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Myocardial blood flow and coronary flow reserve late after anatomical correction of transposition of the great arteries

Frank M. Bengel, MD^a, Michael Hauser, MD^*, Claire S. Duvernoy, MD^a, Andreas Kuehn, MD^*, Sibylle I. Ziegler, PhD^a, Jens C. Stollfuss, MD^a, Mareike Beckmann, MS^*, Ursula Sauer, MD^*, Otto Muzik, PhD, Markus Schwaiger, MD^a and John Hess, MD^*

^a Nuklearmedizinische Klinik und Poliklinik der Technischen Universität München, Munich, Germany
^* Kinderklinik für Herz- und Gefäßerkrankungen, Deutsches Herzzentrum München, Munich, Germany
PET-Center, Children’s Hospital of Michigan, Detroit, Michigan, USA

View larger version (16K): [in a new window]   Figure 1 Myocardial blood flow at rest (normalized to the rate-pressure product) and during adenosine-induced vasodilation in children with early ASO for simple TGA (group A; n = 15; 9 ± 1 years), children with later ASO for more complex TGA with associated anomalies (group B; n = 7; age 13 ± 3 years) and healthy young adults (n = 10; age 26 ± 6 years).

View larger version (70K): [in a new window]   Figure 2 Short-axis images of three cases of children after ASO for TGA. Representative apical, midventricular and basal slices are depicted at rest and during adenosine-induced vasodilation. Images are oriented with anterior wall on the top, lateral wall to the right, septum to the left and inferior wall at the bottom. Case A represents a 9-year old after ASO for simple TGA at 7 days after birth without visually detectable regional abnormalities. Quantitative global MBF was 93 ml/100 g/min at rest and 295 ml/100 g/min during adenosine stress; coronary flow reserve was 3.2. In case B, a moderate adenosine-induced reversible abnormality in the basal anterolateral wall was found at visual analysis (arrowhead). This 9-year old also had early ASO for simple TGA at 11 days after birth. Quantitatively, global MBF was 83 ml/ 100 g/min at rest and 241 ml/100 g/min during adenosine stress; coronary flow reserve was 2.9. Case C shows images of a 16-year old patient with TGA and an associated large VSD (arrows). The defect was closed with a patch during ASO and appears on the images as a fixed abnormality in the basal septal wall. This child, who underwent ASO at an age of 5 years, had MBFs of 83 ml/100 g/min at rest and 252 ml/100 g/min during adenosine stress; coronary flow reserve was 3.0. Sectors containing the structural defect were excluded from quantitative flow analysis in this case.