Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction
Kazufumi Tsuchihashi, MD, PhDa,
Kenji Ueshima, MD, PhD ,
Tatsuro Uchida, MD, PhD ,
Nobuhiro Oh-mura, MD, PhD ,
Kazuo Kimura, MD, PhD||,
Mafumi Owa, MD, PhD¶,
Minoru Yoshiyama, MD, PhD#,
Shunichi Miyazaki, MD, PhD**,
Kazuo Haze, MD, PhD ,
Hisao Ogawa, MD, PhD ,
Takashi Honda, MD, PhD ,
Mamoru Hase, MDa,
Ryu-ichi Kai, MD, PhD ,
Isao Morii, MD, PhD** for the Angina Pectoris-Myocardial Infarction Investigations in Japan
a Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
Second Department of Internal Medicine and Cardiology, Memorial Heart Center, Iwate Medical University School of Medicine, Morioka, Iwate, Japan
Division of Cardiovascular Medicine, Sendai Cardiovascular Center, Sendai, Japan
Department of Cardiovascular Medicine, Omiya Medical Center, Jichi Medical School, Omiya, Saitama, Japan
|| Department of Cardiology, Yokohama City University Medical Center, Yokohama, Japan
¶ First Department of Internal Medicine, Shinsyu University School of Medicine, Matsumoto, Nagano, Japan
# Division of Cardiology, Osaka City University School of Medicine, Osaka, Japan
** Division of Cardiology, National Cardiovascular Center, Suita, Osaka, Japan
 Department of Cardiology, Osaka City General Hospital, Osaka, Japan
 Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto, Japan
 Cardiovascular Center, Saiseikai Kumamoto Hospital, Kumamoto, Japan

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Figure 1 Representative electrocardiographic changes and left ventriculogram of transient left ventricular (LV) apical ballooning (Case 1). (Left) 12-lead electrocardiogram during chest pain (B) demonstrated ST elevation in leads I, aVL, V1 to V5 and reciprocating ST depression in leads II, III and aVF compared with control (A). Fourteen days after onset (C), a coronary T-wave was confirmed. (Right) Left ventriculogram demonstrated LV apical ballooning. After 15 days, almost all of the contracted LV configuration recovered to normal.
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Figure 2 Changes in intracardiac pressure recording (Case 1). Intraventricular pressure recording immediately after onset revealed a significant intraventricular pressure gradient (PG), estimated to be 75 mm Hg, with a systolic ejection murmur (Levine III/VI). In the subacute period, no significant pressure gradient was recorded.
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Figure 3 Electrocardiography and left ventriculographic findings of a representative case (Case 2). (Left) 12-lead electrocardiogram showed ST elevation in leads II, III, aVF and V3 to V6. In the subacute period, the electrocardiogram exhibited a negative T-wave. (Right) Initial left ventriculogram revealed apical ballooning only in the acute period.
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Figure 4 Scintigraphic and positron emission computed tomographic (PET) findings (Case 2). Nuclear cardiographic evaluations showed marked perfusion (Tc-99m sestamibi [MIBI]) metabolic (I-123 beta-methyl-p-iodophenyl pentadecanoic acid [BMIPP] or I-123 metaiodobenzyl-guanitidine [MIBG]) mismatches mainly at the left ventricular apex. However, in the subacute period, this perfusion metabolic mismatch decreased after the functional recovery (three-dimensional left ventriculography by Tc-99m MIBI). After five months, PET by N-13 ammonia showed improvement in the coronary flow reserve (CFR) assessed by dipyridamole administration. EDV = end-diastolic volume; EF = ejection fraction; ESV = end-systolic volume; MBF = myocardial blood flow; SPECT = single photon emission computed tomography.
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