A correlative study of kinetocardiographic and apexcardiographic traces taken at the left sternal border and cardiac catheterization data was conducted on a group of 57 patients with various types of heart disease.
Several parameters derived from kinetocardiograms and apexcardiograms were examined for the correlation with right ventricular systolic pressure. However, there observed little correlation between them, and, it appeared difficult to obtain any reliable estimate of the pressure from these parameters. The pressure calculated from the II_p-T interval by using the Burstin's method was moderately correlated with the pressure directly obtained by catheterization. However, this method seemed inadequate for clinical use, because of its unnegligible error and a difficulty involved in the measurement of the II_p-T interval.
Nevertheless, kinetocardiograms and apexcardiograms were a useful procedure in detection of right ventricular hypertension and, furthermore, yielded some qualitative information on the level of ventricular pressure. The merit of the kinetocardiogram in this regard was discussed in contrast to the apexcardiogram.

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An on-line system to analyze cardiac arrhythmias was developed by the use of a small scale digital computer. Electrocardiographic signals were fed into the computer, being adjusted within the input range by a buffer amplifier. The analog signals of electrocardiograms were converted to the digital values at a rate of 1, 000 times per sec. for a 20sec. period by an analog-to-digital converter installed in the computer. Then, the digitized electrocardiograms were processed by the diagnostic program. The computation time for the parameter measurement and the interpretation of an electrocardiogram by this system was about 15sec. One thousand three hundred and forty-one electrocardiograms were analyzed. A relatively accurate classification was obtained except atrio-ventricular block.
The automated system of this type would serve as a diagnostic aid for physicians in the routine electrocardiographic interpretation, the mass screening of heart diseases and the electrocardiographic monitoring in the intensive care unit or the coronary care unit.

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In view of the apparent contrast in clinical symptoms between the variant form of angina pectoris and conventional effort angina and of tendency towards the decrease of heart rate at the beginning of the former attack, an entirely different mechanism was assumed between these 2 diseases. Based on this assumption, 3 patients with this disease were studied from the viewpoint of catecholamines in blood. As the result, the decrease of catecholamines in blood, especially adrenaline, immediately before and at the beginning of attack, was established. Based on this fact, the mechanism of the development of the attack of the variant form of angina pectoris was explained by the temporary state of obstruction of the large branch of the coronary artery with advanced stenosis due to the increased tonus, following the weakening of the dilation effect of the coronary artery due to decrease of blood adrenaline at rest. The mechanism of development of specific clinical symptoms might be explained too by fluctuations of catecholamines in blood due to stress such as cardiac ischemia or anginal pain.

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In this experiment, attempts were made to clarify the mechanism with which the pulmonary infarction occurs, from coagulofibrinolytic point of view. The following results were obtained.
1) Injection of the human serum (2ml./Kg.) into the rabbits provoked a hypercoagulative state within 2min. after the injection, followed by a decrease afterward with accelerated fibrinolytic activity. The control level was resumed about 1 hour after the injection.
2) Changes in the coagulofibrinolytic system induced by lycopodium spores infusion progressed slowly toward a marked hypercoagulative state with reduced fibrinolytic activity seen 2 to 3 days later. Injection of the blood clots at this time yielded a high mortality among the animals.However the pulmonary infarction tended to occur in the survived.
3) Although natural liquefaction of the blood clots, when injected at the 5th day after the lycopodium spores infusion, was seen in the majority of the cases, intravenous injection of t-AMCHA in combination with the procedure produced the pulmonary infarction in 62.5% of the animals, and further addition of intravenous injection of the human serum yielded the highest rate (88.9%) in producing the infarct.
The tissue activator was a high activity in the infarcted area for 6 hours after the blood clot injection, but showed a decrease below control level after 3 to 5 days.
4) The same procedure performed I month or later after the lycopodium infusion failed to produce the infarct.
5) It is concluded from these observations that the following 3 factors, cessation of the blood flow in the collateral vessels brought by repeated microembolization as can be obtained experimentally by the lycopodium infusion, hypercoagulative state in the blood, and reduction of fibrinolytic activity, are sine qua non in producing the pulmonary infarction. Embolization of the pulmonary artery with large embolus or emboli, and injury in the capillary beds as might be brought about by a heterologous serum injection are additional factors in the occurrence of the infarcts.

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By altering the calcium, sodium and potassium content of the Tyrode solution, the relationship between the shape of the action potential and of the contraction curve in regard to the changes induced by l-isoproterenol, dl-norepinephrine and ouabain, and at the same time the mode of action of these drugs were sought for. In the normal Tyrode solution, shortening of the duration of the action potential at 25% and 50% repolarization showed a significant correlation with the increment of the contractile force, and the total duration of the action potential showed a significant correlation with the time to the peak tension and with the total duration of the contraction curve at the maximal effect period of these drugs. This relationship was found to be more or less true qualitatively also when the extracellular ions were altered variously.
By analyzing the observed changes, it was concluded that l-isoproterenol increases the contraction, employing chiefly the extracellular calcium ions, whereas dl-norepinephrine and ouabain can increase the contraction by mobilizing in addition the intracellular calcium ions in a calcium-free solution. The increase of contraction by l-isoproterenol is mostly independent of the potassiumion, whereas that by ouabain and dl-norepinephrine occurs in connection with this ion. l-Isoproterenol and dl-norepinephrine increase the contraction directly by driving the calcium ions into the cell rather than by exchanging the sodium ions with the calcium ions. The inotropic action of ouabain does not seem to have any relation with either the sodium ions or the calcium ions entering at this phase.

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Effects of calcium on myocardial cells were investigated in the in situ canine heart. Ninety-three experiments were performed on 28 anesthetized dogs. Solutions of high or low calcium concentrations were perfused into the coronary artery through an artificial coronary circuit. Surface and intracellular electrograms were simultaneously recorded. The most prominent effect of low calcium was the prolongation of the membrane action potential duration. The most prominent effects of high calcium were a shortening or disappearance of phase 2 and a decrease in the amplitude of phase 2. The mechanism of S-T segment elevation is discussed in association with these findings. These observations show that true S-T segment elevation can be caused by the faster repolarization of cardiac muscle cells in the injured area.

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A case is presented of ventricular return extrasystoles showing 2 consecutive re-entry sweeps to the atrium. These rare arrhythmias were observed in a patient with atrial septal defect, who had received digitalis for a long period.

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