Sakamoto T, Tei C, Murayama M, Ichiyasu H, Hada Y
Jpn Heart J. 1976 Sep;17(5):611-29. doi: 10.1536/ihj.17.611.
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).
对9例原因不明的巨大T波倒置患者进行了超声心动图和超声心动断层扫描,以寻找可能存在的心肌异常。左胸前导联的深倒置T波超过1.2mV(平均为1.63mV)。所有病例均有原因不明的心电图左心室肥厚,且无缺血发作。常规超声束方向测量左心室短轴显示室间隔(IVS)和后壁(PW)厚度及运动基本正常,因此这些病例的报告常为正常范围。然而,超声心动断层扫描(扇形B超)显示左心室心尖附近有相当局限性的肥厚,当朝着心尖进行扫描时,常规超声心动图也显示乳头肌附着点以下的IVS或PW或两者的相同区域有肥厚(不对称性心尖肥厚:AAH)。对9例特发性肥厚性主动脉瓣下狭窄(IHSS)患者的对照研究显示为不对称性室间隔肥厚(ASH),IVS从基部到心尖几乎同等肥厚。所有病例均有T波倒置,但程度较轻。3例有与AAH患者相当深的T波,且这些病例也有相当程度的心尖肥厚(IHSS的不寻常类型,即AAH和ASH之间的中间类型)。倒置T波深度与心尖/室壁厚度比值之间的密切关系提示,肥厚的心尖部肌肉组织恢复过程改变是迄今原因不明的巨大T波倒置的原因。在揭示AAH与其他形式肥厚型心肌病的联系之前,具有这种T波和心尖肥厚的病例可称为不对称性心尖肥厚(AAH)。