In the present study, we demonstrated that hypertensive left ventricular hypertrophy can be devided angiographically into symmetrical (SH) and asymmetrical septal hypertrophy (ASH) groups. In the SH group, the dynamics of the septal wall and the free wall were almost the same as those of the control group. On the other hand, the ASH group rather resembled the HCM group in the thickness and dynamics of the septal wall and the free wall as well as in the septal configuration. The most characteristic difference of the ASH and HCM groups from the SH group was in the significantly greater thickness of the septal wall at end diastole. However, in view of the developmental mechanism of hypertensive heart, it is interesting to note that the more the septal-free wall ratio increases, the more the thickness of the septal wall increases in the SH group.

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First, age changes and progression of atherosclerosis in the human aorta and cerebral arteries were studied morphologically. Secondly, effects of normolipemic high-density lipoprotein (HDL) on the proliferation of medial smooth muscle cells from the monkey aortas induced by hyperlipemic low-density lipoprotein (LDL) were investigated in vitro. Atherosclerosis developed in cellulofibrous intimal thickening in the human arteries. The first hitological evidence of the intimal proliferation of the middle cerebral arteries leading to the cellulofibrous intimal thickening was observed at bifurcations in 6 month-old fetuses. The initial event in the morphogenesis of the intimal thickening was believed to be the endothelial injuries caused by hemodynamic forces, namely, shear stress and turbulence of the blood flow at bifurcations of the arteries. The endothelial injuries resulted in increased endothelial permeability which permitted the entry of blood plasma into the tunica intima to proliferate myointimal cells (intimal smooth muscle cells) derived from the tunica media. The intimal thickening increased gradually with advancing age associated with the increase of the number of myointimal cells and of the amount of glycosaminoglycans and collagen and elastic fibers in the intima with individual variation. It might be considered that the cellulofibrous intimal thickening of the arteries, which was observed in normal subjects from fetal life up to adolescence and was regarded as the physiological development of the arterial wall, was actually a complex of changes resulting from mechanical injuries and related to age. Repeated proliferation of the intima formed the multilayered intimal thickening in cases over the age around ten. The so-called physiological intimal thickening also occurred in the aorta, markedly in the thoracic and abdominal aorta. The thickened intima was more vulnerable to injurious factors affecting the arterial walls than the less thickened intima. When hypertension, hyperlipemia or any kind of vascular injuries affected the arterial walls, enhancement of endothelial permeability and stagnation of the insudated blood plasma in the intima occurred more easily in the thickened intima. Particularly, the marginal areas of the thickened intima showed more increased permeability of the endothelial cells.

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Relation of the intimal change in aging of various arteries to progression of atherosclerosis and the morphology of regression of atherosclerotic lesion were discussed. The course of regression of experimental atherosclerosis in rabbits and its histological findings were described.

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Fibromuscular intimal thickening begins to occur early in the pediatric age, with or without lipid deposition. Fatty streaks also appear first in infant. Fatty streaks occur almost always in close association with intimal thickening. Some fatty streaks remain unchanged as those seen in the ascending aorta. Intimal thickening and lipid deposition generally increase with age. The prevalence of those lesions is very high in infants and children. The degree and extent of those lesions display wide individual variability. Finally, intimal thickening is considered to be an integral part of atherosclerosis and to represent the first stage of atherosclerosis. Atherosclerotic lesions, at least a part of them, are derived from thrombosis in association with endothelial denudation. Hyperlipidemia accelerates the atherosclerotic process. Lipid-rich atherosclerotic lesions may regress to some degree under a long normolipidemic state but leave intimal fibrous scarring. Therefore primary prevention of atherosclerosis should be directed as well as secondary prevention.

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The physical properties of the lipids accumulating as spherical inclusions in human atherosclerotic lesions were explored both in vivo and in vitro conditions. They were mostly anisotropic within the cytoplasma of cells and in an average diameter of 1.96 μ. When suspended in hydrophilic media, say of physiological saline solution, in 4 hours they swelled 2.4 times in volume and changed into isotropic form. They were resilient and deformable in three dimensional configuration, and lyotropic in polar media. When dried they underwent a phase shifting from liquid crystal to true solid crystal. These physical properties of lipid inclusions gained in a new significance for their role in metabolic deterioration of intima cells, rupture and necrosis of foam cells, and destruction of the intimal and medial architectures, which set on mesenchymal reactions leading eventually to thickening and hardening of the arteries.

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Clinical and experimental studies have provided an increasing amount of evidence that atherosclerosis is preventable and that regression is feasible. Although the elimination of risk factors would be a form of primary prevention such is hardly feasible in our modern industrial age. Thus the combination of elimination or at least decrease in risk factors and a direct treatment of the arterial wall should help to bring about this prevention and regression. Metabolic changes and/or dysfunction of the vessel wall particularly endothelial cells has been given increasing attention. Energy and cyclic nucleotide metabolism in endothelial cells have been studied in the initiation, progression and regression of atherosclerosis. Several compounds were found to exert beneficial effects on metabolism in the endothelial cells and clinical favorable effects have been documented. Chemotherapy for the treatment of "endotheliopathy" and atherosclerosis will no doubt be the object of intensive studies.

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Total cholesterol level measured in 8, 303 children and youth in Tokyo. Age ranged from 6 to 18 years. The change of total cholesterol level relates to sex and age, and girls showed higher level than boys. Not a small number of children revealed elevated total cholesterol level but some children shoed very low level. HDL-cholesterol was determined and prevalence of ischemic coronary heart disease risk factors was studied. The elevation of total cholesterol level in senior high school students was caused by either increase of HDL-cholesterol or increased total minus HDL-cholesterol fraction. High school boys with obesity were found to have higher serum total cholesterol level accompanied by low HDL-cholesterol level. High school boys of parents with myocardial infarction were found to have higher total cholesterol level. Majority of Japanese senior high school students were found to have one or more coronary heart disease risk factors. The necessity of prevention for ischemic coronary heart disease starting from childhood in Japan is emphasized.

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