• Wendy Whiteside, Justin T Tretter, Jamil Aboulhosn, Osamah Aldoss, Aimee K Armstrong, Martin L Bocks, Matthew J Gillespie, Thomas K Jones, Mary Hunt Martin, Jeffrey J Meadows, Christina M Metcalf, Mariel E Turner, Thomas Zellers, and Bryan H Goldstein.
• From the Heart Institute, Cincinnati Children's Hospital Medical Center, OH (W.W., J.T.T., C.M.M., B.H.G.); Division of Cardiology, Ahmanson/Adult Congenital Heart Disease Center, Los Angeles, CA (J.A.); Division of Pediatric Cardiology, Department of Pediatrics, University of Iowa Children's Hospital (O.A.); Division of Pediatric Cardiology, Department of Pediatrics, University of Michigan C. S. Mott Children's Hospital, Ann Arbor (A.K.A., M.L.B.); Division of Cardiology, the Children's Hospital of Philadelphia, PA (M.J.G.); Seattle Children's Hospital, University of Washington (T.K.J.); Division of Cardiology, Department of Pediatrics, University of Utah, Salt Lake City (M.H.M.); Division of Cardiology, UCSF Benioff Children's Hospital, University of California (J.J.M.); Division of Pediatric Cardiology, Columbia University College of Physicians and Surgeons, Morgan Stanley Children's Hospital of New York Presbyterian (M.E.T.); and Division of Cardiology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas (T.Z.). wendywhiteside@gmail.com.
• Circ Cardiovasc Interv. 2017 Sep 1; 10 (9).

BackgroundTranscatheter pulmonary valve replacement (TPVR) is an established therapy for dysfunctional right ventricular (RV) outflow tract conduits. TPVR in patients with congenitally corrected transposition of the great arteries, subpulmonary left ventricle, and left ventricular outflow tract (LVOT) conduit dysfunction has not been studied. Unique anatomic and physiological aspects of this population may contribute to distinct risks and outcomes.Methods And ResultsAcross 10 US centers, 27 patients with a dysfunctional LVOT conduit were evaluated in the catheterization laboratory between December 2008 and August 2015 with the intent to perform TPVR. TPVR was successful in 23 patients (85%). Five serious adverse events occurred in 4 cases (15%), including pulmonary hemorrhage, hypotension requiring vasoactive support, conduit disruption requiring covered stent (n=2), and acute RV dysfunction with flash pulmonary edema. After TPVR, the LVOT peak systolic ejection gradient decreased from median of 35 to 17 mm Hg (P<0.001); pulmonary insufficiency was trivial/none in all but 1 patient, where it was mild. Worsening of systemic RV dysfunction or tricuspid regurgitation was seen in 12 patients (57%) and was associated with a significantly lower post-TPVR LVOT peak systolic ejection gradient (median 17 versus 21 mm Hg; P=0.02) and higher post-TPVR RV sphericity index (median 0.88 versus 0.52; P=0.004). Post-TPVR, there were 2 late deaths because of RV failure and 1 cardiac transplantation because of progressive RV dysfunction and tricuspid regurgitation.ConclusionsTPVR in dysfunctional LVOT conduits is feasible but associated with an important rate of TPV nonimplantation and procedural serious adverse events. Worsening systemic RV function and tricuspid regurgitation may develop after LVOT TPVR.© 2017 American Heart Association, Inc.

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