End-stage ventricular dysfunction is the first cause of mortality in adults with functionally univentricular heart (FUVH). Its physiopathology remains unclear. End-stage dilated and hypertrophic cardiomyopathies experience reduced capillary density (RCD). In FUVH physiology, volume overload leads to ventricular dilatation, then myocardial hypertrophy. We therefore hypothesize that FUVH also demonstrate RCD.
Average CD was measured in 13 post-mortem human adult hearts: 5 failing FUVH, 8 controls. Hearts were preserved in 10% formalin. Free wall left ventricular longitudinal and transversal tissue samples were harvested. A morphometric study was realized after immunohistochemical staining of factor VIII. Capillary surface area was quantified by optical density on 50 different samples per patient. The CD was calculated: (capillary surface area) / (total ventricular surface area) (x100%) using Image J software. Results were expressed as mean ± sd.
Among the 13 hearts, 6 allowed a correct interpretation of the CD: 3 failing FUVH (2 tricuspid atresia, 1 double-inlet left ventricle) and 3 controls (congenital heart disease with normal left ventricular function : 2 atrial septal defects with Eisenmenger syndrome, 1 tetralogy of Fallot with pulmonary atresia). There was no significant difference in arterial oxygen saturation between the 2 groups (71 ± 1% in FUVH vs 85 ± 0,8% in controls). Myocardial CD was significantly decreased in FUVH compared to controls (3.58 ± 1.23% vs 7.69 ± 3.29%, p<0.0001).
In conclusion, myocardial CD is decreased in end-stage FUVH. Further studies with more patients are needed to assert the responsibility of RCD for the ventricular dysfunction.