title: Hemodynamic impact of transseptal access to the ascending aorta in a porcine model.
abstract: OBJECTIVE
  To evaluate the hemodynamic impact of transseptal sheath access to the ascending aorta using increasing sheath diameters.
  
  
  METHODS
  Transseptal puncture was performed in 6 pigs (62±9 kg) facilitating guidewire passage across the left heart to the descending aorta to establish transseptal through-and-through access into the ascending aorta. Hemodynamic parameters were evaluated during 6- to 16-F sheath deployments and after sheath retraction according to a standardized protocol. Fluorescent microspheres were injected for quantitative assessment of myocardial and cerebral perfusion and left-right shunting volume.
  
  
  RESULTS
  Cardiac output, heart rate, and central venous pressure (CVP) were stable throughout the study in all animals. The ratio between pulmonary artery pressure and mean arterial pressure was significantly higher during sheath deployment compared to after retraction (p<0.01), indicating transient mitral valve insufficiency. The ratio between left atrial pressure and CVP was significantly higher with the sheath in place (p<0.01), signaling transient left-right shunting; the hemodynamic alteration disappeared after sheath retraction. Myocardial perfusion (p=0.224), cerebral perfusion (p=0.209), and left-right shunting volume (p=0.111) were not significantly affected by the transseptal access.
  
  
  CONCLUSIONS
  Transseptal access to the ascending aorta in a porcine model is feasible without persisting hemodynamic impairment or severe influence on myocardial or cerebral perfusion even with up to 16-F sheaths. Potential adverse effects need to be addressed before clinical use of this alternative access to the ascending aorta, aortic arch, and its side branches.
authors.affiliation: Department of Vascular Medicine, University Heart Center Hamburg, Germany.
authors.forename: Sabine
authors.initials: S
authors.lastname: Wipper
authors.forename: Christina
authors.initials: C
authors.lastname: Lohrenz
authors.forename: Klaas
authors.initials: K
authors.lastname: Peymann
authors.forename: Detlef
authors.initials: D
authors.lastname: Russ
authors.forename: Jan Felix
authors.initials: JF
authors.lastname: Kersten
authors.forename: Sebastian William
authors.initials: SW
authors.lastname: Carpenter
authors.forename: Axel
authors.initials: A
authors.lastname: Larena-Avellaneda
authors.forename: Christian
authors.initials: C
authors.lastname: Detter
authors.forename: Sebastian
authors.initials: S
authors.lastname: Debus
authors.forename: Tilo
authors.initials: T
authors.lastname: Kölbel
mesh_terms: D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D062186:Arterial Pressure; D006328:Cardiac Catheterization / Q000009:adverse effects / Q000295:instrumentation*; D062906:Cardiac Catheters; D002302:Cardiac Output; D002496:Central Venous Pressure; D002560:Cerebrovascular Circulation; D003326:Coronary Circulation; D004867:Equipment Design; D005260:Female; D006339:Heart Rate; D006439:Hemodynamics; D008297:Male; D008944:Mitral Valve Insufficiency / Q000209:etiology / Q000503:physiopathology; D023421:Models, Animal; D011677:Punctures; D015641:Radiography, Interventional; D034421:Sus scrofa; D014655:Vascular Resistance