Abstract
Dilated cardiomyopathy is an important cause of congestive cardiac failure in infants and children. Mobilizing hematopoietic progenitor cells is a promising intervention to this deadly disease. Aim. Evaluate granulocyte colony stimulating factor (GCSF) as therapeutic modality in children with idiopathic dilated cardiomyopathy (IDCM). Subjects and Methods. This case-control prospective study was conducted on 20 children with IDCM following up at Cardiology Clinic Children's Hospital, Ain Shams University (group 1) who were compared to another 10 age-, sex-, duration-of-illness-, and systolic-function-matched children with IDCM as control (group 2). They were subjected to history taking, clinical examination, echocardiography, and peripheral blood CD34+ cell assessment before and one week after GCSF intake for 5 consecutive days (by group 1 but not group 2). Results. A significant improvement in echocardiographic data and CD34+-T-cell increase was found in group 1 one week after GCSF intake and for the next 6 months CD34+ T cells percentage of change showed no significant correlation with the that of the left ventricular dimensions and systolic function. Conclusion. Administration of GCSF to children with IDCM resulted in clinical and echocardiographic improvement not correlated to mobilized CD34+ T cells, implying involvement of additional mechanisms over simple stem cell mobilization.
Highlights
Dilated cardiomyopathy is an important cause of chronic congestive cardiac failure in infants and children
This case-control prospective study was conducted on twenty children with idiopathic dilated cardiomyopathy following up at cardiology clinic Children’s Hospital, Ain Shams University
This study provides new insights into investigation of a new therapy for pediatric dilated cardiomyopathy patients with advanced heart failure
Summary
Dilated cardiomyopathy is an important cause of chronic congestive cardiac failure in infants and children. A variety of etiological factors have been listed, most patients with echocardiographically documented dilated cardiomyopathy do not possess a demonstrable cause [1]. Poor myocardial function in dilated cardiomyopathy triggers a sequence of compensatory mechanisms that favor myocardial and peripheral vascular remodeling by necrosis, fibrosis, and apoptosis which do more harm than good [2]. Medical intervention will remain the cornerstone of management until advances in surgical techniques become more widely available [3]. Mobilizing hematopoietic progenitor cells to repair the failing heart is a promising intervention to halt the progression of this deadly disease. Low doses of GCSF, five microgram per kilogram per day, were found to improve systolic function in adults with advanced systolic heart failure [2]
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