In order to study the etiology of postmyocardial infarction syndrome, the experiments were conducted on both the intact heart muscle antigen and infarcted heart muscle antigen. Whereas no substantial difference was noted between both antigens by either of the agar gel diffusion test and immunoelectrophoresis, the hemagglutination test and hemagglutination in-hibition test revealed the specific antigenicity of each antigen in association with the antigenicity common to both. By analysis of the anti-heart muscle antibody the activity was demonstrated to be present on 2 different spots on the DEAE cellulose column chromatography.
The hemagglutination test using the intact heart muscle antigen was positive in 27% of myocardial infarction and in 6.7% of angina pectoris, while 39 healthy controls gave invariably negative results. Postmyocardial infarction syndrome showed positive reaction to the infarcted heart muscle antigen in all of 6 cases and to the intact heart muscle antigen in 83%.
The hemagglutination titer was higher in postmyocardial infarction syndrome than ordinary myocardial infarction with either of the infarcted or intact heart muscle antigens, and the titer with the former antigen was higher than that with the latter in both diseases.

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Kinin activity and kininogen content of the venous blood from the ischemic arm was measured in 13 volunteers.During the ischemic arm exercise test, the arm became cyanotic and petechias appeared. The vol-unteers complained of numbness at first and then pain. On releasing the ischemia, the pain and numbness tided out immediately, whereas hyper-emia appeared and petechia increased.
During the ischemic arm exercise test, plasma kinin activity showed a tendency to increase while kininogen content to decrease.
It was supposed that kinins were produced from the kininogen during the ischemia and participated in producing pain sensibility.

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A variable, e(t)=p(t)/v(t), is proposed for formulating the ventricular pumping of blood, as a concept of the reciprocal of ventricular compliance, where t=time, p(t)=time course of the intraventricular pressure and v(t)=that of the intraventricular volume. For actual computation, e(t)=p(t)/{v(o)-∫^t_oi(t)dt} where v(o)=v(t) at t=o or enddiastolic volume and i(t)=aortic blood flow. v(o)=(1-ρ)^-1•v_s, where ρ=residual volume ratio measured by a thermodilution method and v_s=stroke volume or integral of i(t) in the cardiac cycle. e(t) is calculated of areflexive left ventricles of dogs under various v(o) controlled by occlusion of the vena cava. In spite of conspicuous changes of p(t), i(t) and v(t), e(t) has ap-proximately unchanged time course and magnitude in a wide range of v(o). A model of ventricular pumping is presented with e(t).

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QRS waves of the spatial magnitude ECG of 70 normal young men and 127 cases of old myocardial infarctions were examined quantitatively. QRS waves of the normal spatial magnitude ECG showed definite patterns and were classified in 5 groups, namely simple triangular configurations (Type A), small notch at the initial (Type B), at the terminal (Type C) or at the both portions (Type D) of the main QRS waves and with large terminal notch (Type E). Among them Type D was considered as the basic pattern of the normal spatial magnitude ECG.
QRS waves of the spatial magnitude ECG changed characteristically in old myocardial infarctions. These abnormal findings consisted of increase of the amplitude and duration of initial notch, slow ascent of ascending limb, prolongation of peak time, decrease of peak magnitude, splitting of QRS waves and increase of the amplitude and duration of terminal notch. These abnormalities were seen in 79.5% of whole cases of infarctions. Abnormalities of QRS waves of infarction type of the spatial magnitude ECG were observed in 67.9% of old myocardial infarctions, whose conventional ECG became less prominent so as not to satisfy the criteria of abnormal Q wave described by Massie et al. with the advancement of recovery process. It was considered that the sequential curves of the changes of the spatial magnitudes of QRS vectors, which had not been taken as to be important previously, had very important diagnostic informations for myocardial infarctions and that the spatial magnitude ECG was very useful for the diagnosis of old myocardial infarctions or latent myocardial injuries whose conventional ECG showed only equivocal changes.

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In 38 isolated bull-frog hearts, ventricular fibrillation was initiated by changing perfusion fluid from Ringer's solution to the low sodium and potassium solution; i.e. iso-osmotic solutions of glucose, fructose, sucrose, tris-hydroxymethylaminomethane, and so on. The ventricular fibrillation thus induced was easily reversible to sinus rhythm and highly reproducible as well, and it could be prevented by the presence of either sodium or potassium ion. During the event, the atrium continued to beat with regular sinus rhythm, except for one deteriorated case which developed atrial fibrillation. One of the precipitating factors was the hydrostatic pressure exerted onto the cardiac cavity.
ECG findings seen in these experiments were characterized by the following:
(1) Immediately after the perfusion medium was replaced, QRS complexes became wider and more bizarre from beat to beat, and QT interval shortened progressively, together with directional T wave change in Y lead, until ventricular fibrillation developed in 20 to 40 sec.
(2) The QRS complex of the first beat of ventricular fibrillation had a short coupling interval with a deflection in the same direction as those of the preceding sinus beats.
(3) The subsequent rapid ventricular rhythm was comparatively regular in its initial stage at the rate of 250 to 400 per min., getting more and more irregular in amplitude and frequency in the course of time.
The mechanisms involved in the production of the ventricular fibrillation have been discussed.

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Two cases of the common atrium associated with persistent left superior vena cava directly connecting into the left side of the atrium are reported. In both patients, the mitral cleft was repaired and the atrial septum was newly constructed with a large teflon-patch. The left superior vena cava was ligated in Case 1, and in Case 2 a tunnel to transfer the emptying orifice of the left superior vena cava to the right side of the atrium was made from a pericardial pedicle. The former was reoperated upon due to the severe residual mitral insufficiency but died after mitral valve replacement. The latter was discharged with a good condition.

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Four cases with ascending aortic aneurysm-two saccular aneurysms, one with dissecting aneurysm of DeBakey's type I and one with aneurysmal dilatation of the ascending aorta associated with aortic regurgitation-successfully operated upon by means of cardiopulmonary bypass, are presented, and the special considerations of surgery of these conditions are described.

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A patient with splenic arteriovenous fistula was reported. The characteristic feature of this case was that the arteriovenous fistula was intrasplenic and associated with 2 splenic arterial aneurysms of great and small size. In our opinion, this arteriovenous fistula is congenital in origin.
Resection of the aneurysms and splenectomy were carried out with success. A brief review was done on the 16 cases among the previous reports documented in literature.

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