1 ion of this procedure for children born with tricuspid atresia.

2  suggest a genetic basis for the syndrome of tricuspid atresia.

3 yndrome, 10 had pulmonary atresia, and 1 had tricuspid atresia.

4 ies: tetralogy of Fallot (15 patients, 25%), tricuspid atresia (12 patients, 20%), Ebstein's anomaly

5 (95% confidence interval, 45.8 to 64.4); and tricuspid atresia, 74.6% (95% confidence interval, 62.4

6        We examined a total of 53 hearts with tricuspid atresia and 58 normal hearts matched for age.

7  was previously identified in a patient with tricuspid atresia and large secundum atrial septal defec

8 ct ventricular septum, single ventricle, and tricuspid atresia born in 1996 to 2003 were identified f

9 lar septal defects, tetralogy of Fallot, and tricuspid atresia, defects that resemble those associate

10 with the nonfenestrated Fontan procedure for tricuspid atresia has been gratifying, with most survivo

11                The myocardium of hearts with tricuspid atresia is consistently more fibrotic than nor

12 (n = 16) or secondary (n = 26) palliation of tricuspid atresia (n = 13), hypoplastic left heart syndr

13 ere hypoplastic left heart syndrome (n=346), tricuspid atresia (n=103), tetralogy of Fallot (n=127),

14                                              Tricuspid atresia (TA) is a common form of congenital he

15 tive heart failure at E13 with a syndrome of tricuspid atresia that includes an absent tricuspid valv

16 present clinical status of 216 patients with tricuspid atresia who had a nonfenestrated Fontan proced

17 l Wnt signaling in the myocardium results in tricuspid atresia with hypoplastic right ventricle assoc

18 s with double-inlet left ventricle (DILV) or tricuspid atresia with transposed great arteries (TA-TGA

19 t ventricle in 10, unbalanced AV canal in 5, tricuspid atresia with transposition of the great vessel