In Japan the incidence of myocardial infarction or Q^1-1 of Min-nesota Code is 0.24%-0.54% in epidemiological survey, and the incidence of total cases with Q^1-1-Q^1-3 is about 1.0%. The incidence of ischemic heart disease in epidemiological survey is 2.1 %, and the death from arteriosclerotic heart disease including coronary heart disease (B26a) in vital statistics is 3.7%. The incidence of reported myocardial infarct in autopsy cases is 2.04%. The incidence of death from ischemic heart disease was increased in crude death rate and also in age adjusted death rate in Japan.
Myocardial infarction and ischemic heart disease are found more in male and increased with ages. There is some difference of death rate from ischemic heart disease, the incidence of myocardial infarct in autopsy cases and the incidence of ischemic heart disease in epidemiological survey according to the areas in Japan. The some areas, of which death rate from ischemic heart disease was higher than adjacent areas, were dis-cussed.

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The autopsies performed at the Kuakini Hospital during a 10-year period (1957-1967) on patients of Japanese ancestry in Hawaii were re-viewed to determine the frequency of hypertension and adrenocortical ad-enomas.
There was a total of 948 autopsied patients of Japanese ancestry of which 313 (33%) were hypertensive with a higher frequency in females (37.6%) than in males (31.6%). There were 51 (5.4%) cases with adenomas and 44 (4.6%) with hyperplasia in the entire group. But of these, 48 (15.3%) cases with adenomas and 40 (12.8%) with hyperplasias were in the hypertensive group, with an increasing incidence with age.
Perhaps, as Conn has postulated, a number of these patients with adrenal adenomas in the hypertensive group in this study, may have had primary aldosteronism. Moreover, the possibility that some of the patients with nodular hyperplasia having had primary aldosteronism cannot be dis-carded.

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A clinicopathological study was made on 6 cases (5 women and a man) of so-called functional aortic regurgitation. A new etiological concept was proposed for this category of aortic regurgitation as degenera-tive type due to a prolapse of the posterior cusp of aortic valve. Prolapse of the cusp was explained by an interruption of the transverse ridge due to fibrinoid, hyalinoid, atheromatous or calcified lesions.

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By utilizing endomyocardial biopsy, the clinical diagnosis and clas-sification of primary myocardial disease is possible. This procedure will immediately eliminate the possibility of such secondary myocardial diseases as sarcoidosis, amyloidosis, glycogen storage disease and myocarditis.
Histopathologic differentiation of primary myocardial disease was investigated by analyzing the pathologic and diagnostic significances of endocardial and myocardial lesions at probable sites of pathology of 126 autopsied or biopsied cases of different diseases and in numerous biopsy specimens from 173 cases of myocardial disease. At varying intervals following biopsy, 9 cases were autopsied. Biopsy and autopsy findings correlated well.
The following histopathological findings were noteworthy.
1. Endocardial thickening: This is a characteristic finding in endo-cardial fibroelastosis. Other endomyocardial diseases can be diagnosed when various causal genetic factors are excluded.
2. Myocardial hypertrophy: Size of muscle fibers, fragmentation of myofibrils, vacuolization, pyknosis and pleomorphism of nuclei and derangement of muscle bundles should be noted.
Interstitial fibrosis accompanies the advanced cases.
3. Myocardial degeneration or fibrosis: Vacuolization, hydropic degeneration, swelling, pleomorphism, basophilic or mucoid degeneration and deposition of other abnormal substance are to be recorded. Artifacts should be disregarded.
When attempting to establish a histopathologic biopsy diagnosis, such factors as inflammatory, toxic, thrombogenic, anoxic, hemodynamic, mechanical and metabolic conditions should be excluded as far as possible.
It should be emphasized that an endomyocardial biopsy is one of the most important diagnostic means to determine the classification when combined with other diagnostic methods.
Finally, we must reaffirm that the negative biopsy report does notdeny the presence of the disease.

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The isolated rat heart is perfused with adenosine-8-C¹⁴, or a mixture of ATP-8-C¹⁴ and ATP-γ-P³² of known isotope (C¹⁴/P³²) ratio. The results indicate that any difference between the rate of incorporation of adenosine-C¹⁴ or ATP-C¹⁴ into myocardial nucleosides and nucleotides fraction did not show significance, and also that any difference of the C¹⁴ distribution in the perfusates between adenosine-C¹⁴ and ATP-C¹⁴ perfused by the isolated rat hearts did not show singnificance.
When perfused with C¹⁴-and P³²-ATP of known isotope ratio, ATP isolated from the myocardium showed an isotope ratio (C¹⁴/P³²) approximately 5 times greater than that of ATP in perfusion fluid.
These results suggest that ATP might be first degraded and later resynthesized intracellularly.

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Effects of epicardial perfusion using dilute hydrogen peroxide for the ischemic myocardium were studied. Rabbits with ligated coronary arteries were used for this experiment. Following conclusions were obtained from this experiment.
1) Preventable effect for the onset of ventricular fibrillation was recognized with H₂O₂ perfusion.
2) Effectiveness for the cardiac resuscitation in situation of ventricular fibrillation was observed during H₂O₂ application.
3) Ischemic changes in ECG were improved after the perfusion.
4) Shock due to myocardial ischemia was improved by perfusion and nearly normal arterial pressure maintained during the H₂O₂ perfusion.
5) Myocardial oxygen tension increased immediately after the perfusion started.
6) Decreased M-Nade oxidase within myocardium was sustained after the H₂O₂ application.
7) Application of dilute hydrogen peroxide, in the form of epicardial perfusion, may prove to be useful for the ischemic myocardium.

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1) Unilateral pulmonary artery occlusion with an inflatable balloon was carried out in dogs, monitoring end-tidal CO₂ concentration from the occluded lung as an indicator of the pulmonary blood flow.
2) As the balloon was inflated gradually up to the complete occlusion, the pulmonary arterial pressure was elevated stepwise in parallel with stepwise reduction in the end-tidal CO₂ concentration or CO₂ output. The elevation in the mean pulmonary arterial pressure, which was observed consistently, was 72% above the control value with the right sided occlusion and 42% with the left, when the complete occlusion was accomplished.
3) Although further inflation of the balloon was attempted to distend the pulmonary artery, no additional elevation in the pulmonary arterial pressure was observed.
4) When a branch of the pulmonary artery or a lobar artery was occluded, an elevation of a lesser extent in degree in the pulmonary arterial pressure was obtained.
5) No difference in changes in the pulmonary arterial pressure between the internal occlusion and the external ligation was seen.
6) The systemic arterial pressure showed no consistent change during the procedure except for transient "initial drop" seen in most of the experiments.
7) It was concluded that the elevation was solely due to its mechanical effect.

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Distribution and mode of excitation of the cardiac sympathetic receptors following mechanically induced circulatory changes were examined in dogs anesthetized with pentobarbital sodium under artificial respiration and the following results were obtained:
The receptors, from which the afferent impulses originated and traveled in the left upper thoracic white rami, were distributed on the surface of the left ventricle, left atrium, left coronary artery, ascending and descending thoracic aortae, main pulmonary artery, left pulmonary veins, pericardium, pleura of left side and in some cases on the surface of the right ventricle near the anterior descending artery. On the other hand, the afferent impulses recorded from the right upper thoracic white rami were from the right ventricle, right atrium, main pulmonary artery, right pulmonary veins, right side of aortic root, superior and inferior caval veins, pericardium, pleura of right side and in some cases from the surface of the left ventricle near the anterior descending artery.
The afferent impulses from the left ventricle appeared spontaneously at each ascent or in some cases, on the contrary, at each descent of the left ventricular tension or pressure. The impulses increased with post-extrasystolic potentiation of the left ventricular contraction. Also, they increased with an increase in left ventricular contraction produced by occluding the aorta. On the other hand, carotid sinus stimulation resulted in a decrease in number of the impulses per beat. The impulses increased during occlusion of the anterior descending branch of the left coronary artery with or without tugging. Also, they increased markedly following coronary embolism.
It was concluded from these findings that the afferent sympathetic fibers originated from the receptors in the left or right ventricle traveled respectively in the left or right upper thoracic white rami and that the cardiac receptors which are considered to participate in pain sensibility were activated by mechanically induced circulatory alterations.

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A case of total anomalous pulmonary venous drainage, in which the connection with the systemic circuit consisted of a common vein passing through the diaphragm to enter the region of the portal vein, was presented.
Thirty-eight cases were added from the literature to Jonson's 17 cases and diagnostic and surgical aspects of this rare malformation were discussed.

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