Architecture of myocardial cells in human cardiac ventricles with concentric and eccentric hypertrophy as demonstrated by quantitative scanning electron microscopy.

Scanning electron microscopy (SEM) was used to compare the shapes, size, and connections of cardiocytes in the midwall myofibers in the left ventricles of 5 normal hearts (266 +/- 16 g), 5 hears with concentric hypertrophy (564 +/- 99 g) and 5 with eccentric hypertrophy (651 +/- 114 g), obtained at autopsy and fixed in formalin. In the myofibers from normal and hypertrophied hearts, intercalated discs demarcated cardiocytes which consisted of a cylindrical trunk and one or more series and/or lateral branches; cell connections at the intercalated discs had 6 common basic patterns. The length (L), width (W) and L/W ratio of the cells and the size and number of the series and lateral branches per cell were measured in 50 cells from each heart and averaged for comparison studies. The cells in the concentrically hypertrophied ventricles were much thicker than normal (33.0 +/- 2.8 vs 18.2 +/- 1.4 microns, P less than 0.01) but not significantly longer (81.2 +/- 9.5 vs 71.2 +/- 9.6 microns, NS), so that the L/W ratio was greatly decreased (2.6 +/- 0.3 vs 4.1 +/- 0.7, P less than 0.01). The cells in the eccentrically hypertrophied ventricles were markedly thickened (25.9 +/- 2.4 microns, P less than 0.01) and elongated (4.2 +/- 0.4, NS) remained the same as in normal hearts. In both types of hypertrophy, series and lateral branches were significantly thicker and longer than in normal hearts; the number of series branches per cell was also significantly increased. The number of lateral branches per cell did not differ between the normal and concentrically hypertrophied hearts (2.2 +/- 0.7 vs 2.3 +/- 0.6, NS), but it was decreased by approximately one-half in the eccentrically hypertrophied hearts (1.2 +/- 0.3, P less than 0.05). The potential significance of these differences in SEM findings of cardiocytes is discussed with special reference to the differences in the cause, anatomy, and pathophysiology of concentric and eccentric hypertrophy in adult human hearts.