Hemodynamic Characteristics and Outcomes of Pulmonary Hypertension in Patients Undergoing Tricuspid Valve Repair or Replacement

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Abstract

Background: The impact of pulmonary hypertension (PH) on outcomes after surgical tricuspid valve replacement (TVR) and repair (TVr) is unclear. We sought to characterize PH in patients undergoing TVR/TVr, based on invasive hemodynamics and evaluate the effect of PH on mortality. Methods: We identified 86 consecutive patients who underwent TVR/TVr with invasive hemodynamic measurements within 3 months before surgery. We used Kaplan-Meier survival and restricted mean survival time (RMST) analyses to quantify the effects of PH on survival. Results: The mean age was 63 ± 13 years, 59% were female, 45% had TVR, 55% had TVr, 39.5% had isolated TVR/TVr, and 60.5% had TVR/TVr concomitant with other cardiac surgeries). Eighty-six percent of these patients had PH with a mean pulmonary artery pressure of 30 ± 10 mm Hg, pulmonary vascular resistance (PVR) of 2.5 (interquartile range: 1.5-3.9) Wood units (WU), pulmonary arterial compliance of 2.3 (1.6-3.6) mL/mm Hg, and pulmonary arterial elastance of 0.8 (0.6-1.2) mm Hg/mL. Cardiac output was mildly reduced at 4.0 ± 1.4 L/min, with elevated right-atrial pressure (14 ± 12 mm Hg) and pulmonary capillary wedge pressure (19 ± 7 mm Hg). Over a median follow-up of 6.3 years, 22% of patients died. Patients with PVR ≥ 2.5 WU had lower RMST over 5 years compared with patients with PVR < 2.5 WU. Conclusion: PH is common in patients undergoing TVR/TVr, with combined pre- and postcapillary being the most common type. PVR ≥ 2.5 WU is associated with lower survival at 5-year follow-up.

Original languageEnglish (US)
Pages (from-to)488-497
Number of pages10
JournalCJC Open
Volume3
Issue number4
DOIs
StatePublished - Apr 2021

Bibliographical note

Funding Information:
K.W.P. is funded by NIH K08 HL140100, the Cardiovascular Medical Research and Education Fund, a Lillehei Heart Institution Cardiovascular Seed Grant, and the United Therapeutics Jenesis Award. S.L.A. is funded by Canada Foundation for Innovation (229252 and 33012), a Tier 1 Canada Research Chair in Mitochondrial Dynamics and Translational Medicine (950-229252), the Queens Cardiopulmonary Unit (QCPU), and a grant from the William J. Henderson Foundation. S.Z.P. is funded by NIH T32 HL144472, a University of Minnesota Clinical and Translational Science award (NIH UL1 TR0029494) and a University of Minnesota Medical School Academic Investment Educational Program Grant. T.T. is funded by the Cardiovascular Medical Research and Education Fund.

Publisher Copyright:
© 2020 Canadian Cardiovascular Society

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