In regard to the mechanism by which congestive heart failure arises, two main concepts have been advocated : the so-called "forward-failure" and "backward-failure" theories. But certain features of congestive heart failure are not satisfactorily explained by either theory. Professor M. Maekawa has developed a "modified backward-failure" theory, from which he concludes that with the inability of the heart to eject enough blood to meet the demands of the tissues, there exists not only a diminished forward output of blood from the heart, but also a disturbance of sucking the blood from the veins into the atrium, and both go hand in hand to develop congestive heart failure. The purpose of this study is to present from a pathologic point of view the factors or mechanisms which induce clinical manifestation of congestive heart failure. Special attention is focused on (1) cardiac dilatation and hypertrophy, (2) the pathologic changes in various organs where the heart had failed, and (3) the relationship between the pathologic changes in the heart and those in various organs.The material available for this study consisted of 46 autopsies performed on subjects with congestive heart failure at the Department of Pathology, Univeristy of Kyoto from March, 1927, through August, 1950. The clinical records and autopsy protocols were studied, and histological material was available in 23 cases. The weight of various organs was compared with the calculated normal weight for age and sex in 5, 000 autopsies performed at the Department of Pathology, University of Kyoto. The summary and conclusion of this study is as follows : 1. In subjects with congestive heart failure, cardiac weight was 900-260 g.; increase in cardiac weight over calculated normal, 361-10%; the ratio of the cardiac weight to the body weight, 2.5-0.78%. The thickness of the left ventricular wall measured at the anterior middle part of the heart was 2.7-1.2 cm., and that of the right, 1.5-0.4 cm. These results indicate that almost all hearts which had failed showed more or less a tendency to enlarge and this enlargement occurred at the site where the strain existed or the chamber retrograde from the site of disturbance.2. Though the microscopic study revealed various myocardial, valvular or vascular abnormalities none was specific for the heart which had failed, nor could they explain the development of heart failure ; cardiac failure could not be attributed to these cardiac lesions alone. In many cases of rheumatic heart disease, inflammatory changes and lesions of coronary arteries were found.3. Though venous congestion of the lungs or the liver was striking, kidneys showed only a slight evidence of venous congestion. This indicates that the passive venous congestion is localized in the organs proximal to the heart.4. As for main pathologic changes, the lungs showed congestion, and thickening of alveolar wall, and in one case extensive fibrosis was found. The liver showed congestion, degeneration, atrophy or necrosis of the liver-cells, increase in connective tissue and cirrhosis ; spleen, enlargement or atrophy and hyaline degeneration of arteries ; kidneys, only a slight congestion and sometimes infarction. Besides these findings in cases of hypertension, arteriosclerosis and syphilis, arterioscleroic kidney was found as a complication.5. In about 50% of the cases, the liver showed an evidence of increase in connective tissue, or cirrhosis. But no definit relationship between these changes and ascites was found.6. Cardiac hydrothorax was found in about 50% of the cases, in which the right hydrothorax was more frequent than the left and even in the case of biliateral hydrothorax the larger effusion was localized in the right pleural cavity.

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Nehb's leabs, leads D, A and J, which was proposed by W. Nehb in 1938 were hardly regarded in the American and British literature. But in Germany Nehb's leads were appraised as considerably valuable in the diagnosis of myocardial infarction and some of the Japanese investigators also supported Nehb's opinion.In this paper, the value of the Nehb's leads in the diagnosis of infarction has been examined by the correlation between the electrocardiographic and post-mortem findings of 30 cases in the series of 35 cases of myocardial infarction. Of these 30 cases, in the majority the Wilson precordial leads, the Goldberger unipolar limb leads and the standard limb leads, and in few cases from two to five CF leads and the standard limb leads were taken together with the Nehb's leads.The author considered that in the diagnosis of infarction in the Nehb's leads one should also attach importance first to the appearance of an abnormal Q wave and in addition refer to the typical RS-T variations of infarction, similarly in the other leads.In 6 of 22 cases, in which the infarct was revealed in the posterior wall of the left ventricle at autopsy, lead D showed a deep Q wave which is more than one-third of the amplitude of R wave, and in 5 of these 6 cases, this change was accompanied by the elevation of RS-T segment and/or a inverted or flat T wave. This pattern was considered as the diagnostic change of posterior infarction. In 13 of the remaining 16 cases, lead D showed RS-T variations without a deep Q wave. The lesion in the posterior wall of these cases, in which an abnormal Q wave was recorded in lead D, was extensive in general. In only one of the cases, in which posterior infarct was confined to less than apical one-third of the posterior wall of the left ventricle at autopsy and the pattern of posterior infarct could not be found in the standard and unipolar limb leads, an abnormal Q wave was found in lead D in the acute stage of infarction. However, it is worthy of note in the diagnosis of posterior infarction that lead D displayed signs of infarction in 3 cases, in which signs of posterior infarction could not be found in leads _aV_F, III and II.In 8 of 13 cases with anterior or anterolateral infarction, leads A and J showed an abnormal Q wave and/or typical elevation of the RS-T segment and a coronary T wave. Consequently, these 8 cases were dignostic of anterior infarction in a broad sense. But, in all of these 13 cases, the multiple unipolar precordial leads could not only diagnose the infarction in all cases, but also were far more excellent than the Nehb's leads in the localization diagnosis of infarction. Lead A and J were of little value, when the multiple unipolar precordial leads were employed.

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Frogs were sensitized with the same antigen shown in report I. After a period of 2∼3 weeks, the isolated frog's heart, which was fixed after Straub's method, was affected with (1 : 100) solution of labbit myocardial phosphatid and after then perfused with the mixture of rabbit myocardial phosphatid and fresh oxen sera. Amplitude of heart contraction was increased by the test solution in report II, but not increased in this experiment. Therefore, sensitized frog's heart was desensitized with phosphatid.

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