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Background: Chronic lung allograft dysfunction (CLAD) remains the primary cause of death in lung transplant recipients (LTRs) despite improvements in immunosuppression management. Despite advances in knowledge regarding the pathogenesis of CLAD, treatments that are currently available are usuallyineffective and delay progression of disease at best.There are currently no evidence-based guidelines and minimal publications regarding the optimal treatment ofCLAD.Objective: To complete a comprehensive review of the literature for the prevention and medical management of CLAD. Methods:We identified the major domains of the medical management of CLAD and conducted a comprehensive search of PubMed and Embase databases to identify articles published from inception to December 2021 related to CLAD in LTRs. Studies published in English pertaining to the pharmacologic prevention and treatment of CLAD were included; highest priority was given to prospective, randomized, controlled trials if available. Prospective observational and retrospective controlled trials were prioritized next, followed by retrospective uncontrolled studies, case series, and finally case reports if the information was deemed to be pertinent. Reference lists of qualified publications were also reviewed to find any other publications of interest that were not found on initial search.In the absence of literature published in the aforementioned databases, additional articles were identified by reviewing abstracts presented at the International Society for Heart and Lung Transplantation and American Transplant Congress annual meetings between 2010-2021. Conclusion:CLAD should be identified as early as possible along with prompt intervention to optimize the possibility of stabilizing or improving lung function. More robust clinical data is needed to validate the use of all currently available and investigational treatment options for CLAD to identify the optimal pharmacotherapy management for this patient population.

Those with elevated right ventricular systolic pressures were at lower risk of arrhythmia (p<0.001). Patient survival did not differ for patients receiving amiodarone therapy (compared to non-amiodarone atrial arrhythmia patients). These groups also did not differ in ventilator time, length of stay, and long-term survival. Conclusion: In this cohort, intravenous amiodarone therapy in lung transplant patients with new onset atrial arrhythmias did not result in any identifiable pathology. Clinical outcomes for these two study groups were similar. These results suggest that amiodarone can be safely used in this population.

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