Impact of secondary pulmonary hypertension on lung transplant outcome

Torin P. Fitton, Tomasz R. Kosowski, Christopher J. Barreiro, Vincent Chan, Nishant D. Patel, Marvin C. Borja, Jonathan B. Orens, John Conte

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22 Citations (Scopus)

Abstract

Introduction: Secondary pulmonary hypertension (SPH), defined as a mean pulmonary artery pressure (PAM) greater than 25 mm Hg, complicates end-stage lung diseases of varying etiology. Although previous studies have suggested that SPH does not adversely affect outcome, no study has assessed the impact of the degree of SPH. Methods: A retrospective review of the lung transplant database was used to identify patients who underwent either single-lung (SLT) or bilateral lung transplantation (BLT) complicated by SPH. SPH patients were stratified into low SPH (PAM = 30-40 mm Hg) and high SPH (PAM ≥ 40 mm Hg). Each group was further sub-categorized into SLT or BLT. Patients with a heart-lung transplant or primary pulmonary hypertension were excluded. Recipients without pulmonary hypertension transplanted over the same time were used as controls. Data are reported as controls vs low SPH vs high SPH. Results: One hundred-four patients received lung transplants between August 1998 and March 2003. There were 45 patients (18 men and 27 women) with SPH. Of these, 28 patients had low SPH, and 17 patients had high SPH. Forty-two patients (18 men and 24 women) without PH were the controls. There were no significant differences between groups except pre-operative oxygen dependence (81% vs 100% vs 94%, respectively) and use of CPB (28.6% vs 57.1% vs 64.7%, respectively). Pao2-Pao2 gradients and Pao2/Fio2 ratios were significantly worse in the high SPH group (116.2 vs 132.9 vs 186.3; p < 0.006) and (277.8 vs 234.3 vs 214.4; p < 0.026) respectively. There was no statistical difference in length of mechanical ventilation or duration of intensive care unit stay between groups. PAMs were significantly different pre-operatively (22.2 ± 0.8 vs 34.0 ± 0.6 vs 47.8 ± 2.0; p < 0.001) and post-operatively (20.9 ± 1.1 vs 23.7 ± 1.3 vs 24.8 ± 2.1; p < 0.001). There were no operative deaths. There were 3 early deaths in the control group, 1 in the low SPH group, and 3 in the high SPH group, none were related to pulmonary hypertension. Actuarial survival at 12, 24, and 48 months was not significantly different among the groups nor between SLT or BLT with SPH. Conclusion: Although SPH increases the risk of reperfusion injury; survival is equivalent with mild or moderate pulmonary hypertension. Either SLT or BLT may be used in patients with SPH without compromising outcome. This has the added benefit of expanding the donor pool.

Original languageEnglish (US)
Pages (from-to)1254-1259
Number of pages6
JournalJournal of Heart and Lung Transplantation
Volume24
Issue number9
DOIs
StatePublished - Jan 1 2005

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Pulmonary Hypertension
Transplants
Lung
Lung Transplantation
Survival

All Science Journal Classification (ASJC) codes

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine
  • Transplantation

Cite this

Fitton, T. P., Kosowski, T. R., Barreiro, C. J., Chan, V., Patel, N. D., Borja, M. C., ... Conte, J. (2005). Impact of secondary pulmonary hypertension on lung transplant outcome. Journal of Heart and Lung Transplantation, 24(9), 1254-1259. https://doi.org/10.1016/j.healun.2004.08.009
Fitton, Torin P. ; Kosowski, Tomasz R. ; Barreiro, Christopher J. ; Chan, Vincent ; Patel, Nishant D. ; Borja, Marvin C. ; Orens, Jonathan B. ; Conte, John. / Impact of secondary pulmonary hypertension on lung transplant outcome. In: Journal of Heart and Lung Transplantation. 2005 ; Vol. 24, No. 9. pp. 1254-1259.
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abstract = "Introduction: Secondary pulmonary hypertension (SPH), defined as a mean pulmonary artery pressure (PAM) greater than 25 mm Hg, complicates end-stage lung diseases of varying etiology. Although previous studies have suggested that SPH does not adversely affect outcome, no study has assessed the impact of the degree of SPH. Methods: A retrospective review of the lung transplant database was used to identify patients who underwent either single-lung (SLT) or bilateral lung transplantation (BLT) complicated by SPH. SPH patients were stratified into low SPH (PAM = 30-40 mm Hg) and high SPH (PAM ≥ 40 mm Hg). Each group was further sub-categorized into SLT or BLT. Patients with a heart-lung transplant or primary pulmonary hypertension were excluded. Recipients without pulmonary hypertension transplanted over the same time were used as controls. Data are reported as controls vs low SPH vs high SPH. Results: One hundred-four patients received lung transplants between August 1998 and March 2003. There were 45 patients (18 men and 27 women) with SPH. Of these, 28 patients had low SPH, and 17 patients had high SPH. Forty-two patients (18 men and 24 women) without PH were the controls. There were no significant differences between groups except pre-operative oxygen dependence (81{\%} vs 100{\%} vs 94{\%}, respectively) and use of CPB (28.6{\%} vs 57.1{\%} vs 64.7{\%}, respectively). Pao2-Pao2 gradients and Pao2/Fio2 ratios were significantly worse in the high SPH group (116.2 vs 132.9 vs 186.3; p < 0.006) and (277.8 vs 234.3 vs 214.4; p < 0.026) respectively. There was no statistical difference in length of mechanical ventilation or duration of intensive care unit stay between groups. PAMs were significantly different pre-operatively (22.2 ± 0.8 vs 34.0 ± 0.6 vs 47.8 ± 2.0; p < 0.001) and post-operatively (20.9 ± 1.1 vs 23.7 ± 1.3 vs 24.8 ± 2.1; p < 0.001). There were no operative deaths. There were 3 early deaths in the control group, 1 in the low SPH group, and 3 in the high SPH group, none were related to pulmonary hypertension. Actuarial survival at 12, 24, and 48 months was not significantly different among the groups nor between SLT or BLT with SPH. Conclusion: Although SPH increases the risk of reperfusion injury; survival is equivalent with mild or moderate pulmonary hypertension. Either SLT or BLT may be used in patients with SPH without compromising outcome. This has the added benefit of expanding the donor pool.",
author = "Fitton, {Torin P.} and Kosowski, {Tomasz R.} and Barreiro, {Christopher J.} and Vincent Chan and Patel, {Nishant D.} and Borja, {Marvin C.} and Orens, {Jonathan B.} and John Conte",
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Fitton, TP, Kosowski, TR, Barreiro, CJ, Chan, V, Patel, ND, Borja, MC, Orens, JB & Conte, J 2005, 'Impact of secondary pulmonary hypertension on lung transplant outcome', Journal of Heart and Lung Transplantation, vol. 24, no. 9, pp. 1254-1259. https://doi.org/10.1016/j.healun.2004.08.009

Impact of secondary pulmonary hypertension on lung transplant outcome. / Fitton, Torin P.; Kosowski, Tomasz R.; Barreiro, Christopher J.; Chan, Vincent; Patel, Nishant D.; Borja, Marvin C.; Orens, Jonathan B.; Conte, John.

In: Journal of Heart and Lung Transplantation, Vol. 24, No. 9, 01.01.2005, p. 1254-1259.

Research output: Contribution to journalArticle

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AU - Fitton, Torin P.

AU - Kosowski, Tomasz R.

AU - Barreiro, Christopher J.

AU - Chan, Vincent

AU - Patel, Nishant D.

AU - Borja, Marvin C.

AU - Orens, Jonathan B.

AU - Conte, John

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Y1 - 2005/1/1

N2 - Introduction: Secondary pulmonary hypertension (SPH), defined as a mean pulmonary artery pressure (PAM) greater than 25 mm Hg, complicates end-stage lung diseases of varying etiology. Although previous studies have suggested that SPH does not adversely affect outcome, no study has assessed the impact of the degree of SPH. Methods: A retrospective review of the lung transplant database was used to identify patients who underwent either single-lung (SLT) or bilateral lung transplantation (BLT) complicated by SPH. SPH patients were stratified into low SPH (PAM = 30-40 mm Hg) and high SPH (PAM ≥ 40 mm Hg). Each group was further sub-categorized into SLT or BLT. Patients with a heart-lung transplant or primary pulmonary hypertension were excluded. Recipients without pulmonary hypertension transplanted over the same time were used as controls. Data are reported as controls vs low SPH vs high SPH. Results: One hundred-four patients received lung transplants between August 1998 and March 2003. There were 45 patients (18 men and 27 women) with SPH. Of these, 28 patients had low SPH, and 17 patients had high SPH. Forty-two patients (18 men and 24 women) without PH were the controls. There were no significant differences between groups except pre-operative oxygen dependence (81% vs 100% vs 94%, respectively) and use of CPB (28.6% vs 57.1% vs 64.7%, respectively). Pao2-Pao2 gradients and Pao2/Fio2 ratios were significantly worse in the high SPH group (116.2 vs 132.9 vs 186.3; p < 0.006) and (277.8 vs 234.3 vs 214.4; p < 0.026) respectively. There was no statistical difference in length of mechanical ventilation or duration of intensive care unit stay between groups. PAMs were significantly different pre-operatively (22.2 ± 0.8 vs 34.0 ± 0.6 vs 47.8 ± 2.0; p < 0.001) and post-operatively (20.9 ± 1.1 vs 23.7 ± 1.3 vs 24.8 ± 2.1; p < 0.001). There were no operative deaths. There were 3 early deaths in the control group, 1 in the low SPH group, and 3 in the high SPH group, none were related to pulmonary hypertension. Actuarial survival at 12, 24, and 48 months was not significantly different among the groups nor between SLT or BLT with SPH. Conclusion: Although SPH increases the risk of reperfusion injury; survival is equivalent with mild or moderate pulmonary hypertension. Either SLT or BLT may be used in patients with SPH without compromising outcome. This has the added benefit of expanding the donor pool.

AB - Introduction: Secondary pulmonary hypertension (SPH), defined as a mean pulmonary artery pressure (PAM) greater than 25 mm Hg, complicates end-stage lung diseases of varying etiology. Although previous studies have suggested that SPH does not adversely affect outcome, no study has assessed the impact of the degree of SPH. Methods: A retrospective review of the lung transplant database was used to identify patients who underwent either single-lung (SLT) or bilateral lung transplantation (BLT) complicated by SPH. SPH patients were stratified into low SPH (PAM = 30-40 mm Hg) and high SPH (PAM ≥ 40 mm Hg). Each group was further sub-categorized into SLT or BLT. Patients with a heart-lung transplant or primary pulmonary hypertension were excluded. Recipients without pulmonary hypertension transplanted over the same time were used as controls. Data are reported as controls vs low SPH vs high SPH. Results: One hundred-four patients received lung transplants between August 1998 and March 2003. There were 45 patients (18 men and 27 women) with SPH. Of these, 28 patients had low SPH, and 17 patients had high SPH. Forty-two patients (18 men and 24 women) without PH were the controls. There were no significant differences between groups except pre-operative oxygen dependence (81% vs 100% vs 94%, respectively) and use of CPB (28.6% vs 57.1% vs 64.7%, respectively). Pao2-Pao2 gradients and Pao2/Fio2 ratios were significantly worse in the high SPH group (116.2 vs 132.9 vs 186.3; p < 0.006) and (277.8 vs 234.3 vs 214.4; p < 0.026) respectively. There was no statistical difference in length of mechanical ventilation or duration of intensive care unit stay between groups. PAMs were significantly different pre-operatively (22.2 ± 0.8 vs 34.0 ± 0.6 vs 47.8 ± 2.0; p < 0.001) and post-operatively (20.9 ± 1.1 vs 23.7 ± 1.3 vs 24.8 ± 2.1; p < 0.001). There were no operative deaths. There were 3 early deaths in the control group, 1 in the low SPH group, and 3 in the high SPH group, none were related to pulmonary hypertension. Actuarial survival at 12, 24, and 48 months was not significantly different among the groups nor between SLT or BLT with SPH. Conclusion: Although SPH increases the risk of reperfusion injury; survival is equivalent with mild or moderate pulmonary hypertension. Either SLT or BLT may be used in patients with SPH without compromising outcome. This has the added benefit of expanding the donor pool.

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Fitton TP, Kosowski TR, Barreiro CJ, Chan V, Patel ND, Borja MC et al. Impact of secondary pulmonary hypertension on lung transplant outcome. Journal of Heart and Lung Transplantation. 2005 Jan 1;24(9):1254-1259. https://doi.org/10.1016/j.healun.2004.08.009