European Heart Journal Advance Access originally published online on March 27, 2008
European Heart Journal 2008 29(18):2201; doi:10.1093/eurheartj/ehn129
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In vivo molecular imaging of angiogenesis, targeting 
vβ3 integrin expression, in a patient after acute myocardial infarction
1 Department of Nuclear Medicine, Technical University, Klinikum rechts der Isar, Ismaninger Straße 22, 81675 Munich, Germany
2 Department of Cardiology and Intensive Care Unit, Heart Center Munich-Bogenhausen, Staedtisches Klinikum Muenchen GmbH, Klinikum Bogenhausen, Munich, Germany
* Corresponding author. Tel: +49 89 4140 2963, Fax: +49 89 4140 4950. Email: marcusmakowski{at}gmail.com
A 35-year-old Caucasian male presented with chest pain and nausea in the emergency room. The initial ECG displayed sinus-rhythm with ST elevation in I, aVL, V1–5, ST-depression in III, and aVR and pathological Q waves in V1–5. The laboratory results showed severely elevated cardiac enzymes.
Percutaneous coronary intervention (PCI) with stenting of the completely occluded proximal left anterior descending (LAD) was performed without complications.
Two weeks after the myocardial infarction and PCI, the patient underwent MRI and PET/CT evaluation based on a clinical research protocol (study approved by the ethics committee). Cine-MRI (steady-state-free-precession) displayed an impaired systolic function (left ventricular ejection fraction, 33%). Fifteen minutes after contrast injection (0.2 mmol gadolinium-diethlenetriamine pentaacetic acid), a nearly complete transmural delayed enhancement (>75%) was observed in the anterior-, anteriorseptal-, anteriorlateral-, and apical-wall (Panels A, D).
The positron emission tomography (PET) examination (Biograph 16 PET/CT, Siemens, Germany) with 13N-ammonia revealed a severely reduced myocardial blood flow in the distal anterolateral, apical and inferoseptal region. (Panels B, E).
A novel 
vβ3-targeting PET agent (18F-Galakto-RGD) was used to assess integrin expression, which potentially represents angiogenesis involved in the regeneration process after myocardial infarction. The vβ3 integrin is a key mediator of angiogenesis and thus may be an important diagnostic and therapeutic target associated with myocardial repair processes after ischaemic injury. Focal tracer retention was localized in the infarcted area defined by the extent of delayed enhancement MRI and severely reduced myocardial blood flow (MBF) (Panels C, F). This signal may indicate the myocardial healing taking place within the infarcted area as demonstrated in animal models.
Panel A and D. CMR with delayed enhancement (arrows) extending from the anterior wall to the apical region in the four- (A) and two-chamber (D) view. Panel B and E. Identically reproduced location and geometry with severely reduced myocardial blood flow using 13N-ammonia, corresponding to the regions of delayed enhancement by CMR (arrows). Panel C and F. Focal 18F-RGD signal co-localized to the infarcted area. This signal may reflect angiogenesis within the healing area (arrows). Panel G and I. Polar map (I: 3D) of myocardial blood flow assessed by 13N-ammonia indicating severely reduced flow in the distal LAD-perfused region. Panel H and J. Co-localized 18F-RGD signal corresponding to the regions of severely reduced 13N-ammonia flow signal, reflecting the extent the of vβ3 expression within the infarcted area.
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