persistent elevation of cardiac enzymes in a patient with hypertrophic cardiomyopathy: With special reference to electrocardiographic, echocardiographic and 201-thallium myocardial scinti-graphic findings.

  • HAMADA M.
    The 2nd Department of Internal Medicine, Ehime University School of Medicine
  • SHIGEMATSU YUJI
    The 2nd Department of Internal Medicine, Ehime University School of Medicine
  • FUJIWARA YASUSHI
    The 2nd Department of Internal Medicine, Ehime University School of Medicine
  • SUMIMOTO TAKUMI
    The 2nd Department of Internal Medicine, Ehime University School of Medicine
  • HIWADA KUNIO
    The 2nd Department of Internal Medicine, Ehime University School of Medicine
  • KOKUBU TATSUO
    The Department of Internal Medicine, Kinki Central Hospital

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抄録

A 17-year-old female patient with hypertrophic cardiomyopathy whose serum cardiac enzymes (creatine phosphokinase = CPK, lactic dehydrogenase = LDH) showed persistent elevation was presented. Percent of CPK-MB and LDHl in 6-year-follow-up period ranged from 3.2% to 8.5%, and 58.0% to 63.2%, respectively. This finding strongly suggests the existence of a small amount of continuous myocardial necrosis for a long time. The influence of cardiac enzyme release on the heart was assessed by serial checks of electrocardiogram, echocardiogram and 201-thallium myocardial scintigram. In serial checks of electrocardiograms, markedly decreased R wave amplitude ranging between 31% and 47% was observed in II, III, aVF and V3-6. On echocardiograms, asymmetric septal hypertrophy and a narrow left ventricular cavity were observed in all echocardiograms through the follow-up period. But, in most recent apical two-dimensional echocardiograms, hourglass appearance of the left ventricle due to a distinct cavity-formation at the apex was observed. In 201-thallium single photon emission computed tomogram, hypoperfusion area markedly extended in anterior and lateral parts. These changes in electrocardiograms, echocardiograms and 201-thallium myocardial scintigrams seemed to reflect myocardial necrosis. Our case points to a mechanism for hypertrophic cardiomyopathy to change, over time, to dilated cardiomyopathy-like features.

収録刊行物

  • Jpn Circ J

    Jpn Circ J 54 354-360, 1990

    社団法人日本循環器学会

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