Richard E Tracy
Cardiac myocytes respond to volume overload by undergoing hypertrophy in two phases: Proportionate increase in breadth and length and Continuation only of lengthening after the chamber dilates beyond a defined threshold. These responses have upper limits that are in need of explanation. Hearts were retrieved from 104 forensic autopsies. Myocyte breadths were measured in H&E-stained paraffin sections from LV and RV free walls. Mean myocyte lengths were calculated from chamber diameter and wall thickness (at full systole in these preparations) using a previously defined regression equation. Using body weight as an estimate for volume overload, myocyte breadth obeyed the expected two phase pattern. This pattern differed between ventricles in only one well defined way: the limiting mean breadths in the right and left respectively were 17.5 μm and 21.9 μm. Hence, in the RV it is not the attained size that imposed the limit on further hypertrophy of the mean myocyte because that attained size imposed no such limit in the LV. The behaviour of overworked myocytes is virtually identical in the two ventricles and it seems reasonable to propose that this identity should affect also the upper limit to size. Log normal distributions generally fit reasonably well in both RV and LV with no ceiling exerted upon the most enlarged cells, which further supports the lack of effect by attained size. A body of theory emerges which provisionally places a causal role for hypertrophy on the simple operation of geometry constrained by a fixed number of myocytes. The theory emerged without need to introduce any proposed contractile weakening. If this theory is confirmed by further observations using improved methodology then this conclusion would sharply constrain what subcellular mechanisms might mediate these events.
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