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

Mahima Vijayaraghavan, Kurt W. Prins, Sasha Z. Prisco, Sue Duval, Ranjit John, Stephen L. Archer, E. Kenneth Weir, Rochus Voeller, Andrew W. Shaffer, Thenappan Thenappan

Research output: Contribution to journalArticlepeer-review

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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  • Journal Article

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