Human cardiac myosin heavy chain isoforms in fetal and failing adult atria and ventricles

Reiser, Peter J., Michael A. Portman, Xue-Han Ning, and Christine Schomisch Moravec. Human cardiac myosin heavy chain isoforms in fetal and failing adult atria and ventricles. Am J Physiol Heart Circ Physiol 280: H1814-H1820, 2001.--The goal of this study was to test the hypothesis that the relative amounts of the cardiac myosin heavy chain (MHC) isoforms MHC-[Alpha] and MHC-[Beta] change during development and transition to heart failure in the human myocardium. The relative amounts of MHC-[Alpha] and MHC-[Beta] 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-[Alpha] (mean [is less than] 5% of total MHC). There was a small significant decrease in the level of [MHC-[Alpha] in the ventricles between 7 and 12 wk of gestation. Fetal atria expressed predominantly MHC-[Alpha] (mean [is greater than] 95%), with MHC-[Beta] being detected in most samples. The majority of adult nonfailing right and left ventricular samples had detectable levels of MHC-[Alpha] ranging from 1 to 10%. Failing right and left ventricles expressed a significantly lower level of [MHC-[Alpha]. [MHC-[Alpha] comprised -90% of the total MHC in adult nonfailing left atria, whereas the relative amount of MHC-[Alpha] 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