Hemodynamics, angiocardiography, electrocardiography, and vectorcardiography were analysed in 15 cases of ruptured aneurysm of the sinus of Valsalva and in 20 cases of ventricular septal defect with aortic regurgitation.
(1) Systolic pressure in the pulmonary artery and ratio of pulmo-nary to systemic blood flow (Qp/Qs) is well related with anatomical findings in ruptured aneurysm of the sinus of Valsalva, whereas not in ventricular septal defect with aortic regurgitation.
(2) Severity of aortic regurgitation is well related with that of ventricular septal defect and pulmonary stenosis in ventricular septal defect with aortic regurgitation.
(3) Rv₅+Sv₁ is well correlated with Qp/Qs in ruptured aneurysm of the sinus of Valsalva, and with degree of aortic regurgitation in ven-tricular septal defect with aortic regurgitation.
(4) Terminal vector in horizontal plane is located at right posterior quadrant in ruptured aneurysm of the sinus of Valsalva, whereas at left posterior quadrant in ventricular septal defect with aortic regurgitation.

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Eighty cases of primary cardiomyopathy were classified clinically into 4 categories. Fifteen of them were autopsied and their pathological classification was shown. Among these 80, clinical pictures of 15 obstructive and 51 non-obstructive cases were outlined. The clinical picture of these 66 cases was, in general, similar to that reported from western countries.
Although specific infectious diseases were omitted from the group, myocardial inflammation was suggested as a possible cause of the myocardial disease in 7 non-obstructive cases.
History as a chronic alcoholic, which has long been neglected in Japan as a cause of cardiomyopathy, was revealed in 6 cases of non-obstructive cardiomyopathy. Their clinical findings suggested a gradually progressing disease of the myocardium, which involved diffusely all cardiac chambers. Predominant right heart involvement was not observed.
The gray area between obstructive and non-obstructive cardiomyopathy was discussed and possible inclusion of the former cases in the latter group was suggested.

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Among 87 infants and children with congestive heart failure due to L-R shunts, 67 (77.1%) developed symptoms and signs of heart failure during infancy. The mode of onset was characteristically insidious, and varied with different types of L-R shunts.
Symptoms and signs commonly observed were tachycardia, tachypnea, prolongation of the time needed for feeding, hepatomegaly, cardio-megaly and roentgenological evidences of pulmonary congestion. The hepatomegaly, a sign of right ventricular failure was almost invariably noted in infants with failure, even in those of PDA, who, as traditionally believed, pertained to the left ventricular decompensation.
Large pulmonary blood flow and high pulmonary arterial pressure were the altered hemodynamics most commonly encountered. The pulmonary blood volume was usually increased, which could be limited or even compromized by the mechanisms, such as pulmonary vasocon-striction or vascular obstructive disease, and shortening of the mean pulmonary transit time. Augmentation of the pulmonary blood flow alone seemed to be not causing significant respiratory distress, such as tachypnea unless left ventricular failure supervened.
Five important factors were pointed out in our present studies as contributing to the development of heart failure due to L-R shunts: 1) Abnormally rapid decrease of the pulmonary vascular resistance following birth. 2) Large size of the defect. 3) Level of the systemic-pulmonary communication. 4) Presence of associated cardiac anomalies. 5) In-fection.

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Time course of pressure/volume ratio of the left ventricle in systole has been proposed as a good index of its pumping properties; the ratio is an approximately steady function of time with its time course almost un-altered by changes in left ventricular end-diastolic volume (preload) and arterial loading conditions (afterload). It is the purpose of the present investigation to compare the ratio in a positive inotropic state with a control in experiments on the dog. The results indicate that the maximum value of the ratio in systole is increased and the time course is shortened by positive inotropism (stimulation of the left stellate ganglion), but that the contour of the time course is approximately unchanged by positive inotropism.

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A simple circulatory device to substitute sufficiently the total cardiac functions was tried. Double valved cannulae were inserted via the right and left ventricular walls to the pulmonary artery and the aorta and con-nected to pulse pressure generators. The pump accepted blood through the inflow valve in the ventricle during negative pressure phase and ejected to the artery through the outflow valve during positive pressure phase.
Over 20 dogs' experiments showed that this complete cardiac bypass method could maintain the left and right atrial pressures, the pulmonary and systemic arterial pressures and cardiac output at physiological condi-tions under ventricular fibrillation. The results of long-term pumping in 10 dogs were over 20 hours pumping in 5 dogs, over 30 hours in 3 dogs and the maximum pumping term was 46 hours.

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The effects of ganglionic blockade were studied on the changes in coronary blood flow and myocardial contraction produced by electrical stimulation of the left cardiac sympathetic nerves in anesthetized open-chest dogs. Stimulation of the left ventral ansa subclavia (AS) and the ventrolateral cervical cardiac nerve (VLCCN) produced 2 peaks of increase in coronary blood flow, in myocardial contractile force (MCF) and in left ventricular pressure (LVP). The first peak was, in some experiments, preceded by an initial transient decrease in coronary blood flow. Bilateral cervical vagotomy or intravenous injection of atropine did not affect the initial changes in coronary blood flow.
In dogs pretreated with intravenous propranolol or practolol, the stimulation of either AS or VLCCN evoked a prolonged decrease in coronary blood flow without appreciable changes in systemic blood pressure and myocardial contractility. The decrease in coronary flow resulting from AS stimulation was blocked not only by intravenous injection of phentolamine but also by hexamethonium (C₆) given into the pericardial cavity or in the coronary artery. On the other hand, the decrease elicited by stimulation of VLCCN was abolished by phentolamine but not influenced by intracoronary and intrapericardial C₆, while hypotension and brady-cardia produced by cervical vagosympathetic stimulation were completely blocked by C₆.
From the present data, it may be concluded that in coronary vessels there exist adrenergic alpha receptors corresponding to the sympathetic vasoconstrictor nerve of which preganglionic fibers terminate in the stellate and inferior cervical ganglia, and that the intracardiac ganglion cells play little role in the coronary vasoconstrictor response after beta adrenergic receptor blockade.

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Myocardial amino acid transport activity was estimated in experimental cardiac hypertrophy with an aid of a nonmetabolized amino acid analogue, C¹⁴-α-aminoisobutyric acid (C¹⁴-AIB). Myocardial AIB uptake was lower than the reported value for skeletal muscle and decreased linearly with increasing heart weight. These differences were discussed in relation to tissue activity to grow. With banding the aorta, myocardial AIB uptake increased within 3.5 days, but only in hearts which have hypertrophied significantly.

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Post-extrasystolic ST, T changes were analyzed in the exercise vector-cardiogram, using Frank's lead system.
(1) The magnitude of ST vector of the post-extrasystolic sinus beat after exercise was not changed in a normal subject, slightly increased in a hypertensive patient and a patient with aortic stenosis and insufficiency, slightly decreased in a patient with intermediate type and markedly increased in patients with angina pectoris, comparing to that of the preceding sinus beat of extrasystole.
(2) The magnitude of the maximal T vector of the post-extrasystolic sinus beat after exercise was decreased in a normal subject, a hypertensive patient and a patient with aortic stenosis and insufficiency, and was increased in a patient with intermediate type. The direction of the maximal T vector of the post-extrasystolic sinus beat after exercise was not changed in non-ischemic patients and changed spatially in ischemic patients.
(3) There were no marked changes in the shape of T loop of the post-extrasystolic sinus beat after exercise in non-ischemic patients and increased widening or narrowing of T loop was seen in the post-extrasystolic sinus beat of ischemic patients, comparing to T loop in the preceding sinus beat of extrasystole.
(4) It is concluded that there was the specific pattern of the post-extrasystolic ST, T changes for local ischemia, that is, they occurred in a way that ST, T changes of ischemic type produced by exercise were accentuated.

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An aged case of atrial flutter with complete A-V block was presented. This combination of arrhythmias was emphasized to be rare, and histological study of the conduction system revealed a fresh degenerative change superimposed on the severe degenerative and fibrotic changes at the penetrating portion of the A-V bundle, which finally produced a complete A-V block.

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A case is reported of anomalous drainage of a persistent left superior vena cava to the left atrium associated with stenotic right superior vena cava. The anomaly was reflected by mild cyanosis and superior vena cava syndrome. Surgical relief was accomplished by transposing the left superior vena cava to the right appendage and widening the right superior vena cava with a pericardial patch graft.

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