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

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 ch ange during development and transition to heart failure in the human myocar dium. The relative amounts of MHC-alpha and MHC-beta in ventricular and atr ial samples from fetal (gestational days 47-110) and nonfailing and failing adult hearts were determined. The majority of the fetal right and left ven tricular samples contained small relative amounts of MHC-alpha (mean <5% of total MHC). There was a small significant decrease in the level of MHC-<al pha> in the ventricles between 7 and 12 wk of gestation. Fetal atria expres sed predominantly MHC-alpha (mean >95%), with MHC-beta being detected in mo st samples. The majority of adult nonfailing right and left ventricular sam ples had detectable levels of MHC-alpha ranging from 1 to 10%. Failing righ t and left ventricles expressed a significantly lower level of MHC-alpha. M HC-alpha comprised similar to 90% of the total MHC in adult nonfailing left atria, whereas the relative amount of MHC-alpha in the left atria of indiv iduals with dilated or ischemic cardiomyopathy was similar to 50%. The diff erences in MHC isoform composition between fetal and nonfailing adult atria and between fetal and nonfailing adult ventricles were not statistically s ignificant. We concluded that the MHC isoform compositions of fetal human a tria are the same as those of nonfailing adult atria and that the ventricul ar MHC isoform composition is different between adult nonfailing and failin g hearts. Furthermore, the marked alteration in atrial MHC isoform composit ion, associated with cardiomyopathy, does not represent a regression to a p attern that is uniquely characteristic of the fetal stage.