From the data of the cardiac catheterization the natural history of the ischemic heart disease, especially of the myocardial infarction was studied. 1. Coronary insufficiency was seen in many cases within three months after the initial attack of myocardial infarction, but rarely thereafter. 2. The late mortality and the attack of myocardial infarction were not predicted by decreased oxygen tension in the coronary sinus blood. 3. Cases with signs of left heart failure had a poor prognosis within five years.

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1. ST depression with negative T was the worst sign for prognosis in this study. 2. Then atrial fibrillation, negative T, RBBB and old myocardial infarction followed in this order. 3. The cause of death of the subjects with ECG abnormalities were closely related. to myocardial infarction, sudden death and congestive heart failure and high frequency of cerebral hemorrhage were encountered in ST depression with negative T. 4. In our 10 years experience the incidence of ECG abnormalities and prognosis significantly depended upon high blood pressure.

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With the data obtained in 1, 413 cases of HHD followed up for 5-15 years, investigations were made into the natural history of HHD treated in the current standard of medical care. HHD is a clinical expression of EH, and is significant particularly in Japan as a factor associated with cerebrovascular fatality. It is especially of importance to regard the degree of this lesion as a measure for the evaluation of the over-all severity of EH.

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The plasma catecholamine determination was undertaken in normal subjects and patients with congestive heart failure. It was found that the concentration of plasma catecholamine was intimately related with its urinary excretory levels, and showed a marked increase in cardiac failure, however this increase had no connection with the underlying diseases but was related to the severity of heart failure. In physical exercise, the increase in plasma catecholamine in cardiac patients was greater than that in normal subjects. The effects of digitalis and sympatholytic agents on catecholamine levels were also observed as well as on clinical progress of cardiac patients. It has been proved that the increased sympathetic activity in cardiac failure would have an important role for improvement of pathological state.

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An elevation of serum levels of CPK, LDH, GOT and concentration of LDH-1 in isoenzymes was observed in two middle aged female patients with hypothyroidism. During treatment with thyroid hormone these enzyme activities fell parallel to the improvement of thyroid function tests, cardiomegaly and findings of electrocardiogram. An increase in CPK, LDH and GOT activity indicates that the source of these serum enzymes may be heart or skeletal muscle. Among two organs heart was considered to be an major source of increased serum enzymes by further analysis of LDH isoenzymes.

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A 15-year-old boy with congenital heart disease showed two types of wide QRS complexes in the limb leads. One type appeared during sinus rhythm with a QRS axis of ca. -45°, and the other during isorhythmic A-V dissociation with a QRS axis of ca. +110°. Transitions between the two rhythms were gradual, and several intermediate QRS complexes intervened. Possibility of parasystolic fusion of upper and lower pacemakers during transitions was discussed.

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In open-heart surgery various forms of cardiac arrest have been utilized, such as potassium citrate arrest, acetylcholine arrest, anoxic arrest, hypothermic arrest and electrical ventricular fibrillation. The introduction of reliable techniques for the correction of acquired valve disease by open-heart surgery has necessiated long period of extracorporeal circulation and prolonged cardiac arrest. But prolonged arrest induced by any method that does not include coronary perfusion with oxygenated blood may be harmful. On the other hand, during electrical ventricular fibrillation, with the coronary perfusion maintained, no significant biochemical or structural changes of myocardium have been demonstrated. However, the periods of electrical ventricular fibrillation reported previously were all within 60 minutes and no detail data of this method for the period of more than 60 minutes has been reported. On this paper, electrical ventricular fibrillation was maintained with coronary perfusion for than 120 minutes, and myocardial metabolism, microscopic structure and myocardial after defibrillation were studied. Methods The experiment was performed on a total of 20 mongrel dogs weighing 10-19kg, but extra-corporeal circulation for about 3 hours was satisfactorily maintained on only 8 of 20 dogs. The heart was perfused through the cannulated brachiocephalic artery by the constant pressure of 130cmH₂0 with blood supplied from oxygenator. In group 1 (2 dogs), beating heart was maintained for 165 minutes, with coronary perfusion. In group 2 (3 dogs), fibrillating heart was produced by the alternating current of 10 volts, 1 second, maintained for 120 minutes, and defibrillated by the alternating current of 120 volts, 0.1 second. In group 3 (3 dogs), fibrillating heart was maintained by the continuous current of 5 volts for 120 minutes, and defibrillated by the alternating current of 120 volts, 0.1 second.

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Myocardial infarction ranks high among the causes of death In adults and the establishment of its prophylactic measures and therapeutic means is one of the primary tasks assigned to today's medicine. In the pathogenesis of myocardial infarction, coronary atherosclerosis plays an important role. Many attempts have so far been made in order to prevent the progress of atherosclerosis, but none of them have led to a directly effective therapeutic means for myocardial infarction. Therefore, the improvement of oxygen supply has been tried through increasing endocardial blood supply. Once coronary sclerosis is established, however, blood flow is not expected to be improved beyond a limited extent. It may be advisable to take a different approach to prevent myocardial infarction by a mechanism of action other than coronary vasodilation. The author studied various models of experimental myocardial infarction, and selected the model described by Rona et al. (1959) because of its easy duplicability, simplicity in procedure and histopathological similarity to myocardial infarction in men. The present study was undertaken to investigate biochemical and histopathological changes induced by large multiple doses of isoproterenol in rats and to obtain information about effects of some drugs on these changes. Methods: 1. Male Wistar rats, weighing 190 to 250g, were used in this study. Cardiac necrosis enlargement were induced by dl-isoproterenol at a dose of 80mg/kg s.c. daily for two days, and examined at various stages. Time course changes in the development of myocardial necrosis were examined by biochemical and histopathological procedures. Effects of some drugs on myocardial necrosis were also investigated. 2. Biochemical determination Serum enzymes: Serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) were measured by the method of Reitman and Frankel, and creatine phosphokinase (CPK) by the Kuby's method. Serum lipids: Cholesterol and triglycerides were determined by the method of Technicon's autoanalyzer methodology N-24a and methodology N-70 respectively. Serum free fatty acids (FFA) were measured by the Novak's method (the animals unfasted). Hematocrit (Ht.): By high speed centrifugation.

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