Pressure-overload left ventricular hypertrophy in children demonstrates proportional capillary angiogenesis, whereas in adults, hypertrophy appears to be associated with failure of compensatory angiogenesis.

Fluctuations in body weight as occur with aging make body weight an unreliable reference for normalizing heart weight. We compared heart weight normalized by tibial length, which remains constant after maturity, with that normalized by body weight in 5- to 28-mo-old male Wistar rats. When normalized by tibial length or body weight, relative to the 5-mo heart, the senescent left ventricle undergoes 17 vs. 38% hypertrophy, respectively, and the right ventricle undergoes 0 vs. 28% hypertrophy, respectively. Histological measurements in the 25- compared with the 5-mo-old left ventricles reveal 6% larger myocyte diameters and 12% larger cellular cross-sectional areas, indicating about 15% hypertrophy; this value agrees more closely with the estimates based on tibial length than with those based on body weight. To allow prediction of left ventricular weight in a living rat, a regression equation using body weight, age, and tibial length was derived. This enabled us to perform a longitudinal aging study that verified that the above results were not biased by selective survival. Thus, in conditions in which body weight changes, cardiac hypertrophy can be more accurately quantified by relating heart weight to tibial length than to body weight. This approach may have applicability for assessing relative sizes of other organs as well.

SUMMARY1. Cardiomegaly has been produced in rats by sideropenic anaemia, by isoprenaline or thyroxine or by the application of both drugs, by artificial increase in resistance to blood flow and by long-term adaptation to hvpoxia and physical stress. The ratio of the growth of muscle to the growth of collagen in the heart has been studied.2. All possible variations in the ratio occurred depending on the type of stimulus used for inducing cardiomegaly and on the dynamics of the development of cardiomegaly. In cardiomegaly induced by sideropenia and by thyroxine the growth of muscle was not accompanied by the growth of collagen. Exposure to hypoxia or isoprenaline administration increased only the growth of collagen in the hypertrophic heart. in all other forms of cardiomegaly muscle and collagen formation were stimulated to the same extent.3. It is concluded that when certain organs hypertrophy during adult life several factors may determine the relative rapidity of growth of the muscular or parenchymal and the collagenous stromal components of the tissue.

The length and width of enzymatically isolated individual rat cardiac myocytes were concurrently measured during normal and stimulated cardiac growth. In normal rats weighing between 75 and 750 g the length and width increased by 64 and 68% while their ratio remained constant (ca. 5.3). The cell volume, calculated on the basis of a cylindrical model, increased almost 5 times. The rates of increase in the volume of an average myocyte and in left ventricular mass were found to be similar, indicating that normal myocardial growth could be explained by hypertrophy of existing myocytes and no proliferation would be required. In cardiomegaly induced by aortic constriction in the adult rat, an increase in cell volume was observed while no significant changes in the length-to-width ratios could be detected. The cell volumes of the hypertrophic hearts corresponded to those observed in hearts of similar weight obtained from larger normal rats and the stimulated cardiac growth could also be explained solely by hypertrophy of existing cells.

Changes in hemodynamic load cause alterations in cardiac myocyte size, with regional variations in myocyte size distribution possible within the ventricular wall. We studied regional changes in cellular dimensions and their distribution in two models of cardiac hypertrophy and in cardiac atrophy in the rat. Combined volume-pressure overload was produced by 3,3',5-triiodo-L-thyronine (T3) treatment; atrophy was produced by heterotopic isotransplantation. Our previous data from long-term pressure overload after aortic constriction were used for comparison. Isolated