European Heart Journal Advance Access originally published online on February 23, 2006
European Heart Journal 2006 27(18):2246; doi:10.1093/eurheartj/ehi820
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Apical ballooning without apical ballooning
Medizinische Klinik II, Universität zu Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany
* Corresponding author. Tel: +49 451 500 2421; fax: +49 451 500 2363. E-mail address: bonnemei{at}medinf.mu-luebeck.de
A 63-year-old woman presented with a sudden exacerbation of chronic obstructive lung disease and elevated levels of cardiac troponin T (0.5 ng/mL). The electrocardiogram exhibited sinus tachycardia, P-pulmonale, and diffuse T-wave inversion. The echocardiogram displayed markedly impaired left ventricular function. In view of these diagnostic findings and ongoing dyspnoea, the patient was referred for emergency cardiac catheterization.
Left ventricular angiography demonstrated a depressed ventricular function with an unusual pattern of wall motion abnormalities, characterized by a circular mid-ventricular balloon-like dyskinesis and marked apical hypercontractility, comparable with the shape of an artichoke heart in the end-systolic frame (Panels A and B). Coronary angiography revealed insignificant coronary artery disease (Panel C). In the subacute phase, 18F-FDG positron emission tomography (PET) (Panel D) and I-123-MIBG scintigraphy (Panel E) revealed decreased uptake of the mid-ventricular basal and lateral wall, indicating both decreased viability and functional sympathetic denervation in the area corresponding to the wall motion abnormities. After 10 days of supportive medical therapy and clinical recovery, follow-up angiography revealed that left ventricular function returned to normal (Panel F).
These findings are consistent with the syndrome of ‘Takotsubo cardiomyopathy’ or ‘apical ballooning’, except for the name giving phenomenon. The disease is characterized by a transient apical ballooning of the left ventricle in post-menopausal women and thought to be caused by sympathetic hyperactivity. The precise mechanisms underlying the wall motion abnormalities are unclear. The present case illustrates that dyskinesis can occur with a mid-ventricular circular pattern and even exclude the apex, which was even hypercontractile in our patient.
Panel A. Left ventricular angiogram on hospital admission: end-diastolic (a) and end-systolic (b) frame of left ventricular angiography exhibiting mid-ventricular lateral and basal wall dyskinesis and apical hypercontractility. Left ventricular ejection fraction 31%.
Panel B. Scheme of regional wall motion from the traced endocardial left ventricular contours at end-diastole and end-systole from left ventricular angiogram on hospital admission.
Panel C. Left ventricular angiogram on hospital admission: the left (a) and the right (b) coronary artery reveal no significant coronary artery disease.
Panel D. 18F-FDG PET for assessment of myocardial viability in the subacute phase exhibiting decreased uptake of the mid-ventricular basal and lateral wall.
Panel E. I-123-MIBG scintigraphy for assessment of functional sympathetic innervation in the subacute phase revealed that accumulation was significantly reduced in the mid-ventricular basal and lateral wall.
Panel F. Left ventricular angiogram 10 days after hospital admission: end-diastolic (a) and end-systolic (b) frame of left ventricular angiography exhibiting normalization of left ventricular function. Left ventricular ejection fraction 74%.
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