Saving Tiny Hearts Society

Filing Period

Jan 1, 2011 to Dec 31, 2011

Signed

Jun 21, 2012

Return Version

2011v1.2

Gross Receipts

$389,377

Mission

Major Activities

Activity 2

FETAL & POSTNATAL EFFECTS OF HYPOXIA: This research will determine if there are factors which put infants with complex CHD at increased risk for brain injury due to abnormalities in blood flow to the brain that occur in the womb as a result of congenital heart disease (CHD). This study will show whether brain abnormalities identified at birth by magnetic resonance imaging (MRI) are related to blood flow alterations in the womb, and whether brain abnormalities found at birth are worsened by low brain oxygen levels that occur before, during, and after heart surgery.The specific aims of this study will be to show that abnormalities in blood flow in the brain assessed by ultrasound in fetuses with complex CHD are associated with abnormal brain findings on MRI obtained in the newborn period prior to surgery, and that sustained low oxygen levels in the brain measured in newborns using near infra-red spectroscopy (NIRS) monitoring before, during, and after repair of CHD, are associated with new or worsened findings on brain MRI obtained after surgery. A secondary aim will be to show that blood flow in the brain assessed by ultrasound in fetuses with complex CHD and preoperative brain abnormalities suggestive of delayed brain maturity will be associated with an increased frequency and/or severity of postoperative brain abnormalities shown to be associated with decreased brain oxygen levels. ADDITIONAL STUDY INFORMATION IS AVAILABLE AT WWW.SAVINGTINYHEARTS.ORG/AWARDS/HYPOXIA.HTML

Activity 3

DEFINING NEW PARADIGMS FOR ARRHYTHMIA AND SUDDEN CARDIAC DEATH IN CHILDREN: Human ANK2 mutations result in severe cardiac electrical and structural abnormalities (e.g. potentially fatal ventricular arrhythmias) in children and young adults. Despite the clear link between human ANK2 mutations and potentially fatal cardiac phenotypes in children, essentially nothing is known regarding 1) how human ANK2 mutations affecting ankyrin-B function cause severe structural and electrical dysfunction in the developing heart, or 2) how ankyrin-B expression is regulated in humans. The proposed research will combine a host of synergistic approaches and a newly generated animal model of ankyrin-B (ANK2) deficiency to define the cause of fatal congenital cardiac phenotypes in children with ankyrin-B mutations. We anticipate that the new information gained through the Saving Tiny Hearts Foundation will deliver critical new insight into our understanding of potentially fatal cardiac arrhythmia in children, as well as provide a necessary first step for developing improved diagnostics, as well as therapies for regulating cardiac function in common forms of pediatric heart disease.

Filer

EIN

20-5505536