Erin S DeMartino1, Rodrigo Cartin-Ceba, James Y Findlay, Julie K Heimbach, Michael J Krowka. 1. 1 Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN.2 Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Scottsdale, AZ.3 Department of Anesthesiology, Mayo Clinic, Rochester, MN.4 William J. von Liebig Transplant Center, Mayo Clinic, Rochester, MN.5 Division of Transplantation Surgery, Mayo Clinic, Rochester, MN.
Abstract
BACKGROUND: Pulmonary hypertension (PH) exists when mean pulmonary artery pressure (mPAP) is 25 mm Hg or greater. mPAP of 35 mm Hg or greater, with increased pulmonary vascular resistance from portopulmonary hypertension, has been associated with increased post-liver transplant (LT) mortality. However, mPAP of 35 mm Hg or greater can also occur in the setting of normal pulmonary vascular resistance from a high flow state and/or increased pulmonary venous volume. We describe the frequency of patients with mPAP of 35 mm Hg or greater at LT and correlate their clinical outcomes with hemodynamic characteristics. METHODS: We reviewed hemodynamics of 300 consecutive adult patients undergoing LT. Primary and secondary outcomes were transplant hospitalization mortality and 1-year mortality. RESULTS: Overall, PH was documented in 117 (39%) of 300 transplant recipients. Five patients were receiving ongoing treatment for portopulmonary hypertension at the time of transplant. mPAP of 35 mm Hg or greater was seen in 31 of 300 patients (10.3%; median, 38 mm Hg; range, 35-46 mm Hg). No intraoperative deaths occurred. Transplant hospitalization mortality was 0% for those with mPAP of 35 mm Hg or greater (vs 2.2% if mPAP < 35 mm Hg, P = 1.0). One-year mortality was similar for patients with and without mPAP of 35 mm Hg or greater (3.2% vs 6.0%, P = 1.0). No deaths were associated with right heart failure. CONCLUSIONS: At the time of LT, 39% of recipients had PH (mPAP ≥ 25 mm Hg) and 10.3% had mPAP ≥ 35 mm Hg. When associated with a high flow state and/or increased volume, transplant hospitalization and 1-year posttransplant outcomes were not adversely affected.
BACKGROUND: Pulmonary hypertension (PH) exists when mean pulmonary artery pressure (mPAP) is 25 mm Hg or greater. mPAP of 35 mm Hg or greater, with increased pulmonary vascular resistance from portopulmonary hypertension, has been associated with increased post-liver transplant (LT) mortality. However, mPAP of 35 mm Hg or greater can also occur in the setting of normal pulmonary vascular resistance from a high flow state and/or increased pulmonary venous volume. We describe the frequency of patients with mPAP of 35 mm Hg or greater at LT and correlate their clinical outcomes with hemodynamic characteristics. METHODS: We reviewed hemodynamics of 300 consecutive adult patients undergoing LT. Primary and secondary outcomes were transplant hospitalization mortality and 1-year mortality. RESULTS: Overall, PH was documented in 117 (39%) of 300 transplant recipients. Five patients were receiving ongoing treatment for portopulmonary hypertension at the time of transplant. mPAP of 35 mm Hg or greater was seen in 31 of 300 patients (10.3%; median, 38 mm Hg; range, 35-46 mm Hg). No intraoperative deaths occurred. Transplant hospitalization mortality was 0% for those with mPAP of 35 mm Hg or greater (vs 2.2% if mPAP < 35 mm Hg, P = 1.0). One-year mortality was similar for patients with and without mPAP of 35 mm Hg or greater (3.2% vs 6.0%, P = 1.0). No deaths were associated with right heart failure. CONCLUSIONS: At the time of LT, 39% of recipients had PH (mPAP ≥ 25 mm Hg) and 10.3% had mPAP ≥ 35 mm Hg. When associated with a high flow state and/or increased volume, transplant hospitalization and 1-year posttransplant outcomes were not adversely affected.
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