title: Hemodynamics and arteriovenous malformations in cavopulmonary anastomosis: the case for residual antegrade pulsatile flow.
abstract: OBJECTIVE
  Continuous flow in Fontan circulation results in impairment of pulmonary artery endothelial function, increased pulmonary vascular resistance, and, potentially, late failure of Fontan circulation. Bidirectional cavopulmonary shunt is the interim procedure in palliation of patients with single-ventricle physiology, but pulmonary arteriovenous malformations occur in many patients. In a porcine chronic model of cavopulmonary shunt, we studied pulmonary hemodynamics, pulmonary arteriovenous malformation occurrence, and gas exchange capabilities. We hypothesized that residual antegrade pulsatile pulmonary flow may attenuate the deleterious effects of nonpulsatile Fontan-type circulation.
  
  
  METHODS
  Thirty pigs underwent a sham procedure (n = 10, group I), a cavopulmonary shunt with right pulmonary artery ligation (n = 10, group II, nonpulsatile), or a cavopulmonary shunt with proximal right pulmonary artery partial ligation (n = 10, group III, micropulsatile). Three months later, in vivo hemodynamics, blood gas exchange, pulmonary arteriovenous malformation occurrence, and lung histology were assessed.
  
  
  RESULTS
  At 3 months, group II right lungs demonstrated significantly increased pulmonary artery pressure, pulmonary vascular resistance, and evidence of pulmonary arteriovenous malformations compared with groups I and III (all P < .001). Group III lungs also showed increased pulmonary artery pressure and pulmonary vascular resistance compared with the sham group, but significantly less than group II. Group III right lungs had the best gas exchange performance, with less histologic changes compared with group II.
  
  
  CONCLUSIONS
  We developed a viable chronic large animal model of bidirectional cavopulmonary anastomosis. Residual antegrade pulsatile flow in the setting of a cavopulmonary shunt prevents pulmonary arteriovenous malformation formation and attenuates, but does not suppress, the development of pulmonary hypertension. From a clinical standpoint, these data would support keeping a small amount of antegrade pulsatile flow during creation of a cavopulmonary shunt.
authors.affiliation: Department of Cardiothoracic Surgery, Hôpital Louis Pradel, Hospices Civils de Lyon, Lyon, France. Electronic address: roland.henaine@chu-lyon.fr.
authors.forename: Roland
authors.initials: R
authors.lastname: Henaine
authors.forename: Mathieu
authors.initials: M
authors.lastname: Vergnat
authors.forename: Olaf
authors.initials: O
authors.lastname: Mercier
authors.forename: Alain
authors.initials: A
authors.lastname: Serraf
authors.forename: Vincent
authors.initials: V
authors.lastname: De Montpreville
authors.forename: Jean
authors.initials: J
authors.lastname: Ninet
authors.forename: Emile A
authors.initials: EA
authors.lastname: Bacha
mesh_terms: D000818:Animals; D062186:Arterial Pressure; D018729:Fontan Procedure / Q000009:adverse effects*; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology; D008026:Ligation; D008168:Lung / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology; D023421:Models, Animal; D011651:Pulmonary Artery / Q000293:injuries* / Q000503:physiopathology / Q000601:surgery*; D011652:Pulmonary Circulation; D011659:Pulmonary Gas Exchange; D011667:Pulmonary Veins / Q000293:injuries* / Q000503:physiopathology; D011673:Pulsatile Flow; D013552:Swine; D013997:Time Factors; D017211:Treatment Failure; D014655:Vascular Resistance; D057772:Vascular System Injuries / Q000209:etiology* / Q000503:physiopathology
keywords: 11.3; 17; 20; 9; CPS; Fio(2); PA; PAP; PVP; PVR; Pco(2); Po(2); SVC; Sao(2); arterial oxyhemoglobin saturation; cavopulmonary shunt; inspired oxygen fraction; partial pressure of carbon dioxide; partial pressure of oxygen; pulmonary artery; pulmonary artery pressure; pulmonary vascular resistance; pulmonary vein pressure; superior vena cava