Abstract
BACKGROUND
Primary graft dysfunction is a risk factor of early mortality after lung transplant. Models identifying patients at high risk for primary graft dysfunction are limited. We hypothesize high postreperfusion systolic pulmonary artery pressure is a clinical marker for primary graft dysfunction.
METHODS
This is a retrospective review of 158 consecutive lung transplants performed at a single academic center from January 2020 through July 2022. Only bilateral lung transplants were included and patients with pretransplant extracorporeal life support were excluded.
RESULTS
Primary graft dysfunction occurred in 42.3% (n = 30). Patients with primary graft dysfunction had higher postreperfusion systolic pulmonary artery pressure (41 ± 9.1 mm Hg) than those without (31.5 ± 8.8 mm Hg) (P < .001). Logistic regression showed postreperfusion systolic pulmonary artery pressure is a predictor for primary graft dysfunction (odds ratio 1.14, 95% CI 1.06–1.24, P < .001). Postreperfusion systolic pulmonary artery pressure of 37 mm Hg was optimal for predicting primary graft dysfunction by Youden index. The receiver operating characteristic curve of postreperfusion systolic pulmonary artery pressure at 37 mm Hg (sensitivity 0.77, specificity 0.78, area under the curve 0.81), was superior to the prereperfusion pressure curve at 36 mm Hg (sensitivity 0.77, specificity 0.39, area under the curve 0.57) (P < .01).
CONCLUSIONS
Elevated postreperfusion systolic pulmonary artery pressure after lung transplant is predictive of primary graft dysfunction. Postreperfusion systolic pulmonary artery pressure is more indicative of primary graft dysfunction than prereperfusion systolic pulmonary artery pressure. Using postreperfusion systolic pulmonary artery pressure as a positive signal of primary graft dysfunction allows earlier intervention, which could improve outcomes.
Lung transplantation is becoming an increasingly more common lifesaving therapy for patients with end-stage lung disease. With changes in donor selection, organ preservation, and perioperative management, the median survival of lung transplant patients has increased from 4.7 years to 6.7 years.1,2 Nevertheless, lung transplant outcomes remain inferior to those of other solid organ transplants.3 One important driver of these worse outcomes is primary graft dysfunction (PGD).
PGD is a severe lung injury that occurs within the first 72 hours after lung transplantation and is defined by the presence of diffuse pulmonary opacities on chest imaging and hypoxemia, without another identifiable cause.4 Multiple studies have identified risk factors for PGD, citing variables throughout all stages of the transplant process, from donor and recipient characteristics, to harvesting and storage procedures, to implantation-reperfusion techniques.5–7 Yet, even though PGD is a well-known significant risk factor for both short- and long-term mortality, the incidence remains over 50%.6–10 Ischemia-reperfusion injury is known to play a significant role in the development of PGD and is characterized by microvascular permeability and endothelial cell dysfunction with neutrophil infiltration.11,12 Furthermore, elevated pretransplant mean pulmonary artery pressure is one of the most significant risk factors for PGD.13 However, whether elevated postreperfusion pulmonary artery pressure is associated with and can predict PGD is unknown.
If an elevated postreperfusion pulmonary artery pressure could predict who develops significant PGD, this would allow for expedited treatment with therapies such as inhaled pulmonary vasodilators or extracorporeal membrane oxygenation (ECMO), which both have been shown to improve outcomes for patients diagnosed with PGD.14–17 Therefore, our study objectives were twofold: First, determine if elevated postreperfusion pulmonary artery pressure is associated with PGD; and second, assess if postreperfusion pulmonary artery pressure is a reliable predictor of PGD.
PATIENTS AND METHODS
STUDY DESIGN.
This study was approved by the Northwestern University institutional review board (STU00213616) including a waiver of consent. This is a retrospective review of 158 patients who underwent lung transplants at a single academic center from January 2020 through July 2022. Only patients who underwent bilateral lung transplant were included (N = 99); patients on ECMO support as bridge to transplant were excluded as ECMO could impact the pre–lung transplant systolic pulmonary artery pressure (sPAP) (n = 28). Assuming a PGD incidence of 50%, sample size calculations showed 66 patients were necessary for a confidence level of 90% with 10% margin of error. Data collected included patients’ characteristics, preoperative laboratory values, pre- and postreperfusion sPAP, intraoperative and postoperative outcomes, and donor characteristics. Our institution uses the following donor criteria: ratio of arterial oxygen partial pressure to fractional inspired oxygen >300, no chest x-ray film abnormalities, and no obvious pneumonia on computed tomography scan. Our institution does not use any extended criteria, donation after circulatory death, and ex vivo donors. Prereperfusion sPAP was determined from the patient’s right heart catheterizations at time of listing. Swan-Ganz catheters were placed after anesthesia induction by an anesthesiologist during all transplants. Postreperfusion sPAP was determined from the patient’s Swan-Ganz catheter intraoperative record at the conclusion of the lung transplantation operation, off inhaled nitric oxide (iNO). iNO was started during all lung transplants at the time of hilar dissection and weaned off either at the time of reperfusion for those lung transplants performed off ECMO or after ECMO decannulation. PGD was the primary outcome variable, recorded as the most severe score during the initial 72 hours posttransplant, and defined according to modified International Society of Heart and Lung Transplantation criteria.4
STATISTICAL ANALYSIS.
Recipient and donor demographics, prereperfusion and postreperfusion sPAP, and intraoperative and postoperative outcomes were compared between those patients with PGD grade 0/1 and PGD grade 2/3. Continuous variables were compared using t test and reported as mean SD. Categorical variables were compared using χ2 tests and reported as a number (percentage). P values less than .05 were accepted as statistically significant. Univariate logistic regression analyses were performed to assess the ability of recipient and donor demographics, preoperative laboratory values, prereperfusion and postreperfusion sPAP, and intraoperative outcomes to predict PGD grade 2/3. Those variables with a P value less than .1 were then used to perform a multivariate logistic regression analysis.
The Youden index was used to determine the optimal postreperfusion sPAP to predict PGD grade 2/3. Receiver operating characteristic curves were then created for prereperfusion and postreperfusion sPAP.
Subsequently, recipient and donor demographics, preoperative laboratory values, and intraoperative and postoperative outcomes, including PGD grade 2/3, were compared between those patients with nonelevated and elevated postreperfusion sPAP. Elevated postreperfusion sPAP was defined as any pressure above the previously determined sPAP by Youden index. EZR software (Saitama Medical Center, Jichi Medical University), a graphical user interface for R (The R Foundation for Statistical Computing), was used to perform all analyses.
RESULTS
PATIENT DEMOGRAPHICS AND OUTCOMES.
A total of 71 patients met inclusion criteria; 36 (50.7%) were female and 30 (42.3%) had a smoking history. The average age of patients was 56.3 years, with an average body mass index of 25.7 kg/m2. There were 41 (57.7%) patients who developed PGD grade 0/1 and 30 (42.2%) patients who developed PGD grade 2/3. There were no significant differences in patient demographics, comorbidities, and etiology of lung failure, as well as donor characteristics between those patients who developed PGD grade 0/1 and PGD grade 2/3. There were also no significant differences in the pretransplant laboratory values between the 2 groups except for platelets (239.7 ± 98.9 vs 284.6 ± 90.2, P = .05, respectively) (Table 1).
TABLE 1.
Patient Characteristics by PGD Grade
| Variable | PGD Grade 0/1 (n = 41) |
PGD Grade 2/3 (n = 30) |
P Value |
|---|---|---|---|
| Recipient factors | |||
| Age, y | 57.9 ±11.4 | 54 ± 12.8 | .17 |
| Female | 18 (43.9) | 18 (60.0) | .27 |
| Body mass index, kg/m2 | 25.2 ± 5.2 | 26.3 ± 5.5 | .41 |
| Body surface area, m2 | 1.9 ± 0.3 | 1.8 ± 0.2 | .47 |
| Smoking history | 20 (48.8) | 10 (33.3) | .29 |
| Hypertension | 17 (41.5) | 11 (36.7) | .87 |
| Diabetes | 14 (34.1) | 7 (23.3) | .47 |
| Etiology of lung failure | |||
| COPD/CPFE | 13 (31.7) | 4 (13.3) | .13 |
| Interstitial lung disease | 10 (24.4) | 6 (20.0) | .88 |
| COVID-19 ARDS | 8 (19.5) | 5 (16.7) | 1.00 |
| Pulmonary arterial hypertension | 6 (14.6) | 6 (20.0) | .78 |
| Connective tissue disease | 2 (4.9) | 5 (16.7) | .21 |
| Other | 2 (4.9) | 4 (13.3) | .40 |
| Laboratory | |||
| Hemoglobin, g/dL | 12.1 ± 2.5 | 11.6 ± 2.3 | .37 |
| White blood cell, 1000/mm3 | 9.4 ± 4.0 | 9.4 ± 3.5 | .96 |
| Platelets, 1000/mm3 | 239.7 ± 98.9 | 284.6 ± 90.2 | .05 |
| Sodium, mEq/L | 139.6 ± 2.8 | 139.4 ± 3.2 | .80 |
| BUN, mg/dL | 14.8 ± 5.5 | 13.2 ± 4.8 | .19 |
| Creatinine, mg/dL | 0.77 ± 0.23 | 0.77 ± 0.22 | .99 |
| AST, U/L | 27.8 ± 22.2 | 24.0 ± 10.6 | .39 |
| ALT, U/L | 20.3 ± 16.7 | 18.9 ±11.7 | .69 |
| Albumin, g/dL | 3.9 ± 0.5 | 3.9 ± 0.5 | .54 |
| Total bilirubin, mg/dL | 0.7 ± 0.5 | 0.5 ± 0.3 | .07 |
| INR | 1.1 ± 0.3 | 1.1 ± 0.1 | .37 |
| Arterial blood gas | |||
| pH | 7.36 ± 0.06 | 7.36 ± 0.08 | .87 |
| Paco2 | 49.6 ± 10.6 | 51.2 ± 15.1 | .63 |
| Pao2 | 264.1 ± 125.1 | 297.0 ±111.1 | .27 |
| Donor | |||
| Age, y | 33.5 ± 12.5 | 36.0 ± 12.3 | .41 |
| Female | 18 (43.9) | 10 (33.3) | .51 |
| Cause of death | |||
| Anoxia | 17 (41.5) | 14 (46.7) | .85 |
| Head trauma | 17 (41.5) | 9 (30.0) | .46 |
| Other | 7 (17.1) | 7 (23.3) | .72 |
Values are presented as mean ± SD or n (%). ALT, alanine aminotransferase; ARDS, acute respiratory distress syndrome; AST, aspartate aminotransferase; BUN, blood urea nitrogen; COPD, chronic obstructive pulmonary disease; COVID-19, coronavirus disease 2019; CPFE, combined pulmonary fibrosis and emphysema; INR, international normalized ratio; PGD, primary graft dysfunction.
OUTCOMES ASSOCIATED WITH PGD GRADE 2/3.
PGD grade 2/3 occurred in 30 (42.2%) patients. One-year survival was reduced in recipients with PGD grade 2/3 compared with those with PGD grade 0/1 ((P = .02)) (Supplemental Figure 1).
Intraoperatively, patients who developed PGD grade 2/3 had significantly higher postreperfusion sPAP (41±9.1 mm Hg) compared with those with PGD grade 0/1 (31.5 ± 8.8 mm Hg) (P < .001). There were no significant differences between PGD grade 2/3 and PGD grade 0/1 patients in prereperfusion sPAP or other intraoperative outcomes. Postoperatively, patients with PGD grade 2/3 had significantly longer intensive care unit admissions (25.4 vs 12.2 days, P < .001) and overall hospital stays (29.4 vs 19.8 days, (P = .02)) (Table 2).
TABLE 2.
Intraoperative and Postoperative Outcomes of Lung Transplant Recipients by PGD Grade
| Variable | PGD Grade 0/1 (n = 41) |
PGD Grade 2/3 (n = 30) |
P Value |
|---|---|---|---|
| Pulmonary artery pressure | |||
| Prereperfusion sPAP | 45.9 ± 19.7 | 51.3 ± 21.9 | .28 |
| Postreperfusion sPAP | 31.5 ± 8.8 | 41.0 ± 9.1 | <.001 |
| Intraoperative outcomes | |||
| Operative time, h | 7.7 ± 1.2 | 8.0 ± 1.0 | .25 |
| Intraoperative blood transfusion: pRBC | 1.7 ± 2.0 | 2.1 ± 1.9 | .34 |
| Intraoperative blood transfusion: FFP | 0.4 ± 1.0 | 0.7 ± 1.5 | .28 |
| Intraoperative blood transfusion: platelets | 0.3 ± 0.7 | 0.1 ± 0.3 | .10 |
| Ischemic time, h | 5.8 ± 1.9 | 5.4 ± 0.9 | .24 |
| Venoarterial ECMO use | 35 (85.4) | 28 (93.3) | .50 |
| Venoarterial ECMO time, h | 3.3 ± 1.7 | 3.2 ± 0.6 | .79 |
| Post-operative outcomes | |||
| Acute kidney injury | 11 (26.8) | 15 (50.0) | .09 |
| Dialysis | 1 (2.4) | 4 (13.3) | .20 |
| Stroke | 1 (2.4) | 2 (6.7) | .78 |
| Bowel ischemia | 0 (0) | 1 (3.3) | .87 |
| Digital ischemia | 0 (0) | 2 (6.7) | .34 |
| Intensive care unit stay, d | 12.2 ± 8.8 | 25.4 ± 21.8 | <.001 |
| Posttransplant ventilator, d | 5.2 ± 7.0 | 11.3 ± 19.4 | .07 |
| Hospital stay, d | 19.8 ± 11.8 | 29.4 ± 21.4 | .02 |
Values are presented as mean ± SD or n (%). ECMO, extracorporeal membrane oxygenation; FFP, fresh frozen plasma; PGD, primary graft dysfunction; pRBC, packed red blood cells; sPAP, systolic pulmonary artery pressure.
PREDICTORS OF PGD GRADE 2/3.
Univariate logistic regression analysis of recipient, donor, and operative characteristics revealed chronic obstructive pulmonary disease/combined primary fibrosis and emphysema lung failure (odds ratio [OR] 0.33, 95% CI 0.1–1.15, P = .08), preoperative platelets (OR 1.01, 95% CI 1–1.01, P = .06), total bilirubin (OR 0.27, 95%CI 0.06–1.24, P = .09), and postreperfusion sPAP (OR 1.13, 95% CI 1.05–1.21, P < .001) as predictive of PGD grade 2/3 development (Supplemental Table 1). On subsequent multivariate logistic regression analysis, only postreperfusion sPAP (OR 1.14, 95%CI 1.06–1.24, P < .001) remained predictive of PGD grade 2/3 development (Table 3).
TABLE 3.
Multivariate Logistic Regression Analysis to Predict PGD Grade 2/3
| Variable | OR | 95% CI | P Value |
|---|---|---|---|
| Etiology of lung failure | |||
| COPD/CPFE | 0.37 | 0.07‒1.95 | .24 |
| Laboratory | |||
| Platelets, 1000/mm3 | 1.00 | 0.998‒1.01 | .19 |
| Total bilirubin, mg/dL | 0.25 | 0.04‒1.46 | .12 |
| Pulmonary artery pressure | |||
| Postreperfusion sPAP | 1.14 | 1.06‒1.24 | <.001 |
COPD, chronic obstructive pulmonary disease; CPFE, combined pulmonary fibrosis and emphysema; OR, odds ratio; PGD, primary graft dysfunction; sPAP, systolic pulmonary artery pressure.
POSTREPERFUSION sPAP and PGD Grade 2/3.
When determining the postreperfusion sPAP most predictive of PGD grade 2/3, a postreperfusion sPAP of 37 mm Hg had the highest Youden index (56.4) (Supplemental Table 2). The receiver operating characteristic curve of postreperfusion sPAP at 37 mm Hg had a sensitivity of 0.77, specificity of 0.78, and area under the curve of 0.81 (Figure 1) for predicting PGD grade 2/3, which was significantly superior to the curves of prereperfusion sPAP at 36 mm Hg (sensitivity 0.39, specificity 0.76, area under the curve 0.54, P < .01) and the difference between prereperfusion and postreperfusion sPAP (sensitivity 0.951, specificity 0.233, area under the curve 0.559, P < .01) (Supplemental Figures 2 and 3, respectively).
FIGURE 1.
Receiver operating characteristic curve for postreperfusion systolic pulmonary artery pressure predicting primary graft dysfunction grade 2/3 at 37 mm Hg.
FACTORS AND OUTCOMES ASSOCIATED WITH ELEVATED POSTREPERFUSION sPAP.
Thirty-two (45.1%) patients had elevated postreperfusion sPAP (postreperfusion sPAP 37 mm Hg). There were no significant differences in recipient and donor characteristics or preoperative laboratory values between patients with elevated and nonelevated postreperfusion sPAP, except for preoperative platelets (284.8 ± 109.3 vs 237.2 ± 81.4, P = .04, respectively), blood urea nitrogen (12.4 ± 3.5 vs 15.5 ± 6, P = .01, respectively), and arterial oxygen partial pressure (310.6 ± 106.7 vs 250.3 ± 124, P = .04, respectively) (Supplemental Table 3). Additionally, there were no significant differences in prereperfusion sPAP and intraoperative outcomes between the 2 cohorts. Patients with elevated postreperfusion sPAP were significantly more likely to develop PGD grade 2/3 (71.9%) compared with those with non-elevated postreperfusion sPAP (17.9%) (P < .001) (Table 4). Furthermore, those patients with elevated postreperfusion sPAP had significantly decreased 1-year survival (P = .02) (Supplemental Figure 4).
TABLE 4.
Intraoperative and Postoperative Outcomes of Lung Transplant Recipients by Postreperfusion sPAP
| Variable | Postreperfusion sPAP <37 mm Hg (n = 39) |
Postreperfusion sPAP ≥37 mm Hg (n = 32) |
P Value |
|---|---|---|---|
| Pulmonary artery pressure | |||
| Prereperfusion sPAP | 49.2 ± 21.2 | 46.9 ± 20.3 | .65 |
| Intraoperative outcomes | |||
| Operative time, h | 7.8 ± 1.2 | 7.9 ± 1.1 | .55 |
| Intraoperative blood transfusion: pRBC | 2.0 ± 2.1 | 1.7 ± 1.7 | .54 |
| Intraoperative blood transfusion: FFP | 0.5 ± 1.2 | 0.6 ± 1.2 | .79 |
| Intraoperative blood transfusion: platelets | 0.3 ± 0.7 | 0.1 ± 0.3 | .17 |
| Ischemic time, h | 5.7 ± 2.0 | 5.6 ± 0.8 | .93 |
| Venoarterial ECMO use | 34 (87.2) | 29 (90.6) | .94 |
| Venoarterial ECMO time, h | 3.3 ± 1.7 | 3.2 ± 0.6 | .72 |
| Postoperative outcomes | |||
| PGD grade 2/3 | 7 (17.9) | 23 (71.9) | <.001 |
| Acute kidney injury | 15 (38.5) | 11 (34.4) | .91 |
| Dialysis | 1 (2.6) | 4 (12.5) | .25 |
| Stroke | 1 (2.6) | 2 (6.3) | .86 |
| Bowel ischemia | 0 (0) | 1 (3.1) | .92 |
| Digital ischemia | 0 (0) | 2 (6.3) | .39 |
| Intensive care unit stay, d | 14.6 ± 9.9 | 21.8 ± 22.2 | .07 |
| Posttransplant ventilator, d | 6.1 ± 7.8 | 9.8 ± 18.8 | .26 |
| Hospital stay, d | 22.3 ± 13.0 | 25.6 ± 21.1 | .42 |
Values are presented as mean ± SD or n (%). ECMO, extracorporeal membrane oxygenation; FFP, fresh frozen plasma; PGD, primary graft dysfunction; pRBC, packed red blood cells; sPAP, systolic pulmonary artery pressure.
COMMENT
Despite multiple studies identifying risk factors for PGD, it remains common and one of the leading drivers of inferior outcomes in lung transplantation compared to other solid organs.5–7 Our study is the first to investigate the association between postreperfusion sPAP and PGD, and its ability to predict patients who will develop significant PGD. We report that postreperfusion sPAP is related to PGD grade 2/3 and a postreperfusion sPAP of 37 mm Hg is a suitable predictor of PGD grade 2/3. Identifying those patients in the early postoperative period who are likely to develop significant PGD—before it can be formally diagnosed—would allow for earlier interventions, which could mitigate PGD severity and improve clinical outcomes.
PGD GRADE 2/3 IS ASSOCIATED WITH ELEVATED POSTREPERFUSION sPAP.
Prior studies have analyzed the association between pretransplant pulmonary artery hypertension and PGD, citing pretransplant pulmonary artery hypertension as a strong recipient risk factor for PGD.5,13,18–20 We analyzed postreperfusion sPAP because it is an easy to obtain parameter after implantation after ischemia-reperfusion has occurred. We report that postreperfusion sPAP is significantly higher in patients with PGD grade 2/3 compared with those with PGD grade 0/1. While we additionally found patients with PGD grade 2/3 had higher pre-reperfusion sPAP compared with those with PGD grade 0/1, we did not find this statistically significant (Table 2).This suggests that postreperfusion sPAP is more highly associated with PGD grade 2/3 than is prereperfusion sPAP.
To further demonstrate this strong association, when we stratified patients by postreperfusion sPAP, we found those with elevated postreperfusion sPAP were significantly more likely to experience PGD compared with those with nonelevated postreperfusion sPAP (Table 4). There were no significant differences in prereperfusion sPAP between those patients with elevated and nonelevated postreperfusion sPAP, proposing that postreperfusion sPAP is not due to elevated prereperfusion sPAP. There were no major differences in donor and recipient demographics and intraoperative outcomes, in both the analysis between those patients with PGD grade 2/3 and PGD grade 0/1 and the analysis between those patients with elevated and nonelevated postreperfusion sPAP, suggesting that those were not confounders. Together, these results support the use postreperfusion sPAP as an early clinical indicator of PGD. Using postreperfusion sPAP as a marker for patients who will develop significant PGD would allow for earlier treatment interventions, which could mitigate the effects of PGD, such as placing patients on ECMO prior to leaving the operating room prophylactically or starting inhaled pulmonary vasodilators. Currently, iNO use is justified selectively for PGD patients with severe hypoxemia or elevated pulmonary artery pressures, as prospective, randomized clinical studies investigating the effect of iNO on clinical outcomes for those lung transplant patients with PGD are lacking.21 Therefore, if elevated postreperfusion sPAP was accepted as a surrogate marker for PGD, this would allow for earlier intervention with iNO in these patients, which could improve outcomes.
POSTREPERFUSION sPAP Predicts PGD Grade 2/3 Occurrence.
In addition to the formal criteria for PGD, plasma levels of intracellular adhesion molecule-1, Pselectin, and plasminogen activator inhibitor-1 have been identified as biomarkers of PGD.4,22 However, there is a paucity of studies analyzing the ability for postreperfusion hemodynamic parameters to predict PGD occurrence, which are more easily evaluated than a panel of select biomarkers. Here, we found that postreperfusion sPAP is indeed predictive of PGD grade 2/3 on both univariate (Supplemental Table 2) and multivariate analyses (Table 3). Specifically, we found that a postreperfusion sPAP of 37 mm Hg was an optimal cutoff for predicting those patients who will develop PGD grade 2/3 and superior to prereperfusion sPAP. Given that postreperfusion sPAP is the sPAP after complete implantation of the lung allograft after ischemia-reperfusion has occurred, we feel it likely reflects the early sequelae of PGD.
Many studies investigating PGD have cited endothelial dysfunction as a significant event in the pathogenesis of PGD via mechanisms such as downregulation of endothelial tight junctions or increased endothelial cell permeability.23–25 We believe that these mechanisms are a possible explanation for why PGD patients have significantly higher postreperfusion sPAP. If true, this would further support that PGD causes elevated post-reperfusion sPAP, rather than the converse. Additionally, this direction of causality is supported by studies which have shown that prophylactic administration of iNO does not seem to prevent PGD, but rather iNO improves clinical outcomes for patients with diagnosed PGD.14–16 If PGD was caused by elevated postreperfusion sPAP, one would argue that prophylactic iNO would be more effective in preventing PGD, rather than as an adjunctive treatment. However, as this is a retrospective study, causality cannot be appropriately assessed, and therefore we feel this is an area for future research. Defining the direction of causality between post-reperfusion sPAP and PGD would further guide appropriate treatment for those patients with PGD and elevated pulmonary artery pressures.
LIMITATIONS.
Our study is not without limitations. First, this study only included patients undergoing bilateral lung transplantation, so the results may not be generalizable to single lung transplants. Second, given the smaller sample size, it is difficult to adjust for potential confounders. Third, this study did not account for postoperative inhaled pulmonary vasodilators use, which could have impacted PGD incidence/grade. Finally, this study did not consider all categories of PGD. We have previously described a subset of PGD due to allograft rejection, mediated by preexisting lung restricted autoantibodies, for which this study did not control.26
CONCLUSIONS.
In conclusion, PGD grade 2/3 is associated with elevated postreperfusion sPAP after bilateral lung transplantation; additionally, an elevated post-reperfusion sPAP, defined as 37 mm Hg, after lungtransplant is predictive of significant PGD. Furthermore, postreperfusion sPAP is more indicative of PGD development than prereperfusion sPAP. This study supports the need for further multiinstitutional, large-scale studies to help elucidate the ability of postreperfusion sPAP to serve as a complementary clinical marker of PGD as it could identify patients with significant PGD earlier who may benefit from targeted interventions.
Supplementary Material
FUNDING SOURCES
Emily Cerier is supported by the National Institutes of Health grant T32AI083216 and Thoracic Surgery Foundation; Ankit Bharat is supported by the National Institutes of Health grants HL145478, HL147290, and HL147575.
Footnotes
DISCLOSURES
The authors have no conflicts to disclose.
The Supplemental Material can be viewed in the online version of this article [10.1016/j.athoracsur.2022.12.013] on http://www.annalsthoracicsurgery.org.
Presented at the Forty-second Annual Meeting of the International Society of Heart and Lung Transplantation, Boston, MA, April 27–30, 2022.
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