Calcification of the coronary arteries was studied on 137 hearts over 50 years of age from a randomly selected autopsy. The hearts were unrolled by the Rodriquez-Reiner method and photographed with super soft X-ray before and after injection of the gelatin-containing barioum sulfate fluid into the coronary arteries. The films were observed stereo-scopically and compared to pathologic findings of the coronary arteries. The extent of calcification and that of stenosis in the coronary arteries were significantly correlated and both of them increased with advancing age, but the former was more intimately related with aging than the latter. The greatest calcific involvement was shown in the heart with myocardial infarction, followed by the heart with small myocardial scar.
Calcific lesions were most prevalent and most extensive in the proximal portion of the left anterior descending artery, followed by the left main trunk, the proximal portion of the right coronary artery and the left circumflex artery.
There was no significant difference in calcific involvement between the normal ECG group and the group presenting ST depression, while the heart weights were heavier in those with myocardial infarction or ECG ST depression than in those with normal ECG. No significant correlation were found between the extent of coronary atherosclerosis and antemortem blood pressure or serum total cholesterol.

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Six cases with painless myocardial infarction were clinico-pathologically studied in comparison to 9 cases presenting painful attack of myocardial infarction. Postmortem stereoagniography of the coronary artery was performed on all the hearts. In addition, change of coronary arterial architecture, development of collateral and its relationship to myocardial ischemic change were studied in 21 hearts with myocardial infarction including 10 sudden death.
The group of painless infarction was significantly older than the painful group, while hypercholesterolemia atd hyperglycemia were more prevalent in the painful group. The heart weight was significantly greater and coronary luminal narrowing was more severe in the painful group, but higher degree of coronary calcification was found in the painless group. Scattered, mostly fibrotic myocardial lesions were observed in the heart of the painless infarction in contrast to massive, partly necrotic, ischemic lesions shown in the painless group.
Arterial anastomoses were well developed in the inter-ventricular septum and the subendocardial zone of the left ventricle in the heart with myocardial infarction. Intramyocardial hypervascular plexus was also demonstrated in the fibrotic lesion, of which age was estimated two weeks to three months after acute necrosis.
This hypervascularity was chiefly confined to subendocardium and consisted of vessels which were mostly 10-50 microns in caliber, thin-walled and running circularly parallel with myocardial fiber. This suggests that the hypervascularity contributed to the repair of myocardial necrosis as a collateral channel.

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Arterial blood gas studies were made on sixty healthy elderlies over sixty years of age and the results compared to those of the fifty young adults in good health under the age. Normal values for the aged and the effects of aging on them were evaluated as follows:
1) Mean value of PaO₂ for each age group from the third to the ninth decade is in order: 93.3±5.8torr. (mean±SD), 85.9±5.4, 85.2±5.1, 84.3±5.6, 82.9±6.1, 81.6±7.8, and 79.4±7.7. The same of AaDO₂ is, 4.9±4.7, 11.5±6.8, 16.4±5.6, 14.6±5.6, 16.3±6.6, 18.0±8.5, and 19.2±10.3.
2) The correlation coefficients and regression equations of those values on aging are: PaO₂=-0.2340×(AGE)+96.4520, r=-0.435 and AaDO₂ 0.287×(AGE)+0.642, r=0.502 for the young, and PaO₂=-0.0621×(AGE)+86.413, r=-0.047, and AaDO²=0.095×(AGE)+10.570, r=0.066 for the elderly. Correlativity between the fractions and age for the elderly is less and the abatement rate of regression curve much milder for the aged.
3) Others as PaCO₂ and PH did not disclose any inconsistency. In conclusion, the PaO₂ regression line in this study demonstrates good accordance in the abatement rate for the young with that in the previous reports, but does not for the elderly; that is, much more gradual at the rate in the present report.

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The pathophysiological meanings of IHD risk factors in the occurrence of IHD have not yet been fully clarified. In order to clarify the significance of abnormalities in the carbohydrate-lipid metabolism as one of the IHD risk factors, we studied the correlation between the glucose tolerance as well as FFA patterns in blood to 50g-OGTT and Master exercise test in 66 cases of elderly subjects (74 yrs. in the mean age), to comparison with 20 young healthy subjects 20.5 yrs. in the mean age) and 20 cases of diabetes mellitus without IHD (40 yrs. in the mean age).
As a result, the following were found out:
1) The reduce of glucose tolerance was noted in 40% of 25 cases with Master-negativity and 36.5% of 41 cases with Master-positivity, showing no statistical significance in the higher rate of Master-positivity in the cases with the reduced glucose tolerance. Rather, the frequency of Master-positivity despite normal glucose tolerance (63.4%) was found significantly higher than the frequency (36.6%) of Master-positivity with the abnormal glucose tolerance.
2) A significant difference was noted in the FFA pattern in blood between the Master-negativity and the Master-positivity (P<0.001). The former indicated Type A which is normal in young and healthy subjects, which indicated the recovery of the once-dropped FFA level in blood into the prior level in 180 minutes after glucose-loading, whereas the latter indicated Type B similar to diabetes mellitus, which showed substantial delay in the revovery of the once-dropped FFA level to the prior level.
3) No significant correlation was noted between FFA_f and FFA₁₈₀ in the Master-positive subjects, where as significant positive correlation with a correlation coefficient of r=0.800 (p<0.001) was noted between the two in the Master-negative subjects.
4) The above results suggest the possibility that the reduced glucose tolerance is not always important factor to the occurrence of IHD and that the abnormality in the plasma FFA pattern to the loading of glucose plays a role as the accerelating factor.
5) There was no significant difference between the FFA pattern of Master-positive patients and that of those with diadetes mellitus, whereas significant difference was noted between the two groups in terms of the FFA value before the loading of glucose, i.e. the latter having been statistically higher than that of the former. In other words, it may be considered possible that factors other than disturbances in glucose tolerance may be correlated to the mechanism of the FFA pattern as seen in the Master-positive patients.
6) The effects of prostaqlandin E₁ (PGE₁) upon the Type B-patterns of FFA as seen in the patients with IHD may be elucidated by that the Type B was changed into Type A by the effect of intravenous PGE₁-administration, creating significant correlation between FFA_f and FFA₁₈₀ (r=0.877, p<0.001). This finding may suggest that the excess in the insulin secretion reaction against the loading of glucose may be related to the mechanism of Type B-FFA pattern in IHD and that delay in recovery of the decrease in FFA caused by the above-mentioned excess may have caused the change from Type A into Type B due to the insulin secretion inhibiting effect possessed by PGE₁.
Conclusion: The above result may suggest that the abnormality in FFA pattern in blood against ingestion of carbohydrates as the IHD risk factor plays an important role which can not be neglected. The fact that Type B changes into Type A by PGE₁ may eventually support the hypothesis that the excessive secretion of insulin against loading of sugars may be indirectly related to the accerelation of atherosclerosis.

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Serum amylase activities of 322 out patients (162 males and 160 females) of various ages raging from 11 to 102 years old were examined by the modified Caraway's Method.
The mean serum amylase values in each age group were as follows: 93.8±24.2U/dl in 10-19 years (40 cases), 85.0±24.2U/dl in 20-29 years (45 cases), 86.7±30.2U/dl in 30-39 years (47 cases), 95.1±29.4U/dl in 40-49 years (45 cases), 101.6±32.5U/dl in 50-59 years (46 cases), 113.1±36.6U/dl in 60-69 years (47 cases), 115.4±34.0U/dl in 70-79 years (42 cases), 99.8±29.2U/dl in over 80 years (10 cases). The serum amylase values tended to increase with age whereas it tended to decrease over 80 years.
On the other hand, serum amylase values correlated with urea nitrogen values (r=0.236, n=322), and negatively correlated with serum albumin values (r=0.236, n=322) respectively.
These findings suggested that both pancreatic and renal changes with age could be the cause of the apparent increased serum amylase values in higher age group.

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A clinicopathological study was made on the amyloid deposition in the aged heart as an index of aging. A total of 108 consecutive autopsy cases (57 men and 51 women), ranging in age from 54 to 94 years was the subject. Three blocks from (1) anterior wall of the left ventricle, (2) interatrial and interventricular septum, (3) junction between the superior vena cava and right auricle, were stained by hematoxylin and eosin, azan and pyridine-congo red, and amyloid was identified by fluorescence and green birefringence.
Amyloid was positive in 23 among 57 men (40.4%), 25 among 51 women (49%), 48 among a total of 108 cases (44.4%). Sex difference was not significant. Increase of the incidence from 41% in the 7th and 8th decades to 50% in the 9th and 10th decades was statistically not significant. Amyloid deposits were found in myocardium in 41 cases, mid to small coronary arteries in 30, and endocardium in 4. Myocardial deposits were found in the atrial septum in 32, pectinate muscle of the right atrium in 23, left ventricle in 4, sinoatrial (SA) node in 3, and atrioventricular (AV) conduction system in 2.
Incidence of conduction disturbances was compared between amyloid positive and negative groups, that is 58% (28 among 48 cases) and 52% (31 among 60 cases) was not significant. In 10 cases conduction system was examined by serial sections, and only 1 of them with left axis deviation (LAD) showed small amount of amyloid in the SA node and right bundle branch, giving no corresponding deposition.
Comments: Aged heart is the predilection site of the amyloid deposition. Using a definition of cardiac amyloidosis as a state producing symptoms such as congestive heart failure or conduction disturbances, our results of 44.4% was the incidence of amyloid deposit, not amyloidosis. Deposition of the amyloid in the conduction system occurred rarely wish few conduction disturbances. Serial sections of the conduction system in various conduction disturbances were negative to the amyloid.
From above results, it was concluded that (1) the incidence of amyloid deposit was high in the aged heart, but cardiac amyloidosis was rare, (2) the most of the conduction disturbances found in the aged were not related to the amyloid.

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