Further implicating derangements in active peptide clearance physiology in the etiology of PLE and PB is the fact that the classic member of the neutral endopeptidase class is (the misnamed) Angiotensin Converting Enzyme (ACE) , which actually cleaves a number of these small peptide signaling molecules including VIP and Substance P. Virtually all patients with Fontan physiology are on large doses of ACE-inhibitors to lower systemic afterload. Captopril-induced inhibition of VIP and Substance P inactivation would significantly increase already elevated systemic levels of these signaling peptides and further potentiate the etiology of PLE and PB in Fontan-palliated patients. Variations of neutral endopeptidase inhibitor ("ACE inhibitor" ) drug dosage and/or genotype variation of ACE which causes dramatically altered activity can in part explain the variable incidence of PLE and PB in Fontan physiology patients. In this study, the use and dose of ACE inhibitor that each patient is on will be recorded to see if there is a correlation between ACE inhibitor dose and measured VIP and Substance P levels. There are wide variation of ACE gene genomics that have been described for decades. Intriguingly, approximately 10-15% of all persons have a newly described genomic variation of the ACE gene which leads to profoundly reduced circulating levels of ACE and increased susceptibility to ACE inhibition and 10-15% of patients with Fontans develop PB or PLE.