Infarction of the lateral wall of the left ventricle was demonstrated pathologically in 105 cases, which represents an incidence of 65 per cent in a series of 161 cases. The cases of anterolateral infarction and those of posterolateral infarction have been analyzed in previous reports and the present study was concerned with a correlation of electrocardiographic and pathologic findings in twenty-seven cases of primary lateral infarction. These cases were classified into three groups, according to the distribution of the lesion at autopsy: (A) high, (B) low, and (C) midlateral infarction. 1. A. High lateral infarction, involving chiefly the basal one-half of the lateral wall, but continuing for a variable distance into the apical one-half, was found in fourteen cases. The infarct was limited to the subepicardial layer in one case and was manifested by normal QRS complexes and deeply inverted T waves typical of the findings in pericarditis. Despite the fact that the high lateral infarct was transmural in five cases and subendocardial in the other eight, it was manifested by a diagnostic QR pattern in Lead V 5 or V 6 in only one case. The rarity of abnormal Q waves in Leads V 5 and V 6 of this group contrasted sharply with their frequency in association with infarction of the apical one-third of the anterolateral wall and was ascribed to the fact that high lateral infarcts generally spared most or all of the apical one-third of the anterolateral wall. On the other hand, Lead aV L yielded a QR pattern which was considered diagnostic of lateral infarction in two cases, strongly suggestive in five cases, and suspicious in four cases. Standard Lead I was not an adequate substitute for Lead aV L because it failed to show an initial downstroke in five of the eleven patients with Q waves in aV L, because of greater initial negativity of the right than the left arm. Signs suggestive of infarction in the customary precordial or left arm leads constitute an indication for exploration of the upper precordium and axilla. Leads at the intersection of a horizontal line through the sternal terminus of the third intercostal space with vertical lines in the plane of precordial Positions 3, 4, 5, and 6 were obtained on four patients who were followed to autopsy. In one case, the findings in the customary precordial leads were equivocal, those in Lead aV L were strongly suggestive, but those in the high precordial leads were pathognomonic of the high lateral infarct found at autopsy. The findings in the high precordial leads taken in conjunction with those in the customary leads in the other three cases aided in establishing the diagnosis and in localizing the position of the infarct. 2. B. Low lateral infarction was found in eleven cases and was largely or entirely confined to the apical one-third of the lateral wall in eight of these. Abnormal Q waves diagnostic of infarction were present in Lead V 5, V 6, and/or aV L in five cases, and strongly suggestive QR patterns were found in three others. The electrocardiogram was negative in one case and conformed to the pattern of Wood, Wolferth, and Bellet in the other two cases. The RS-T depression in V 4, V 5, and V 6 could be correlated with acute infarction which involved the subendocardial and mid-zones, but spared the subepicardial layer, and the absence of Q waves was explained by the patchy character of the subendocardial lesion. A similar pattern was recorded in an electrocardiogram taken four and one-half hours after the onset of the pain in one other case, but was subsequently replaced by a QR complex diagnostic of the subendocardial infarct found at autopsy. 3. C. Small mid-lateral infarcts, involving the subendocardial layer of the middle one-third of the lateral wall, were found in two cases. A pattern resembling that of Wood, Wolferth, and Bellet was found in both cases, but could have been produced by a combination of left ventricular hypertrophy and digitalis action in one of these. The absence of Q waves may have been due to the small size of the lesion and the failure to take high axillary leads. QRS-T abnormalities in one or more of the first four precordial leads, which were suggestive of anteroseptal infarction, but were actually a manifestation of the lateral infarction, were found in five cases. Transmission of the potential variations of the infarcted lateral wall to the precordium was facilitated by marked counterclockwise rotation in three of these cases. This situation was the opposite of that in previously reported cases where abnormal Q waves were recorded in Leads V 5 and V 6 as a result of clockwise rotation sufficient to cause reference of the potential variations of an infarcted anteroseptal wall to the axilla.