Heart failure

1. All normal human hearts have essentially the same number of myocardial f ibers and myocardial nuclei. During physiologic growth the number of myocar dial fibers remains constant; the fibers enlarge, but their length-to-width ratio remains constant (harmonic growth). The number of capillaries increa ses with growth, with one capillary per four fibers in the infant and one c apillary per fiber in the adult. However, the width of the spaces of the ca pillary net is essentially the same for all age groups. The number of fiber s and nuclei is roughly the same for the right ventricle as the left; the l eft ventricle is heavier than the right because its fibers are thicker Ther e are fewer layers of fibers in the right ventricle than in the left. It fo llows 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 a thletic 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 an d width but not increasing in number. The growth results in a larger than n ormal mobilizable blood volume. 3. As a result of pathologic demands for increased heart work as, Sor examp le, in hypertension, the "critical" heart weight of 500 gm, is exceeded. In creases in heart weight above the "critical" level are due to increase in t he number of fibers with little further thickening. There is also an increa se in capillaries, with the ratio of one capillary per fiber maintained The coronary insufficiency than occurs with advanced hypertrophy is not princi pally due to a failure of capillary supply but to the fact that with hypert rophy the growth of the coronary arteries and coronary ostia is retarded an d atherosclerotic lesions of the coronary system become more frequent. 4. As a result of the coronary insufficiency a dilatation takes place. Howe ver, the Z-band to Z-band distance (i.e., the length of sarcomeres) of myoc ardial fibers in dilated hearts is the same as for normal hearts. In additi on to longitudinal growth of the muscle fibers in dilatation there are also structural alterations in the myocardium with rearrangements of the archit ectural relationship among the muscle fibers. Therefore, dilatation as enco untered in man is not characterized by overstretched fibers. This is true o f dilatation whether due to coronary sclerosis, myocarditis or excessive hy pertrophy. It is called "structural dilatation" as opposed to the "function al dilatation" of the acutely overloaded heart. There is an increased resid ual 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 tao 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. Th e unit muscle weight may produce a normal amount of energy liberated on con traction 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 t he heart.