right and left
ventricles expressed a significantly lower level of MHC-
. MHC-
comprised ~90% of the total MHC in adult nonfailing left atria,
whereas the relative amount of MHC-
in the left atria of individuals
with dilated or ischemic cardiomyopathy was ~50%. The
differences in MHC isoform composition between fetal and nonfailing
adult atria and between fetal and nonfailing adult ventricles were not
statistically significant. We concluded that the MHC isoform
compositions of fetal human atria are the same as those of nonfailing
adult atria and that the ventricular MHC isoform composition is
different between adult nonfailing and failing hearts. Furthermore, the
marked alteration in atrial MHC isoform composition, associated with
cardiomyopathy, does not represent a regression to a pattern that is
uniquely characteristic of the fetal stage.
development; myocardium; dilated cardiomyopathy; ischemic cardiomyopathy
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