persistent elevation of cardiac enzymes in a patient with hypertrophic cardiomyopathy: With special reference to electrocardiographic, echocardiographic and 201-thallium myocardial scinti-graphic findings.
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- HAMADA M.
- The 2nd Department of Internal Medicine, Ehime University School of Medicine
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- SHIGEMATSU YUJI
- The 2nd Department of Internal Medicine, Ehime University School of Medicine
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- FUJIWARA YASUSHI
- The 2nd Department of Internal Medicine, Ehime University School of Medicine
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- SUMIMOTO TAKUMI
- The 2nd Department of Internal Medicine, Ehime University School of Medicine
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- HIWADA KUNIO
- The 2nd Department of Internal Medicine, Ehime University School of Medicine
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- KOKUBU TATSUO
- The Department of Internal Medicine, Kinki Central Hospital
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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
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- Jpn Circ J
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Jpn Circ J 54 354-360, 1990
社団法人日本循環器学会
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詳細情報 詳細情報について
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- CRID
- 1570291227134977664
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- NII論文ID
- 110002600393
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- NII書誌ID
- AA00690731
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- ISSN
- 00471828
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- 本文言語コード
- en
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- データソース種別
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- CiNii Articles