Importance of adhesion molecules for children with congenital heart disease.
BACKGROUND
The aim of our study was to compare the blood levels of adhesion molecules in children with different heart diseases and pulmonary flow rates.


METHODS
In this study, we evaluated the levels of soluble intercellular adhesion molecule-1 and soluble vascular cellular adhesion molecule-1 in blood samples of 65 children with different congenital heart diseases. The patients were divided into four groups according to their pulmonary blood flow. The first group had increased pulmonary blood flow with pulmonary hypertension and left-to-right shunt. The second group had increased pulmonary blood flow without pulmonary hypertension and left-to-right shunt. The third group had decreased pulmonary blood flow with cyanotic congenital heart disease and the fourth group had normal pulmonary blood flow with left ventricle outflow tract obstruction and aortic stenosis.


RESULTS
The highest soluble intercellular and vascular cellular adhesion molecule-1 levels with the mean values of 420.2 nanograms per millilitre and 1382.1 nanograms per millilitre, respectively, were measured in the first group and the lowest levels with the mean values of 104.4 and 358.6 nanograms per millilitre, respectively, were measured in the fourth group. The highest pulmonary blood pressure levels were found in the first group.


CONCLUSIONS
Endothelial activity is influenced not only by left-to-right shunt with pulmonary hypertension, but also by decreased pulmonary blood flow in cyanotic heart diseases. Adhesion molecules are valuable markers of endothelial activity in congenital heart diseases, and they are influenced by pulmonary blood flow rate.
Department of Pediatric Cardiology, Istanbul, Turkey. ayildirimmd@yahoo.com
Ayşe
A
Yıldırım
Aysu T
AT
Karaağaç
Fusun
F
Güzelmeriç
Nihat
N
Çine
Naci C
NC
Öner
D001024:Aortic Valve Stenosis / Q000097:blood / Q000150:complications / Q000503:physiopathology; D065627:Familial Primary Pulmonary Hypertension; D005260:Female; D006330:Heart Defects, Congenital / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D006344:Heart Septal Defects, Atrial / Q000097:blood / Q000150:complications / Q000503:physiopathology; D006345:Heart Septal Defects, Ventricular / Q000097:blood / Q000150:complications / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood / Q000150:complications / Q000503:physiopathology; D007223:Infant; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008297:Male; D011652:Pulmonary Circulation / Q000502:physiology*; D013771:Tetralogy of Fallot / Q000097:blood / Q000150:complications / Q000503:physiopathology; D018785:Tricuspid Atresia / Q000097:blood / Q000150:complications / Q000503:physiopathology; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*; D014694:Ventricular Outflow Obstruction / Q000097:blood / Q000150:complications / Q000503:physiopathology
C573420:ICAM1 protein, human; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1