Thorac Cardiovasc Surg 2017; 65(S 02): S111-S142
DOI: 10.1055/s-0037-1599027
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Diffuse Fibrosis in the Ventricles of Patients with Transposition of Great Arteries Late after Atrial Switch with and without Pulmonary Stenosis

N. Shehu
1   Department of Paediatric Cardiology and Congenital Heart Defects, Deutsches Herzzentrum München, Technische Universität München, München, Germany
,
C. Meierhofer
1   Department of Paediatric Cardiology and Congenital Heart Defects, Deutsches Herzzentrum München, Technische Universität München, München, Germany
,
N. Mkrtchyan
1   Department of Paediatric Cardiology and Congenital Heart Defects, Deutsches Herzzentrum München, Technische Universität München, München, Germany
,
S. Martinoff
2   Department of Radiology, Deutsches Herzzentrum München, Technische Universität München, München, Germany
,
P. Ewert
1   Department of Paediatric Cardiology and Congenital Heart Defects, Deutsches Herzzentrum München, Technische Universität München, München, Germany
,
H. Stern
1   Department of Paediatric Cardiology and Congenital Heart Defects, Deutsches Herzzentrum München, Technische Universität München, München, Germany
› Author Affiliations
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Publication History

Publication Date:
02 February 2017 (online)

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Objectives: In adult patients with transposition of the great arteries late after atrial switch (Mustard or Senning), each of the ventricles is faced with a profoundly different pressure regimen from the one they are meant to support in normal conditions. As a consequence, the subaortic morphologic right ventricle (RV) becomes progressively hypertrophic, while the subpulmonary morphologic left ventricle (LV) undergoes progressive hypotrophic changes. The extent of diffuse fibrosis in the RV and LV of these patients remains incompletely investigated. Therefore, aim of this study was to assess the degree of ventricular fibrosis by determining myocardial extracellular volume (ECV) in both ventricles.

Methods: We determined ECV by cardiac magnetic resonance (CMR) in 11 patients without pulmonary stenosis (group A) (36.3 ± 5.3 years old) and in 4 patients with pulmonary stenosis (group B) (33.9 ± 4.7 years old), late after atrial switch by acquiring T1-maps of the myocardium before and 10 minutes after injection of Gadolinium-based contrast agent. We compared ECV values: i) between the two ventricles within the first group and ii) between the left ventricles of groups A and B.

Results: LV-ECV was significantly higher compared to the RV-ECV (37 ± 3% vs. 27 ± 2%, p < 0.01) in patients without pulmonary stenosis. The between-group comparison, showed that the LV-ECV of patients with pulmonary stenosis was significantly lower compared with the group without pulmonary stenosis (26 ± 2% vs. 37 ± 3%, p = 0.03).

Conclusion: In patients late after atrial switch, ECV of the regressed, subpulmonary morphologic LV is significantly increased compared to ECV of the hypertrophic, subaortic morphologic RV. Increased ECV in the LV may be due to diffuse fibrosis, induced by long time reduced activity of LV. The presence of an even mild pulmonary stenosis, increasing the LV pressure, may reduce/prevent fibrosis of the LV in these patients.