II. Correlation of electrocardiographic and pathologic findings in large anterolateral infarcts

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-seven cases of infarction of the apical one-third or more of the anterior and lateral walls of the left ventricle. The infarct was distributed transmurally through the apical one-third or more of both the anteroseptal and lateral walls in twenty-four cases; it was transmural in the anteroseptal wall and subendocardial in the lateral wall in fourteen cases; and was confined to the subendocardial one-fourth to three-fourths of both the anteroseptal and lateral walls in nineteen cases. A QS deflection was recorded in Leads V 3 and/or V 4 in twenty-nine of the thirty-eight patients with transmural infarction of the apical one-third or more of the anteroseptal wall of the left ventricle and corresponded closely with the findings at autopsy. An abnormal QR complex was present in both leads in three other cases and was explainable by the pathologic findings. Good correlation between a QS deflection in Lead V 5 or in both V 5 and V 6 and transmural infarction of the apical one-third or more of the lateral wall of the left ventricle was obtained in twelve of twenty-four cases and a satisfactory explanation was found for an abnormal QR complex recorded in one or both of these leads in eight other cases. An abnormal QR or very coarsely notched QS complex was present in Leads V 3 and V 4 in eleven of the nineteen patients with infarction of the subendocardial portion of the anteroseptal aspect of the left apex and conformed closely with the pathologic findings. A smooth or slightly notched QS deflection found in these leads in four additional cases was adequately explained. Good correlation between an abnormal QR pattern in Lead V 5 or in both V 5 and V 6 and infarction of the subendocardial portion of the lateral aspect of the left apex was obtained in twenty-seven of thirty-three cases and a satisfactory explanation was found for a smooth or slightly notched QS complex recorded in one or both of these leads in three other cases. An initial upstroke was recorded in Leads V 3 and V 4 in ten cases, despite the presence of subendocardial or transmural infarction of the anteroseptal aspect of the left apex, and a similar finding was obtained in Leads V 5 and V 6 in seven of these cases, in spite of a comparable lesion in the lateral wall of the left apex. The causes for the registration of an initial R, rather than a Q, under these circumstances, were as follows: (1) displacement of the transitional zone leftward to the anterior axillary or mid-axillary line; (2) left bundle branch block; (3) infarction of the left side of the septum, necessitating activation of intact septal remnants from right to left; (4) early recording of the electrocardiogram soon after the onset of symptoms and before the myocardial changes have progressed to the point of obliterating the response to the activating impulse; (5) patchy infarction with preserved islands of muscle in the subendocardial layer or scattered through the wall; and (6) extensive infarction of the posterior wall of the left ventricle with consequent reduction in the opposing negative potentials available for transmission through the anterolateral infarct to the precordium. The QS complexes associated with recent transmural infarction were usually accompanied by abnormal elevation of the RS-T junction and straightening or upward convexity of the segment, followed by progressive covelike inversion of the T wave in serial tracings. This RS-T pattern indicated the presence of subepicardial muscle that was injured, but not dead. In three cases, the QS complexes were accompanied by slight RS-T elevation, upwardly concave RS-T segment, and upright T waves, which exhibited no significant change in a repeat tracing a few days later. These findings were correlated with recent transmural infarction, which had completely destroyed the subjacent myocardium. Recent subendocardial infarcts were generally accompanied by upward displacement of the RS-T segment, less marked in degree, but similar in contour to that customarily found in transmural infarction and attributable to injury to the subepicardial layer. A less common, but more characteristic finding in recent subendocardial infarction consisted in acute RS-T depression, attributable to injury localized to the subendocardial layer. A positive differentiation between recent and healed infarction could not be made from a single electrocardiogram because of the tendency for abnormal RS-T elevation and/or cove inversion of the T wave to remain as a permanent finding in ventricular aneurysm.