III. Correlation of electrocardiographic and pathologic findings in anteroposterior infarction

Abstract The findings in the Wilson precordial leads and in the standard and Goldberger limb leads have been analyzed and correlated with the pathologic findings in fifty-two cases of coexistent infarction of the anterior and posterior walls of the left ventricle. Autopsy revealed a recent infarct involving the apical one-third or more of the anterior wall and continuing through the septum and around the tip of the left ventricle into the apical one-third or more of the posterior wall in twenty cases, and an old healed infarct of similar distribution in sixteen cases. The pathologic findings were the result of the confluence of independent anterior and posterior infarcts in at least three of these thirty-six cases, and were attributed to simultaneous anteroposterior infarction in the other thirty-three cases because of the anatomical continuity of the lesions and the uniformity in age. Five additional cases were observed with pathologic evidence of simultaneous anteroposterior infarction, complicated by a separate posterobasal lesion. The eleven remaining cases had anatomically separate anterior and posterior lesions. The cases were classified according to the extent of the involvement of the posterior wall into two groups: (a) twenty-two cases of infarction confined to the apical one-third and (b) thirty cases of infarction of more than the apical one-third of the posterior wall. Electrocardiograms were obtained during the acute phase of the posterior infarct in fifteen cases of each group. Lead aV F proved very disappointing for the detection of extensions of a large anterior infarct into the apical one-third of the posterior wall. The pattern in this lead was considered diagnostic of posterior infarction in only two cases, intermittently diagnostic in another, suggestive in three, and negative in sixteen. The negative findings in twelve cases were ascribed to horizontal position, which favored transmission of the potential variations of the right ventricle to the left leg. The negative findings in the other four cases occurred despite intermediate to semivertical position of the heart and were attributable to one or both of the following factors: (1) derivation of the potential variations of the left leg chiefly from those of the intact basal two-thirds of the posterior wall of the left ventricle, and (2) marked reduction in the opposing negative cavity potentials available for transmission through the infarcted apical one-third of the posterior wall, as a result of the extensive lesion of the anterior wall and septum. The influence of cardiac position in one case of infarction of the apical one-third of the posterior wall was exemplified by the registration of an abnormal QR complex in Lead aV F when the heart was in intermediate position and its replacement by a notched R wave when the heart shifted into a vertical position. Lead aV F was a much greater help in the detection of infarcts involving more than the apical one-third of the posterior wall. The findings in this lead were considered diagnostic of the lesion of the posterior wall in eighteen cases, suggestive in five, and negative in the other seven because of the horizontal position of the heart. The continuation of the apical infarct into the middle one-third of the posterior wall increased the incidence of positive findings in Lead aV F . In one case from each group, the findings in Lead aV F were classed as negative despite fulfillment of the requirements for a diagnosis of posterior infarction. A study of the unipolar limb lead in reference to the precordial leads in these cases indicated that the findings in Lead aV F were not due to the posterior lesion, but rather were representative of the potential variations of the infarcted septum, transmitted through the right ventricle to the leg as a result of horizontal position. Typical signs of anteroseptal infarction originally present in one case were obliterated with the development of an extensive posterior infarction. The absence or paucity of diagnostic signs in the precordial leads referable to the anterior infarction in four other cases was regarded as a secondary manifestation of a large posterior infarct and was attributed to reduction in the opposing negative cavity potentials available for transmission through the anterior wall. On the other hand, infarcts limited to the apical one-third of the posterior wall caused no demonstrable alteration in the precordial lead patterns referable to the anterior lesion. Acute RS-T depression in the precordial leads, which is a familiar reciprocal manifestation of recent infarction limited to the posterior wall, was observed in only three of the thirty cases of acute posterior, coupled with recent or old anterior infarction. The downward RS-T displacement in these cases was regarded as a direct manifestation of subendocardial anterior infarction. Further-more, acute RS-T depression was not found in Lead aV F in any of the twenty-eight cases in which acute anterior infarction was accompanied by a recent or old posterior infarction. The standard limb leads were of very limited value in the diagnosis of coexistent anteroposterior infarction. The findings in these leads were not indicative of either lesion in thirteen of the fifty-two cases, and were strongly suggestive of both in only four cases. However, the pattern compatible with anteroposterior infarction was considered a manifestation of posterolateral infarction in one of the latter, and a result of anterolateral plus septal infarction in another.