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Europace Advance Access originally published online on April 27, 2008
Europace 2008 10(9):1115-1116; doi:10.1093/europace/eun107
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org


CASE REPORTS

Severe headache and a broken heart

Hendrik Bonnemeier1,*, Timothy Krauss1, Klaus Brunswig2 and Christof Burgdorf1

1 Medizinische Klinik II, Universität zu Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany; 2 Klinik für Neurochirurgie, Universität zu Lübeck, Lübeck, Germany

Manuscript submitted 12 March 2008. Accepted after revision 2 April 2008.

* Corresponding author. Tel: +49 451 500 4859; fax: +49 451 500 5146. E-mail address: bonnemei{at}medinf.mu-luebeck.de

A 62-year-old sports teacher was admitted to the emergency room with progressively severe headaches, vomiting, left homonymous hemianopsia, weakness of the left arm and leg, and clouding of consciousness progressing over a few hours. The initial electrocardiogram (ECG) revealed new onset of atrial fibrillation with a ventricular rate of 170 bpm (Figure 1G). A computed tomography (CT) brain scan with contrast enhancement (Figure 1A) confirmed the presence of a large right lobar haemorrhage ~6 cm in diameter with some mass effect.


Figure 1
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Figure 1 (A) Contrast CT brain scan on hospital admission showing a large right lobar intracerebral haemorrhage ~6 cm in diameter with some mass effect. (B) Magnetic resonance imaging brain scan on day 4 after admission showing subacute right lobar intracerebral haemorrhage that appears to be a liquid separated from a clot and blood breakdown products. (C) Left ventricular angiogram on day 6 after admission: the left and right coronary arteries reveal no significant coronary artery disease. (D) Reduced uptake of 123I-MIBG SPECT and 18F-FDG PET in the apical area. 99 mTc-MIBI SPECT indicated normal perfusion within this region. (E) Left ventricular angiogram on day 6 after admission: end-systolic and end-diastolic frame of left ventricular angiography exhibiting apicolateral wall dyskinesis and basal hypercontractility. Left ventricular ejection fraction 40%. (F) Transthoracic echocardiogram on day 4 after admission: end-systolic and end-diastolic frame of left ventricular echocardiography exhibiting apicolateral wall dyskinesis and basal hypercontractility. Left ventricular ejection fraction 29%. (G) Electrocardiogram on admission showing atrial fibrillation with a ventricular rate of 170 bpm. (H) Electrocardiogram on day 4 after admission showing novel T-wave inversion in leads II, III, aVF, V3–V6, and downsloping ST-segment depression. (I) Scheme of regional wall motion from the traced endocardial LV contours at end-diastole and end-systole from left ventricular angiogram on day 6 after hospital admission.

 
During conservative treatment, the patient's symptoms resolved within 3 days and his neurological signs also improved quickly. A magnetic resonance imaging brain scan (Figure 1B) revealed no further increase of the lesion. However, a follow-up ECG now exhibited novel T-wave inversion in leads II, III, aVF, V3–V6, and downsloping ST-segment depression (Figure 1H). Furthermore, serum levels of cardiac troponin T (0.18 ng/mL) were elevated. The ECG displayed markedly impaired left ventricular (LV) function (left ventricular ejection fraction 29%) (Figure 1F). In view of these diagnostic findings and moderate dyspnea, the patient was referred for cardiac catheterization. Coronary angiography revealed insignificant coronary artery disease (Figure 1C). Left ventricular angiography confirmed a depressed ventricular function with an unusual pattern of wall motion abnormalities, characterized by an apical and lateral balloon-like dyskinesis and basal hypercontractility (Figure 1E and I). Single-photon emission computed tomography (SPECT) revealed that myocardial iodine-123 metaiodobenzylguanidine (123I-MIBG) uptake and 18F-fluoro-deoxy-glucose (18F-FDG) were reduced in the akinetic LV area, whereas technetium-99 m methoxyisobutylisonitrile (99 mTc-MIBI) SPECT indicated normal perfusion within this region (Figure 1D).

The association between intracerebral hemorrhage and cardiac dysfunction, reflected by ECG-changes, arrhythmia, and elevations of cardiac markers, is well known. However, the underlying pathophysiological mechanisms still remain unclear. Recently, the syndrome of ‘Takotsubo cardiomyopathy’, ‘apical ballooning’ or ‘broken heart syndrome’, characterized by a transient apical ballooning of the LV during states of exaggerated sympathetic activation, has been more and more recognized. Thus, both entities may provide a uniform pathophysiology, characterized by excessive cardiac sympathetic nervous discharge.

Conflict of interest: none declared.


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This Article
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