In order to clarify morphological differences of arteriosclerosis in various visceral arteries, the cerebral, coronary and renal arteries were morphometrically and histologically investigated.
1. Hypertension enhanced the grade of arteriosclerosis of the major cerebral arteries as well as that of the intracerebral small arteries. The enhancement was markedly observed in cases over age 40.
2. The intracerebral arteries in hypertensive cases showed more varied arteriosclerotic changes than those in other organs. These changes were fibrocellular intimal thickening, atherosclerosis, intimal lipoidosis and edema, fibro-nodular arterial lesion which was resulted from organization of arterionecrosis, and intimal lesions associated with arterial pseudocalcification.
3. The grade of coronary sclerosis was also increased by hypertension. The effect of hypertension on the coronary arteries was more slight than that on the cerebral arteries.
4. Newly formed capillaries in the thickend intima were found more frequently in the coronary arteries than the other arteries. These capillaries were observed in those parts of the intima which were thicker than 400μ for the coronary arteries and 900μ for the cerebral arteries.
5. Diffuse intimal thickening occurred earliest in the coronary arteries.
6. Morphological pictures of intramyocardial coronary sclerosis were fibrocellular intimal thickening and mucoid degeneration. For the pathogenesis of the latter not only hypertension but also hypoxia might be responsible.
7. Histological characteristics of intrarenal arteriosclerosis were intimal laminated elastosis and arteriolar hyalinosis. The severity of the former was increased with hypertension and aging. It was suggested that the elastic fibers in the elastosis were produced by intimal smooth muscle cells. The hyalinosis had a close relation to hypertension. It had a positive parallelism with the grade of cerebral arteriosclerosis.
8. It could be concluded that the differences in histological features and the severity of arteriosclerosis among various visceral organs were induced by differences in arterial wall architecture and hemodynamics, both of which varied depending upon the functions of the different organs.

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The coronary arteries obtained from autopsy cases divided into three groups; (a) control 85 cases, (b) myocardial infarct group 10 cases and (c) hypertension group 12 cases, were studied by various methods consisting of (1) gross and histopathology of the arteries from the cases between new-born and elderly patients (eldest 88 year-old) with various histochemical stains for lipids, mucopolysaccharides and hemosiderin, comparing with aortic atherosclerosis in order to make a statistical comparative analysis of aortic and coronary sclerosis and of aging alterations, (2) resin-cast study on normal vascular architecture, (3) immunohistochemical approach with anti beta-liporotein conjugate, (4) scanning electron-microscopy of coronary and aortic intimal surface, and (5) lipid biochemical analysis by a thin-layer chromatography with a densitometric quantification in grossly “normal” intima and fatty lesions of both coronary arteries and aortae.
Main trunk of the coronary arteries have vasal vasa in the outer layer, at most one-third, of the media. Predisposing sites of atherosclerosis are at branching points and bending locations as many investigators have indicated. In even a new-born infant a localized intimal thickening with fibrocellular proliferation and mucopolysaccharide accumulation is demonstrated. In adulthood even grossly “normal” intima of the coronary arteries contain much more lipid substances than the aortic intima. There are no significant differences of triglyceride content between coronary and aortic intimas in this series. The most characteristic pathology of coronary atherosclerosis is a lumenal obstruction by an eccentrically elevated atheroma at the certain predisposing points of the arteries. Studying serial sections of the arteries, vasal vasa tend to dilate and to be hyperemic and to proliferate from the direction of the adventitia into the media and sometimes even into atheromatous plaques. Around such proliferated and dilated vasa the arterial walls are occasionally and focally edematous or have small foci of macrophage accumulation. Coronary sclerosis has high frequency of secondary hemorrhages within atheromatous plaques, which may be caused by a rupture of such vasal vasa. Communication of the ruptured vasal vasa to intramural hematoma was demonstrated on the serial sections. Circulatory disturbances of the vasal vasa may play in parts an important role, even though it may be a secondary phenomenon, in developing and progressing of coronary atherosclerosis resulting in severe lumenal obstruction.

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Renal arteriosclerosis may be roughly classified into two types, namely the physiological and the pathological. The former develops usually with age, but does not reveal signs of hypertension and renal damages. On the contrary, the latter shows these and its extreme types are well known as malignant renal hypertension.
In this paper, following subjects are stated and discussed;
1. The author's classification method of renal arteriosclerosis observed in the physiological as well as the pathological arteriosclerosis group,
2. The developmental modus relating to age of physiological renal arteriosclerosis and some extraordinal fetal or infantile forms, and the result of a comparative observation on the physiological and the arteriosclerotic group (cerebral hemorrhage, cerebral and myocardial infarction),
3. Characteristic pre- and sclerotic arterioarteriolar lesions observed in cases of two types of typical renal malignant hypertension (the malignant phase of chronic glomerulonephritis and nephrosclerosis),
4. Arterioarteriolar lesions in cases of diabetic nephropathy,
5. Slight but colorful forms of the arteriolar lesion in cases of toxemia of pregnancy.
The conclusions of the present report are as follows;
1) renal arteriolar presclerotic lesions, both slight and severe, being finally come to hyalinosis or sclerosis may be caused by hemodynamic imbalances between the pre-glomerular and the glomerular circulation, resulting simultaneously in more proximal arterial wall-damages of from slight to severe intensity,
2) thus very complex features of renal arteriosclerosis may be formed,
3) the most important difference seen between the cases of physiological and those of malignant renal hypertension is not-existence or existence of predominancy of renal arteriolar pre- and/or sclerotic lesions,
4) organ specificity of renal arteriosclerosis may also depend on this hemodynamic disorder mentioned above.
The results of Sheehan & Davis' experimental studies concerning “renal ischemia with failed reflow and good reflow, “ and that of Matsuoka's using an electric stimulation method of a proximal artery may support the present author's opinion.

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There is some difference in the mechanisms of the initiation and progression of the atherosclerosis between the aorta and coronary and cerebral arteries.
In this paper, morphological characteristics of the aorta and coronary and cerebral arteries, and their relationship to the permeability pattern were studied in the rats and rabbits at the ultrastructural level.
In addition, the influence of renovascular hypertension and/or hypercholesteremia on these arteries were studied.
1. In the untreated control rabbits, reaction products of peroxidase were observed in the vesicles and intercellular junction of the endothelium and in the subendothelial space of the aorta and coronary artery. The ferritin particles were observed in the vesicles of the endothelium and in the subendothelial space of the aorta and coronary artery. But, in the cerebral artery, both the reaction product of peroxidase and ferritin particles were observed only in the vesicles of the endothelium, and they were not observed either in the intercellular junction or in the subendothelial space.
2. Unlike the aorta and the coronary artery, the intima of the cerebral artery showed the barrier function against the permeation of the tracers, as revealed by the presence of the tight or gap junction in the intercellular space.
3. In the rats with renovascular hypertension fed cholesterol for 12 weeks, the foam cell lesions and deposition of the fibrinoid materials were observed in the aorta and coronary artery with enhanced junctional and vesicular transport. No foam cell lesion was found in the cerebral artery, though the reaction product of peroxidase was observed in some intercellular space of the endothelium.
4. In the rabbits with renovascular hypertension fed cholesterol for 12 weeks, the foam cell lesions were freqnently observed in the aorta and coronary artery, but in the cerebral artery only small foam cell lesions were observed at the site of branching.
5. It was indicated that the hypertension might play an important role in the evolution of the cerebral atherosclerosis and the intimal cushion might be the predilective site for the development of atherosclerosis.

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In spontaneously hypertensive rats (SHR), functional arterial constriction and dilatation are noted even at the early stage of hypertension, as observed vitalmicroscopically in mesenteric arteries or ophthalmoscopically in retinal arterioles. When hypertension lasts for at least one month, there is a clear increase in labelled amino acid (proline or lysine) incorporation into the collagenous and noncollagenous proteins of the aorta and mesenteric arteries, thus indicating the accelerated synthesis of both proteins. The former case results in hypertensive diffuse arteriosclerosis and the latter induces medial hypertrophy. Here, both are regarded as kind of “protective mechanism” of the arterial walls, but they increase peripheral vascular resistance and further augment or stabilize hypertension. This basic vascular alteration is different in various organs, and this difference in such protective mechanisms is especially disclosed when severe hypertension develops in SHR.
Stroke-prone SHR (SHRSP) develop cerebrovascular lesions (cerebral hemorrhage and/or infarction) in more than 80% of the population, and organ difference in vascular vulnerability is clearly observed: Arterionecrosis is common in the brain, kidney and testis, but rarely noted in the heart. Renal or testicular arteries and arterioles show also productive alteration, and coronary arteries show mainly medial hyperplasia and hypertrophy. However, in intracerebral arteries, such productive arterial changes are rare.
SHR and especially arteriolipidosis-prone rats (ALR), which have been established by selective breeding for greater reactive hypercholesterolemia from among SHR, develop ring-like arterial fat deposits within a few weeks when fed on a hypercholesterolemic diet. These deposits are noted in mesenteric, cerebral and intrarenal arteries, but rarely in the coronary. For the induction of fat deposits in the cerebral arteries, hypertension is important. However, in mesenteric arteries, such deposits are noted even in prehypertensive or antihypertensive agent-treated ALR, thus indicating a marked organ difference in the vulnerability to fat deposition.
These studies indicate that when hypertension is accompanied with lipidemia, it induces not only arterionecrosis but also acute arterial fat deposition. Mesenteric, renal and cerebral arteries are vulnerable to these hypertensive vascular lesions, but only coronary arteries are rather resistant to them. The immunity of coronary arteries to hypertensive lesions is thought to be ascribed to their relative low perfusion pressure, because they are mainly perfused in the diastolic phase.

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A model study was undertaken to investigate disturbances of blood flow through stenotic blood vessels. Both axisymmetric and nonsymmetric models, having different diameter ratios of constriction, were used in the experiments. (1) Experiments with steady flow. A sudden decrease in the critical Reynolds number took place as the degree of axisymmetric constriction increased. Even at Reynolds numbers far below the critical value, a region of flow separation was clearly seen just behind the constriction. An eddying wake inside the separated region spread downstream as the Reynolds number increased. At the critical Reynolds number vortices were formed at the distal end of the wake and shed downstream in succession. Two symmetrical standing eddies were noticed within the separated region behind a hemispherical bulge projecting into the boundary layer. Further increase in Reynolds number resulted in the formation of secondary flow. The horse-shoe vortex, which passed round the front of the bulge in both directions and led to a vortex pair trailing downstream, is a secondary flow ensued from a radial pressure gradient generated by a bluff obstacle within the boundary layer. (2) Experiments with nonsteady flow. A striking feature of a pulsatile laminar flow through a circular cylinder was the appearance of reverse flow near the wall at the end of the decelerating phase. The presence of an axisymmetric constriction caused pulsatile disturbances. With the progress of acceleration, large vortices were formed near the constriction, shed downstream and broken down into turbulence. The turbulent flow thus formed did not diminish during the decelerating phase but spread upstream against the flow direction until the start of next accelerating phase. Pulsation seemed to facilitate not only the production of vortices but also the backward spread of turbulence formed downstream.

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1) The contents of GAG of the various arteries from Japanese autopsied cases were measured. The lower percentage of chondroitin sulfates (CS) and the higher percentage of heparan sulfate (HS) in total GAG were the characteristic features of the grossly normal cerebral, internal carotid, external carotid and femoral arteries.
2) The CS and HS purified from the cerebral arteries and aortas were used for binding study with plasma lipoproteins (LDL and HDL). The binding capacity of CS from both the cerebral arteries and aorta to LDL was higher than that of HS, but that of CS and HS to HDL was not found. The CS from the cerebral arteries contained higher DS%, lower CS-4-S% and bound more strongly to LDL than that from the aorta. These results may suggest the strong binding capacity of DS or inhibitory effect of CS-4-S on binding to LDL. The atherogenesis in the cerebral arteries was discussed in comparison to that of the aorta.

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Regression of experimental atherosclerosis has been introduced by some investigators. This paper represents the regression of atherosclerosis in the respect of vascular permeability, aging of aorta and the reversibility of early atherosclerotic lesions (e. g. fatty streak, cloudy thickening and mural thrombi).
Ultrastructurally, aortic intima consists of three layers and increased in thickness in the aged group (over 60yrs). In this group, most remarkable change is thickening of the inner layer of intima, connective tissue layer. There are atrophy of intimal myogenic cells, extracellular basement membrane-like material deposits and proliferation of disrupted fibrillar elastic and collagen fibers. The result shows the severity of regression of atherosclerotic lesions in such an aged group because of its morphological findings.
Vascular permeability of human common carotid artery by means of 1% ferric citrate infusion is presented. In the aged group, ferric citrate is condensed in the superficial zone of intima and is caught in the elastic lamina of media. It seems to be thought as the decrease of whole vascular permeability. In the advanced atherosclerotic lesions, there is a lowering of ferric citrate permeability. On the other side, initial lesions of atherosclerosis shows high vascular permeability. These findings of vascular permeability reveal that there must be complicated circumstance behind the regression of atherosclerosis.
Early lesions of atherosclerosis seem to be all reversible when the lesions are not severe and the lack of irreversible destruction of intimal structure and fibro-cellular proliferation.
Experimental aortic atherosclerosis of rabbit induced by cholesterol feeding for 8 weeks showed a tendency to the depletion of aortic fatty lesion 6 weeks after returning to the basal diet.
And the author observed the process of organization of experimental aortic thrombi in rabbit. This complete results of experimental atherosclerosis should be reported in detail afterwards.

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Studies on atherosclerosis have been recently focussed on the pathophysiological or metabolic changes of the cellular components of arterial wall and on their roles in atherogenesis and on the regression of atherosclerosis. On the other hand, cyclic AMP is well known as an intracellular second messenger of various hormones and amines to regular the function of cells. This paper is subjected to search on the roles of cyclic nucleotides in progression and regression of atherosclerosis.
Sixteen healthy rabbits were fed 150g daily of commercial diet containing one per cent of cholesterol for 15 weeks. At this point, 4 rabbits were sacrified to measure cyclic nucleotides in aortic wall, compared with those in the aorta of 4 control healthy rabbits. The other 8 rabbits were fed 150g per day of commercial diet for 10 weeks and during this period, four rabbits were given a placebo capsule and the other four received a capsule of 10mg/kg of EG-626, every morning, which was synthesized by Ishikawa and Shimamoto in 1973 as a potent cyclic AMP phosphodiesterase (cAMPP DE) inhibitor.
Statistically significant increases in cAMP phosphodiesterase activity in atherosclerotic lesions were observed in the rabbits fed cholesterol for 15 weeks, compared with these in aortic intima of normal control rabbits. Conversely, the level of cAMP showed a decrease without a statistically significant difference. Histological study revealed typical cholesterol induced atherosclerotic lesions characterized with large amount of foamy cells. In regressive studies, a statistically significant decrease of cAMPPDE activity and in turn increase in the level of CAMP were obtained in atherosclerotic lesions, compared with that in cholesterol-fed rabbits. These changes of cyclic nucleotides were remarkable in the atherosclerotic lesions of EG treated rabbits, which were histologically characterized with the disappearance of foamy cells and the increase of regenerated smooth muscle cells.
These studies suggests that changes in cyclic nucleotides may possibly be a good parameter to evaluate the regressive effect and trials to prevent the increase of cAMP phosphodiesterase activity and the decrease in the level of CAMP may produce the effect protecting arterial wall from fatal hazard by modifying atherosclerotic lesions.

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The role of diet in development of ischemic heart disease (IHD) has been known to be important. Our epidemiological study clearly revealed the significance of hypo-albuminemia caused by a low protein-intake on IHD.
In this study we report both the effects of a low caloric diet with relatively high protein-content on risk factors for IHD and the results of follow-up study for subjects who had treated with the diet. 228 of hospitalized patients, who suffered from ischemic or hypertensive heart disease without necessity of drug-therapy, consumed the formula diet—dialy intake of calories was 1000 containing 130-140g of carbohydrate and 80g of protein—during administration. Of the patients with hypertriglyceridemia (over 100mg/ 100ml) or hypercholesterolemia (over 200mg/100ml), 77 or 86 percent, respectively, were significantly decreased in these levels by the diet therapy for 4 weeks. Additionally, the decreased level of triglyceride was in proportion to the initial level. The proportional relation of decreased level caused by the diet with the initial level of cholesterol was up to 250mg/100ml.
In our recent report in regard to the mechanism of producing hypercholesterolemia, the hydrolysis of triglyceride in very low density lipoprotein was initiative step for control of serum lipid-level. Consequently, these results were estimated that the excess calory-intake might be important factor for producing hyperlipidemia as same as obesity.
On the other hand, low level of serum albumin repaired also by the diet. Moreover, it was clearly showed, that lower exercise capacity examined by the Master's two step test was strinctly correlated with lower level of albumin when the subjects were divided into 3 groups according to degree of exercise-capacity. 375 of patients with IHD, who had received the diet treatment and the physical training during administration with essential details of instruction, were followed up. Percent surviving at 10 years was clearly different when the subjects was divided 3 groups according to whether they had keeped the instruction for the diet and/or physical training or not. Additionally, though the patients, who had remained the exercise capacity of discharge-period up to followed up period, has kept normoalbuminemia, serum albumin in patients who had not remained the exercise capacity of discharge-period extremely decreased after discharge.
These results are clearly indicated that not only the diet but also the physical training plays the most important role for development of IHD and death caused by IHD, especially correlation between serum albumin level influenced by the content of diet-protein and physical activity is the most important problem for IHD in Japan.

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The present study was conducted to assess the various risk factors responsible for the development of atherosclerotic vascular diseases among Japanese with or without dietary modifications.
Eight hundreds and eighty-three of subjects, including 707 males and 176 females, were enroled in this study, and they were divided into 4 groups according to the presence of hyperlipidemia and hypertension.
The mean period of observation for all 883 subjects is 3 years, ranging from 1 to 5 years.
Dietary instructions for hypertension, obesity and hyperlipidemia were given at the first checkup.
The principle of dietary instruction was based on the restriction of salt for hypertensives, low caloric intake for obesity, and the limitation of saturated fat and cholesterol for hyper-cholesterolemics and low calorie with high poly-unsaturated fat for hypertriglyceridemics.
And subsequently ninety subjects whose degree of the adherence to the dietary modification were later revealed were divided into 3 groups on the basis of the cooperability.
(1) Hyperlipidemics at the first check-up revealed the tendency to reduce their serum cholesterol and triglyceride (TG) levels after the dietary instruction.
(2) Subjects with type IV hyperlipidemia were more frequently encountered under the age of 55, while type IIa hyperlipidemia were relatively more prevalent over the age of 55 in male.
(3) At the second check-up, the incidences of hyperlipidemia from non-hyperlipidemics during the observation were in 21% males and in 33% females, among whom type IV and type IIa were respectively the highest.
(4) The incidences of diabets mellitus, obesity and hyperlipidemia were higher in hyperlipidemic groups, and LVH and coronary ischemia were frequently observed in hypertensive groups.
(5) The significant fall of plasma concentrations of cholesterol and TG and apparent improvement of diabetes mellitus, obesity and hyperuricemia were observed in the cooperative group. There were two cases with non-fatal myocardial infarction in the non-cooperative group.
(6) The number of the overall accidents of vascular disease were 14 cases during the observation period.
Concerning the risk factors in these accidents, hyperlipidemia was found in 8 of 9 cases with ischemic heart disease. Hypertension was accompanied with all 4 cases of cerebral thrombosis and one case of subarachnoid hemorrhage.
Obesity and the habit of heavy smoking tended to accumulate in the cases of myocardial infarction.
In conclusion, the present study strongly suggests that dietary control against the risk factors would be a great armamentarium for the prevention of the atherosclerotic catastrophe.

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We have synthetized two compounds —pyridinolcarbamate and phthalazinol— which are commonly active in preventing the edematous arterial reaction of rabbit aorta, and in antagonizing the vasocontracting and platelet-aggregating effect of thromboxane A₂. They have no vasodilative effect in therapeutic doses. The potency of phthalazinol in roughly 10 times greater than that of pyridinolcarbamate. Thromboxane A₂, besides its highly potent vasocontracting and platelet aggregating effect, has been known to inhibit the release of lipid from adipocytes. This profoundly lowers cyclic AMP of adipocytes by inhibiting the activity of adenyl cyclase.
Such evidence shows the importance of research to see whether the two above-mentioned thromboxane A₂ antagonistic substances exert any anti-atherosclerotic effect in man and animals.
(1) Experimental evidence
In the experiments with rabbits, the anti-atherosclerotic effect of pyridinolcarbamate has already been reported. In this paper the anti-atherosclerotic effect induced by the daily administration of phthalazinol (20mg/day, p. o.) on atherosclerotic rabbits, produced by cholesterol-feeding (1% cholesterol pellets for 15 weeks), was introduced. The treatment was performed under a cholesterol-free diet. The 15 weeks and 30 weeks regimes were compared.
The elimination of cholesterol from the aorta was definitely accelerated by phthalazinol as compared with placebo. It became statistically significant in the 30 weeks regimen. The histochemical analysis revealed a significantly faster removal of stainable lipid (by Oil red-O) from atheromatous lesions of the treated group, compared with the placebo group. And it became much more pronounced in the 30 weeks regimen than the 15 weeks regimen, including the differences in the other histochemical parameters, showing a definite enhancement by phthalazinol in regression of atheromatous lesions.
The cerebral thrombosis of rats (Furlow and Bass, 1974), cerebral hemorrhage of stroke strains of spontaneously hypertensive rats, kept on 1% salt water for 5 weeks, cerebral hemorrhage of spontaneously hypertensive rats induced immediately by intracarotid injection of thromboxane A₂ mixture (Shimamoto et al 1976), and experimental cerebral infarction induced by an intracarotid injection of thromboxane A₂ mixture in rabbits and experimental myocardial infarction induced by its intra-coronary injection in rabbits respectively, were significantly prevented by phthalazinol in a dose of 0.1-1.0mg/kg given intravenously. Such preventive effects were considered to come mainly from the thromboxane A₂-antagonistic effect of phthalazinol, if not all.
(2) Clinical evidence
In order to confirm an anti-atherosclerotic effect of a drug (1) an angiological improvement of the plaque, (2) an increase in the nutritional tissue flow of ischemic lesions, and (3) an improvement in prognosis are required.
In clinical applications of pyridinolcarbamate, a double blind trial of 2 years regimen with pyridinolcarbamate (2g/day) and placebo has been performed by Terry et al (1975). They evaluated their data in 38 patients suffering from advanced atherosclerosis of the lower extremities by an angiographical technique. They showed a statistically significant preventive effect on progression of angiological changes of the arteries of their lower leg by pyridinolcarbamate (P<0.001).
The atherosclerotic gangrene of 135 cases was challenged by inositol niacinate (1.2g daily) and by pyridinolcarbamate (1.5g daily) by Mishima et al under the double blind trial. They showed a favorable response with pyridinolcarbamate, significantly more effective than the vasodilator (P=0.0006).
The preventive effect of pyridinolcarbamate on apoplectic attacks, among postapoplectic patients, has been shown by Kato, Goto et al by their well-controlled 4 year observation. A significant improvement in prog

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The main antilipemic agents now in use and at the stage of clinical trial are hereunder enumerated by action. Most of the following drugs are in use selectively according to the type of hyperlipemia:
1. Preventing the absorption of cholesterol β-Sitosterol, Nicomol (Cholexamin), Linoleamides, Cholestane-triol, Alisol A monoacetate etc.
2. Preventing the absorption of bile acid Cholestyramine, Colestipol, Neomycin, Dimethylaminoethyl Sephadex etc.
3. Inhibiting the biosynthesis of cholesterol Clofibrate (CPIB, Amotrol), Simfibrate (Cholesolvin), S-8527 (Lipoclin), Halofenate (MK-185), Tibric acid, Nicotinic acid etc. Anabolic Steroids
i. 2-Hydroxymethylene-17α-methyl-dihydrotestosterone (HMD, Anadrol)
ii. 17β-Hydroxy-17α-methyl-5α-androstano [2, 3-C] furazan (Miotron)
iii. 17β-Hydroxy-17α-methyl-2-oxa-androstan-3-one (Oxandrolone, Vasorome)
iv. 17α-Ethyl-17β-hydroxy-estr-4-ene (Ethylnandrol, Orgabolin)
4. Accelerating the catabolism of cholesterol Thyroid hormone (D-thyroxine), Acetiromate (TBF-43), Estrogen, Unsaturated fatty acids, EPL (Essential phospholipid), Cholagoga etc.
5. Influencing the transport and/or distribution of lipids Heparin and heparinoids, Dextran sulfate, Elastase etc.
6. Reducing the lipoperoxide in the serum Riboflavin tetrabutyrate, dl-α-Tocopheryl nicotinate etc.
It is ascertained by epidemiological survey and experimental studies that there is a correlation between hyperlipemia and atherosclerosis. It is also certain that to reduce the serum lipids is an effective measure to prevent the onset or progress of atherosclerosis. Many antilipemic agents have been developed by these principles. The papers, reporting the effectiveness of antilipemic agents for primary or secondary prevention of coronary atherosclerosis, support these principles.
However, as was recently reported by the Coronary Drug Project of the USA, such papers became occasionally seen as reporting that the treatment by these natilipemic agents is not always effective to prevent the progress of atherosclerosis. It must be said therefore that these reports gave an opportunity for severe reconsideration on the treatment of atherosclerosis with antilipemic agents.
Although the relation of hyperlipemia and atherosclerosis is ascertained as mentioned previously, there are some problems to expect the therapeutic effect by the treatment only with antilipemic agents, since the atherosclerosis is considered to be a multifactorial disease.
The treatment with antilipemic agents can hardly be considered at the present stage to be of no use as a therapy for atherosclerosis since the relation of hyperlipemia and atherosclerosis is already confirmed as mentioned and to reduce the serum lipids is currently authenticated as an effective measure to prevent the progress of atherosclerosis. It must be however pointed out that the development and the use of antilipemic agents require circumspection.

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ヒト大動脈粥状硬化巣内に線維素の存在をみることは多いが, アテローマの進展にどのような役割をはたしているものか明らかでない.
筆者等は15例のヒト大動脈より330個のプラーク (atheromatous plaque, fibrous plaque) を選び, そのプラーク内における線維素の分布, 由来, 意義等について検索した.
プラークは, 線維素の分布形式より3型に分けられる. I型はプラーク内部のアテローマ性脂肪沈着部の辺縁に線維素が分布し, ときに内膜表層部とアテローマ粥との間に連絡がみられるもの, II型はアテローマ粥中にほぼ均等に線維素が分布するもの, III型はプラーク表層部に線維素が斑状, 層状に分布を示すもの等に分けられ, その頻度はII型, I型, III型の順であった. その線維素の由来について血管内腔かうの血漿成分のしみこみ, 出血, vasa vasorum, 血栓からのものが考えられた. I型, II型を示すものは血管内腔, vasa vasorum (主に血管内腔) からのしみこみが考えられ, III型は fibrous cap 内に線維素の存在とともに時には赤血球を混ずることがあり, 壁の破れから血液成分のしみこみ, あるいはアテローマ表層に二次的に形成された血栓に由来するものと思われた. なお, fibrous plaque では, ほとんど線維素の沈着はみられないが, みられたものはIII型の分布形式を示し, 血栓由来を思わせた.
アテローマ粥内に線維素が沈着することにより, 壁の組織障害, 細胞成分の増生をうながし, アテローマ病巣の進展の一因子になると考えられた.

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心筋梗塞の発病が不一致であった54歳の男子1卵性双生児について検討し, 心筋梗塞の進展に及ぼす遺伝と環境因子について分析し下記の結果を得た.
1) 兄の心電図所見は正常範囲内であったが, 弟には陳旧性後壁心筋梗塞が認められた. 心筋梗塞の不一致の期間は, 現在まで8年間と推定された.
2) 環境因子の差異としては, 兄の職業は鮮魚商, 弟の職業は設計技師であり, 経済条件は兄に比べて弟が良好であったことがあげられる. このため食事摂取量は兄に比べて弟が多く, 弟の飲酒量は兄の約10倍であった. 食塩の摂取量も兄に比べて弟が多かった. 喫煙量には差異はみられなかった.
3) Coronary risk factor の相違は, 兄に比べて弟に高度の肥満がみられ, 糖代謝異常も著しく, コレステロール, 中性脂肪の値もたかかったこと, 寒冷昇圧試験および運動負荷時に血圧の上昇が弟に認められたことなどがあげられる.
4) 摂取カロリーの差異は, 弟に著明な肥満をひきおこし, 両者間の糖代謝異常, 高脂血症に差異を招来している. 肥満とNa摂取量の差異は, 弟に血圧上昇を招来し, これらの因子が弟に心筋梗塞を発生せしめたものと考えられる.

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