Frogs were sensitized with the same antigens as shown in report I, and after a period of 2〜3 weeks, the isolated frog's heart, which was fixed after Straub's method, was perfused with (1:100) and (1:500) solution of the mixture of rabbit myocardial phosphatid and fresh oxen sera. The amplitude of heart contraction was increased by the test solution in all sensitized groups, but not increased in the non-sensitized group. Lasting time of heart action after application of test solution was shorter in all sensitized groups than non-sensitized. From the results in report I and II, we were able to understand that frogs were sensitized with the mixture of phosphatid and serum consequently, as Maekawa's theory, even if dissimilar antigens introduced into them.

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In the Part I of this serial studies the author described a generatalisation of electrocardiographic findings of 35 cases of myocardial infarction, and in Part II and III, the correlationship of electrocardiographic and post-mortem findings was discussed on cases of the infarction involving the anterior wall and of the infarction involved the lateral wall of the left ventricle, respectively. In this communication, the findings in the electrocardiograms have been analyzed and correlated with the pathologic findings in 26 cases of infarction in the posterior wall of the left ventricle. Of 26 cases, 12 were men and 14 were women, with the age ranging from 60 to 96 years, except 3 cases. Of these cases, 3 had recent and 23 had healed infarctions at autopsy, but in at least 2 of the latter, the infarction was relatively fresh microscopically, and it was supposed that in at least 7 cases of the latter the electrocardiograms were obtained also in the acute stage. 1. In 10 of 26 cases, the amplitude of Q wave in Lead III was 25 per cent or more of the amplitude of the highest R wave in the standard limb leads and a Q wave was distinctly present in Lead II. In 7 of these 10 cases, in which the unipolar limb leads were also obtained, a Q wave 25 per cent or more of amplitude of the succeeding R wave was recorded in Lead _aV_F. The duration of Q wave from onset to nadir in Lead _aV_F was measured as 0.02 second or more in all of 7 cases and 0.03 second or more in 3 of these 7 cases. And the duration of the Q_aV_F, from the onset to the point of intersection of the upstroke of the succeeding R wave and the base line was measured as 0.03 second or more in all of the 7 cases, and was 0.04 second or more in 4 of the 7 cases. 2. All of the cases in which the electrocardiogram displayed an abnormal Q wave in Leads _aV_F, III and II, was accompanied by RS-T variations in these leads. None of the case in which a deep Q wave in Lead III was recorded without appearance of a Q wave in Lead II was found, except in one case, in which the elevtrocardiogram displayed an abnormal Q_<III> Q_<II> pattern at first and only an abnormal Q_<III> with absence of Q_<III> for a time and subsequently an abnormal Q wave disappeared in any lead. 3. Lead _aV_F was considered as more reliable than the standard limb leads in the diagnosis of posterior infarction. 4. In 2 cases of posterior subendocardial infarction, upward convexity of the RS-T segment on the base line and sharply inverted T wave without an abnormal Q wave were obtained in Leads II, III and _aV_F in the acute stage of infarction. It was considered that these findings were suggestive of posterior infarction. 5. In 13 cases, 50 per cent of all 26 cases, the diagnosis of posterior infarction could hardly be made, because the electrocardiogram of these cases displayed only a RS-T variation or a pattern of an uncomplicated right bundle branch block. 6. In many of the cases with infarction involving the middle third of the posterior wall, an abnormal Q wave was frequently recorded in Leads _aV_F, III and II. On the other hand, this change was seldom found in cases with infarction confined to the apical one-third or the basal one-third of the posterior wall. 7. When the electrocardiogram indicated horizontal or semihorizontal position of the heart, an abnormal Q wave in Lead _aV_F was found in only few of those cases with posterior infarction, unless a large coexistent infarction extended in the interventricular septum at the same time. 8. In posterior infarction, the differential diagnosis of transmural from subendocardial infarction was almost impossible at least from the findings of the standard and unipolar limb leads. 9. In one case of recent infarction, the right precordial leads displayed depression of the RS-T segment, which is familiar reciprocal manifestation of acute posterior infarction, and a tall R wave. Of healed

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In this study, infarction of the interventricular septum was demonstrated pathologically in 24 of all 35 cases. The author had studied the correlation between electrocardiographic and post-mortem findings concerning the septal infarction in these 24 cases. Of 24 cases, 8 were men and 16 were women and their age ranged from 52 to 86, except in 2 cases. Among these 24 cases, 3 had recent and 21 had healed infarctions at autopsy, but it was considered that in at least 5 cases with healed infarctions, the electrocardiogram was obtained when the infarction was in the acute stage. These cases were classified into four groups, according to the distribution of the lesion at autopsy: (1) coexistent septal extension of anterior infarction in 5 cases; (2) septal extension of anteroposterior infarction in 13 cases; (3) extension of posterior infarction into the posterior portion of the interventricular septum in 5 cases; (4) infarction limited to the interventricular septum in 1 case. On the other hand, the cases were classified into three groups, according to the extent of the lesion in the interventricular septum at autopsy: (〓) large, massive infarction involving at least half or more of the inverventricular septum in 7 cases; (〓) minimal infarction confined to only small portion of the interventricular septum or distributed in patchy fashion in the septum in 10 cases; (〓) moderate infarction corresponded to the middle of both above-mentioned groups in 7 cases. The electrocardiographic patterns in these septal infarction were summarized as follows: 1. Interventricular conduction defects, in which QRS interval was 0.12 second or more, were obtained in 3 cases with right bundle branch block, in one case with the so-called arborization block in the form of left bundle branch block, and in one case with prolonged QRS interval, uncomplicated by a bundle branch block. a) In 2 of 3 cases with right bundle branch block, autopsy revealed the anteroposterior infarction accompanied by a three-plus or two-plus infarction in the interventricular septum, and the electrocardiogram showed an abnormal Q wave and a late (delayed) R wave from Lead V_1 to V_4. In a remaining case of right bundle branch block, in which posterior infarct extended into the posterior portion of the interventricular septum, the electrocardiogram showed an abnormal Q wave in Leads _aV_F III and II, but the right precordial leads showed the similar pattern of uncomplicated right bundle branch block. b) In a case with left bundle branch block, an acute infarction limited to the basal portion of the interventricular septum was found at autopsy, and the electrocardiogram showed the pattern of arborization block characterized by the high grade prolongation of QRS interval and low voltage in the standard and unipolar limb leads, without appearance of an abnormal Q wave in any lead. c) In another case of intraventricular conduction defect, which showed QRS interval of 0.12 second, the damage in the free wall of the left ventricle was extensive, but the septal involvement was very small at autopsy, and a diagnostic pattern of septal infarction could not be found in the electrocardiogram. 2. Auriculoventricular block was observed in only one case of incomplete auriculoventricular block which was probably caused by digitalis intoxication in the course of infarction. 3. The cases without intraventricular conduction defect. a) The cases with septal extension of anterior or anteroposterior infarction: When the extent of infarct in the interventricular septum was moderate (〓) or massive (〓), in 10 of 12 cases, an abnormal Q wave was observed in Leads V_1 and V_2 or Lead V_2, and most of them were accompanied by RS-T variations. In the remaining 2 cases, the amplitude of the initial R wave in the right precordial leads decreased abnormally as the electrode was moved from right to left, and finally an abnormal Q wave was recorded in Lead

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Vectorcardiographic changes which appear in the ventricular hypertrophy of heart have been studies often by use of tetrahedral or cube system methods. But they have not been researched serially on the same subject from the beginning to the end of hypertrophy. Moreover, the vectorcardiograms recorded by htese methods have much deformation in their represented vectors compared with those of the theoretical electrical heart axes. Therefore I tried to study tthe vectorcardiographic changes in the ventricular hypertrophy by means of vectorpolyography having least deformation in represented vectors. The experimental hypertrophy of right or left heart ventricle were produced respectively by ligation of pulmonary or abdominal artery. The polyograms were taken spatially in three planes of frontal, horizontal and sagittal one, and the wire model was reconstructed from these polyograms in three planes for the benefit of observation of the changes in the represented vector loops. The roentgenograms were taken also in every cases. The data obtained in these procedures are compiled in table 1, 2, and 3. The results are as follows. CHANGES IN QRS-LOOP. -Changes in QRS-loop were observed not only in its terminal portion, but in the entire loop, especially in its mid-portion. The mid-portion of QRS-loop displaced from initial position to its right upper anterior in right ventricular hypertrophy, and to its left posterior in left ventricular hypertrophy. Namely, in vectorcaidiogram of right ventricular hypertrophy, the mid-portion in frontal plane displaced from initial position to the right, in horizontal plane to the right anterior, and in sagittal plane to the anterior, and in vectorcardiogram of left ventricular hypertrophy, that in frontal plane displaced to the left, in horizontal plane to the left posterior, and in sagittal plane to the posterior. These results could be explained by the rotation and variation of the QRS-loop before the procedure. Rotation of QRS-loop in right ventricular hypertrophy: The initial QRS-loop is rotated counterclockwise around ventrical axis after the procedure when viewed from the cranial side, clockwise around transverse axis when viewed from the right, and clockwise around anteroposterior axis when viewed from the front. Rotation of QRS-loop in left ventricular hypertrophy: The initial QRS-loop is rotated clockwise around vertival axis, counterclockwise around transverse axis, and couterclockwise around anteroposterior axis after the procedure when viewed from the same side as above mentioned. Variation of QRS-loop was observed mainly in the mid-portion of the loop. The QRS-loop budged or bended to right or anteriorly in right ventricular hypertrophy, and posteriorly in left ventriclar hypertrophy. INVERSION OF T-LOOP. - Inversions of T-loop were observed in about 1/3 of right or left ventricular hypertrophy, and began to appear usually within the same interval after procedure. It was also noted that there was gradual increase in the degree and appearance of inversion in proportion to the number of days after procedure. OPENING OF QRS-LOOP. - No apparent correlation could be observed between the opening of QRS-loop and the hypertrophy in these experiments. The most reasons of these changes of QRS-loop in the vectorcardiogram after the occurrence of ventricular hypertrophy were probably in the rotation, thickness of hypertrophied free ventricular wall and deformation of ventricle itself due to enlargement, hypertrophy, and other reasons, because we observed that the rotation or variation of QRS-loop was caused by rotation or deformation of heart ventricle in another experiments. Futhermore, the vectorcardiograms, obtained by calculation under the assumption that the subepicardial muscle surface in hypertrophied ventricle was activated later than that of normal ventricle, were very alike to these in this paper. These facts mean that the variation of VCG

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