In the previous report, the author describeda generalisation of findings obtained by comparing the electrocardiographic patterns with the postmortem findings of 35 autopsied cases. In this communication, the findings in the unipolar precordial leads and in the standard and goldberger limb leads have been analyzed and correlated with the postmortem findings of 21 cases with anterior infarction in this series of 35 cases. Of 21 cases of anterior infarction, 2 had recently developed and 19 had healed infarctions at autopsy, nut in 9 of the latter group electrocardiograms were taken also during the acute stage. To avoid the errors derived from the difference of extent and location of infarction, the author divided the ventricular wall into the six portions, as shown in the previous communication, each infarction being precisely described according to the pathologic findings; for example, the infarction involved the anterior free wall and the anteroseptal portion of the left ventricle, and the half of the interventricular septum, or the infarction involved the anterior free wall and the lateral wall of the left ventricle etc. The correlation between the pathologic findings and the electrocardiographic patterns was discussed after analysis of these data was made. 1. In 15 cases, the infarctions involved the apical one-third to full length of the anterior free wall and the anteroseptal portion of the left ventricle, and the interventricular septum. In 14 of them, the electrocardiographic pattern showed an abnormal Q wave in one or more of Leads V_1 to V_4. In 9 of these 14 cases, an abnormal QS or QR(S) pattern accompanied by abnormal elevation of the RS-T segment was present in two or more leads of Lead V_1 through V_4. In addition 7 of these 9 cases showed an inversion of T wave at least in one of these leads in which the RS-T segment was found to be elevated abnormally. Another 2 cases of the 14 cases in which abnormal Q waves were noted, had right bundle branch block, characterized by the presence of an abnormal Q wave in place of the customary initial R wave, and the depression of RS-T segment and/or the inversion of T wave. In another 2 cases of them, the amplitude of the initial R wave in Leads V_1, V_2 and V_3 decreased as the electrode was moved from right to left, and finally an abnormal QS or QR complex was recorded in Lead V_4 or V_3. The electrocardiogram of the last case in this group displayed an abnormal elevation of the RS-T segment in Leads V_1, V_E, V_<3R> and V_<4R>, and occasionally displayed a qrS complex in Lead V_2. 2. In one case in which the infarct involved the subepicardial one-fourth to two-thirds of the anterior free wall and the subendocardial two-thirds of the anteroseptal portion of the left ventricle and the left side of the anterior small portion of the inter-ventricular septem, the amplitude of the initial R wave in Leads V_1, V_2 and V_3 showed abnormal decrease as the electrode was moved from right to left, and its QRS pattern was accompanied by the marked elevation of the RS-T segment and a inverted T wave. 3. Interpretation of the abnormal QS or QR pattern in Leads V_1 and V_2 in regards to the differentiation of myocardial infarction from non-infarction cases, was discussed in detail. In myocardial infarction, the abnormal Q wave in Leads V_1 and V_2 is indivative of the infarction of the interventricular septem, not of the infarction of the anterior wall. 4. In 2 cases of the infarction involving the free anterior wall and the anteroseptal portion of the left ventricle, and the interventricular septem, an abnormal qrS complex was recorded in Leads V_1, V_2 and V_3, or in V_2. 5. In an apical infarction, confined to the one-fifth of the anterior free wall and the anteroseptal portion of the left ventricle, and the interventricular septum, abnormal reduction of the initial R wave in Lead V_3 and a biphasic T wace in Lead V_4 were

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In the previous report, the author described the general observation of the electrocardiographic changes in 35 autopsied cases of myocardial infarction. In an attempt to correlate the findings in the electrocardiogram of infarction in each portion of the ventricular wall with the post-mortem findings, the author took up and discussed the anterior infarction in Part II of this serial study. In this communication, the findings in the electrocardiograms have been analyzed and correlated with the pathologic findings in 20 cases with lateral infarction in this series of 35 cases. Of these 20 cases, one had a infarction confined to the lateral wall of the left ventricle. In 12 cases, anterior infarcts extended into the lateral wall of the left ventricle, and in 7 cases, posterior infarcts invaded into the lateral wall of the left ventricle. Of these 20 cases, one had a recent infarction, 19 had healed infarctions, but in 2 of the latter, the infarctions were proved to be of relatively fresh one by microscopic examination, and in at least 8 cases of the latter, the electrocardiograms, were obtained also in the acute stage. The cases were classified into the following three groups, according to the location and extent of the lesion in the lateral wall at autopsy: (A) the infarction involving the apical pne-third or more of the lateral wall, (B) the infarction involving the apical one-fifth or more and less than the apical one-third of the lateral wall, and (C) the infarction involving the middle one-third of the lateral wall. 1. Group A included 13 cases. In 2 cases of 3 transmural infarctions in group A, a QS complex was recorded in one or more of Leads V_5, V_6 and V_7. In 3 of 10 subendocardial infarctions, an abnormal QR(S) complex and a inverted T wave and/or depression of RS-T segment were obtained in one or more of Leads V_5, V_6 and V_7. (in one case in Lead CF_5). An abnormal Q wave could not be found and only depression of the RS-T segment and/or inversion of T wave were present in the left precordial leads in another 7 cases of these subendocardial infarctions, except one case in which the number of the employing leads was insufficient. Consequently, it was shown as difficult to differentiate left ventricular hypertrophy, coronary insufficiency and others by means of the electrocardiographic examination in these cases. 2. Relatively small apical infarction of the lateral wall which was classified into group B was found in 4 cases. One of these cases was a tarnsmural infarct and 3 were subendocardial infarcts. In one case of the latter, a borderline Q wave with a notched upstroke of the succeeding R wave was found in Lead V_5. And the electrocardiogram of these 4 cases displayed a depression of the RS-T segment and an inverted or a frat T wave in one or more (in most cases in two or more) of Leads V_5, V_6 and V_7. 3. In one posterolateral infarction of 3 cases which was classified into group C, the electrocardiogram displayed right bundle branch block and was accompanied by an abnormal Q wave in Lead V_7 and by a depressed RS-T segment in Lead V_5. In another 2 cases of this group, the infarct was patchy and relatively small, and the electrocardiogram recorded only slight depression of RS-T segment in Leads V_4, V_5 and V_6, without an appearance of an abnormal Q wave. 4. Of all 20 cases of the lateral infarction, the abnormal Q wave in the left precordial leads was observed in 5 cases, and the borderline Q wave in only 2 cases. In another 13 cases an abnormal Q waev could not be found. The reason of the absence of an abnormal Q wave was discussed. In respect to this problem, it must be concluded that the infarction was limited to the subendocardial layer in the lateral wall in 15 of these 20 cases. In some cases the displacement of the transitional zone to the left, the presence of other extensive infarction elsewhere in the left ventricule and/or the patchy infarction

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Frogs were sensitized with the mixture of Digitamin and oxen sera, the mixture of rabbit myocardial phosphatid and oxen sera, and fresh oxen sera alone by injection of 0.1 c.c. each in lymphsac. 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 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. These results showed that the sensitization of frogs was possible.

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