[Regression of giant negative T waves in hypertrophic cardiomyopathy: cases simulating either dilated cardiomyopathy or severe coronary artery stenosis].
Two cases of hypertrophic cardiomyopathy (HCM), in whom giant negative T waves resolved during 10 years, are reported. Case 1: A 33-year-old man was admitted in 1975 for careful evaluation because of an ECG abnormality. The ECG revealed a giant negative T wave (GNT) in V5 (-15 mm) and high voltage (SV1 + RV5 = 81 mm). The thickness of the apical wall was 18 mm; the anterior wall, 12 mm; the posterior wall, 16 mm; and the interventricular septum, 17 mm on the left ventriculogram and biventriculogram. The coronary angiogram was normal. From these data, this patient was diagnosed as having HCM. However, follow-up studies disclosed resolution of the GNT with decreased high voltage (SV1 + RV5 = 26 mm). The catheterization performed in 1985 showed a decrease of wall thickness: the apical wall to 10 mm; the anterior wall, 9 mm; the posterior wall, 14 mm; and the interventricular septum, 14 mm. Ejection fraction was markedly decreased from 79.8% to 27.1%, and the wall motion was generally reduced. The coronary angiogram was normal. These findings resemble the clinical pictures of dilated cardiomyopathy (DCM). Case 2: A 58-year-old man was admitted in 1974 because of easy fatiguability. His ECG revealed a GNT in V4 (-10 mm) and high voltage (SV1 + RV5 = 75 mm). The patient was diagnosed as having HCM by cardiac catheterization, right ventricular biopsy and other procedures. In 1985, the depth of the GNT and the voltage of SV1 + RV5 regressed significantly (SV1 + RV5 = 26 mm). The thickness of the apical wall was, 12 mm; the anterior wall, 19 mm; the posterior wall, 13 mm; and the interventricular septum 14 mm during recatheterization. Coronary angiography disclosed stenoses of the left main trunk (75%), the left anterior descending artery (99%) and the left circumflex artery (50%). The right coronary artery was totally occluded. In conclusion, these two cases of HCM had similar changes in their ECG during long-term follow-up studies, but the process was different. One case finally showed clinical pictures of DCM; the other, severe coronary stenoses. These suggested that blood flow to the myocardium is an important determinant for the development of clinical features simulating DCM in cases with HCM.
Horita
Y
Y
Division of Cardiology, Ishikawa Prefectural Central Hospital, Kanazawa.
Konishi
K
K
Osato
K
K
Nakao
T
T
Namura
M
M
Kanaya
H
H
Ohka
T
T
Genda
A
A
Takeda
R
R
D000328:Adult; D006328:Cardiac Catheterization; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis*; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D003251:Constriction, Pathologic / Q000175:diagnosis; D017023:Coronary Angiography; D003327:Coronary Disease / Q000150:complications / Q000175:diagnosis*; D003937:Diagnosis, Differential; D004562:Electrocardiography; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D012075:Remission, Spontaneous; D013318:Stroke Volume