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Review
. 2024 Jun 24;14(13):1340.
doi: 10.3390/diagnostics14131340.

Impact of Pre-Transplant Left Ventricular Diastolic Pressure on Primary Graft Dysfunction after Lung Transplantation: A Narrative Review

Jean Philippe Henry  1 , François Carlier  2 , Julien Higny  1 , Martin Benoit  1 , Olivier Xhaët  1 , Dominique Blommaert  1 , Alin-Mihail Telbis  1 , Benoit Robaye  1 , Laurence Gabriel  1 , Antoine Guedes  1 , Isabelle Michaux  3 , Fabian Demeure  1 , Maria-Luiza Luchian  1
Affiliations
Review

Impact of Pre-Transplant Left Ventricular Diastolic Pressure on Primary Graft Dysfunction after Lung Transplantation: A Narrative Review

Jean Philippe Henry et al. Diagnostics (Basel). .

Abstract

Lung transplantation (LT) constitutes the last therapeutic option for selected patients with end-stage respiratory disease. Primary graft dysfunction (PGD) is a form of severe lung injury, occurring in the first 72 h following LT and constitutes the most common cause of early death after LT. The presence of pulmonary hypertension (PH) has been reported to favor PGD development, with a negative impact on patients' outcomes while complicating medical management. Although several studies have suggested a potential association between pre-LT left ventricular diastolic dysfunction (LVDD) and PGD occurrence, the underlying mechanisms of such an association remain elusive. Importantly, the heterogeneity of the study protocols and the various inclusion criteria used to define the diastolic dysfunction in those patients prevents solid conclusions from being drawn. In this review, we aim at summarizing PGD mechanisms, risk factors, and diagnostic criteria, with a further focus on the interplay between LVDD and PGD development. Finally, we explore the predictive value of several diastolic dysfunction diagnostic parameters to predict PGD occurrence and severity.

Keywords: E/e’; diastolic dysfunction; left ventricle function; lung transplantation; primary graft dysfunction.

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Conflict of interest statement

This work was conducted without external funding. François CARLIER declares travel grants from Takeda, outside of the scope of the work. Jean Philippe HENRY, PhD candidate, received a grant from the “Fondation Mont-Godinne”. This grant was not used to support this paper. The other authors have no relevant financial or non-financial interests to disclose in relation to the current article.

Figures

Figure 1
Figure 1
The common mechanisms of PGD and LVDD and the interplay of the recipient’s LVDD, PH and RVF in the mechanism of PGD. HFpEF: Heart Failure with preserved Ejection Fraction; LVDD: Left Ventricular Diastolic Dysfunction; LVEDP: Left Ventricular End-Diastolic Pressure; RV: Right Ventricular; RVH: Right Ventricular Hypertrophy; * Mean pulmonary artery pressure > 20 mmHg, measured by right heart catheterization; ** Defined as a wall thickness greater than 5 mm.
Figure 2
Figure 2
Predictive value of different diastolic dysfunction variables on PGD. Aggarwal et al.: [25]; Avriel et al.: [40]; DT: Deceleration Time; IRT: Isovolumic Relaxation Time; LA: Left Atrial; LVDD: Left Ventricular Diastolic Dysfunction; Li et al.: [72]; mPCWP: Mean Pulmonary Capillary Wedge Pressure; PACS: Peak Atrial Contraction Strain; PALS: Peak Atrial Longitudinal Strain; PAPs: Pulmonary Arterial Systolic pressure; PGD: Primary Graft Dysfunction; Porteous et al.: [12]; RA: Right Atrial; RV: Right Ventricle; 3D-RVEF: Three-Dimensional Echography Right Ventricular Ejection Fraction; RV FWLS: Right Ventricular Free Wall Longitudinal Strain; TAPSE: Tricuspid Annular Plane Systolic Excursion; Yadlipadi et al.: [73].
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