Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2 mV (average was 1.63 mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wasll (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH). Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH). The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).