Natural decline in pulmonary function following bilateral lung transplantation: a single-centre study

Extract

Lung transplantation is an established treatment option for well-selected patients with end-stage pulmonary disease, when other therapeutic options are no longer available. Although post-transplant survival has much improved in recent years, the development of chronic lung allograft dysfunction (CLAD), which affects 40–50% of all patients by 5 years post-transplant, remains the major cause of morbidity and mortality [1]. CLAD is defined by a progressive and persistent decline in the forced expiratory volume in the first second (FEV₁) of at least 20% compared to the postoperative best value. Several different phenotypes of CLAD have been identified, based on the physiology of the lung function decline, such as obstructive (bronchiolitis obliterans syndrome; BOS), restrictive (restrictive allograft syndrome) or a combination (mixed phenotype), along with the presence or absence of persistent opacities on chest imaging [2, 3]. One of the problems that may arise when interpreting post-transplant lung function decline is that the natural decline in FEV₁ after lung transplantation is unknown at present.