A 60-year-old female with a history of hypertension, hypercholesterolaemia, and diabetes mellitus presented two hours after sudden onset of severe persistent chest pain. Electrocardiography showed ST-segment elevation in the inferolateral leads (figure 1A). Coronary angiography revealed a subtotal occlusion of a small left marginal side branch (figure 1B; arrow) and a normal right coronary artery, which could not explain the full typical pattern of apical ballooning as demonstrated by left ventricular angiography (figures 1C and D; arrows). At presentation, troponin I was slightly elevated (0.70 μg/l) while the creatine kinase was normal (maximum levels were 14.50 μg/l and 828 U/l, respectively).
Figure 1.
Electrocardiographic (A) and angiographic findings (B-D) two hours after the onset of pain in a patient with subtotal occlusion of a small marginal side-branch (B; arrow) and full pattern of apical ballooning (D; arrows).
Five hours after presentation, magnetic resonance imaging (figures 2A and B) showed apical ballooning (arrows) but no scar. Seven days later, the left ventricular function had recovered (figures 2C and D) but gadolinium-delayed enhancement indicated a focal scar in the lateral region (figure 2D;arrow in insert).
Figure 2.
Magnetic resonance imaging five hours after presentation (A and B) and after seven days (C and D) showed recovery of left ventricular function and the presence a focal scar in the lateral region (D; arrow in insert).
Transient apical ballooning of the left ventricle – also called takotsubo cardiomyopathy – mimics serious acute coronary syndromes with severe chest pain and electrocardiographic changes ranging from STsegment elevation to T-wave inversion. The syndrome is triggered by extreme physical exertion or excessive mental stress and has been related to stroke, asthma, pneumonia, metabolic and endocrinological disorders, and surgery.1-4
In the present case, we searched for triggers of this rare syndrome and only found a small myocardial infarction that resulted from the distal occlusion of a coronary branch. We are not aware of a previous publication that has described a full pattern of apical ballooning being triggered by a very focal myocardial necrosis.
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Acknowledgments
Faculty of Science and Technology, Enschede, the Netherlands Correspondence to: C. Gurlek Department of Cardiology, Medical Spectrum Twente, Thoraxcentre Twente, PO Box 50000, 6500 KA Enschede, the Netherlands E-mail: c.von.birgelen@ziekenhuis-mst.nl
References
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