Heart size.

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Abstract
The 1st part of this review analyzes some factors expected to influence muscle work, and the 2nd part discusses the evidence supporting constancy of workload, together with some clinical implications. The data on heart growth come from comparisons of growing animals of the same species, from adult mammals of widely differing sizes, and from experimental or disease states which produce altered hemodynamics. Correlating the data from these 3 areas is difficult because they have been obtained with varying techniques, usually with different purposes in mind. This necessarily limits the precision with which quantitative relations can be established. If the relation between heart size and hemodynamics could be more precisely quantitated, smaller deviations from the normal would be recognizable. These small deviations then could be used to distinguish between different forms of myocardial hypertrophy, and to interpret clinical data. The data reviewed suggest that normal heart muscle grows to match the workload imposed upon the ventricle. Since the work can vary both in the systolic pressure produced and in the volume of blood ejected, different types of growth are produced. When the muscle is normal this growth results in a constant relation between systolic pressure and the ratio of wall thickness to ventricular radius, irrespective of heart size. This relation may be used to determine the progression of hypertrophy, and deviation from the relation can be used as a measure of [human] myocardial disease.