1. All normal human hearts have essentially the same number of myocardial fibers and myocardial nuclei. During physiologic growth the number of myocardial fibers remains constant; the fibers enlarge, but their length-to-width ratio remains constant (harmonic growth). The number of capillaries increases with growth, with one capillary per four fibers in the infant and one capillary per fiber in the adult. However, the width of the spaces of the capillary net is essentially the same for all age groups. The number of fibers and nuclei is roughly the same for the right ventricle as the left; the left ventricle is heavier than the right because its fibers are thicker. There are fewer layers of fibers in the right ventricle than in the left. It follows from this that the inner surface area of the right ventricle must be greater than for the left.

2. The average weight of the normal heart in man is about 300 gm. Through athletic exertion it can attain a weight of 500 gm. This increase is due to an extension of physiologic growth, with the fibers increasing in length and width but not increasing in number. The growth results in a larger than normal mobilizable blood volume.

3. As a result of pathologic demands for increased heart work as, for example, in hypertension, the “critical” heart weight of 500 gm. is exceeded. Increases in heart weight above the “critical” level are due to increase in the number of fibers with little further thickening. There is also an increase in capillaries, with the ratio of one capillary per fiber maintained. The coronary insufficiency that occurs with advanced hypertrophy is not principally due to a failure of capillary supply but to the fact that with hypertrophy the growth of the coronary arteries and coronary ostia is retarded and atherosclerotic lesions of the coronary system become more frequent.

4. As a result of the coronary insufficiency a dilatation takes place. However, the Z-band to Z-band distance (i.e., the length of sarcomeres) of myocardial fibers in dilated hearts is the same as for normal hearts. In addition to longitudinal growth of the muscle fibers in dilatation there are also structural alterations in the myocardium with rearrangements of the architectural relationship among the muscle fibers. Therefore, dilatation as encountered in man is not characterized by overstretched fibers. This is true of dilatation whether due to coronary sclerosis, myocarditis or excessive hypertrophy. It is called “structural dilatation” as opposed to the “functional dilatation” of the acutely overloaded heart. There is an increased residual ventricular volume in the dilated heart, but it is not mobilizable.

5. Structural dilatation is the morphologic substrate of the decompensated heart. The cross section area of muscle capable of contracting is too small for the increased volume of the ventricle. Cardiac insufficiency results, not from overstretching of the fibers or inadequate oxygen consumption per fiber length in the Starling sense, but for strictly mechanical reasons. The unit muscle weight may produce a normal amount of energy liberated on contraction but it is no longer adequate to expel a normal stroke volume from a ventricle of these dimensions. In other words, the essence of myocardial failure is the discrepancy between the amount of energy necessary to expel a stroke volume and the amount of energy available. In these studies it has been shown that in most clinical cardiac disorders with heart failure the discrepancy can be adduced from changes in the quantitative morphology of the heart.