Abstract:Angiogenesis is largely an adaptive response to tissue hypoxia, which occurs in a wide variety of situations. Interestingly, the extent of hypoxia-induces angiogenesis in the cardiac muscle of children diagnosed with congenital cyanotic heart defects is not well established. Thus, the aim of this study was to 1) estimate the cardiac muscle microvessel density (MVD) in children diagnosed with cyanotic (study group) and non-cyanotic (control group) heart defects and to 2) evaluate the prognostic significance of MVD value in the development of ventricular dysfunction in the postoperative period. The study group included 42 children diagnosed with cyanotic heart defects. The control group comprised 33 patients with a diagnosis of non-cyanotic heart failure. The collected tissue included cardiac muscle sections from the right atrium and interventricular or interatrial wall during surgical correction of the defect. Immunocytochemistry with monoclonal mouse anti-human antibodies against CD31, CD34 and CD105 was employed to estimate the MVD value. The mean cardiac muscle MVD, defined by CD34 expression, was 596.7 ± 32.6 microvessels per 1 mm 2 in the study group, which was not significantly different from the mean MVD in the control group (461.2 ± 30.5). Interestingly, in non-cyanotic heart defects, an inner area of subendocardial meshwork was estimated to have 75.3 ± 7.0 microvessels per 1 mm 2 , compared to 92.8 ± 10.9 microvessels per 1 mm 2 (p = 0.0082) in patients with cyanotic heart defects. No significant correlations between MVD value and ventricular dysfunction were found. Cyanotic heart defects resulting in chronic hypoxia might provoke angiogenesis in the subendocardial meshwork of the heart wall. The process seems to be independent of the type of cyanotic heart disease and most likely takes place during antenatal development. A ventricular dysfunction observed in some cases of cyanotic heart defects could not be predicted by the estimation of MVD.