Sustained cavity obliteration and apical aneurysm formation in apical hypertrophic cardiomyopathy
Kinya Matsubara, MD*,*,
Takashi Nakamura, MD ,
Toshiro Kuribayashi, MD ,
Akihiro Azuma, MD and
Masao Nakagawa, MD
* Department of Medicine, Kyoto Municipal Hospital, Kyoto, Japan
Second Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan

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Figure 1 Cavity obliteration (CO) (white arrow) was detected by M-mode echocardiogram through the short-axis plane of the apical portion. Mild CO resolved before early diastole. Moderate or severe CO persisted up to early diastole or up to late diastole, respectively. Every short-axis view of the apical portion displayed marked apical hypertrophy.
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Figure 2 Reversible perfusion defect obtained from a 58-year-old male patient with his typically moderate cavity obliteration exhibited in Figure 1. In exercise thallium single photon emission computed tomography (201Tl-SPECT), there was a perfusion defect during exercise in the apical portion but no defect 3 h later. The left ventriculogram displayed spade-shaped deformation during diastole and cavity obliteration in the midventricle and apical portion during systole (arrowhead).
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Figure 3 Irreversible perfusion defect obtained from a 78-year-old female patient, with her typically severe cavity obliteration and apical hypertrophy exhibited in Figure 1. In exercise thallium single photon emission computed tomography (201Tl-SPECT), there was a perfusion defect during exercise in the apical portion, which persisted up to 3 h later. The left ventriculogram displayed a spade-shaped deformation during diastole because of predominant apical hypertrophy. During systole a cystic cavity in the apical portion (arrow) was separated from the basal cavity by fairly long cavity disappearance, not mimicking hourglass. This cavity deformation suggests apical cavity obliteration with apical aneurysm rather than midventricular obstruction.
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