The field of heart transplantation continues to evolve, with major changes in allocation systems and the increasing use of extended-criteria donor hearts, including hearts from donation after circulatory death donors, hearts supported with ex-vivo perfusion, and hearts from hepatitis C viremic donors. The use of such non-traditional donor hearts has made transplantation available to a larger number of recipients, but the demand continues to outpace the supply. Given this persistent donor heart shortage, much attention has been paid to the topic of donor-recipient size matching. Prior studies have challenged traditional criteria for size matching, 1-3 while others have attempted to identify the optimal metric for matching donor and recipient heart size by comparing criteria, such as height, weight, body mass index (BMI), body surface area (BSA), and predicted heart mass (PHM). [4][5][6][7] This 36th annual adult heart transplant report is based on data submitted to the International Society for Heart and Lung Transplantation (ISHLT) Thoracic Organ Transplant Registry on 146,975 heart transplants in recipients of all ages (including 131,249 adult heart transplants)

This 36 th adult lung and heart-lung transplant report summarizes data from 69,200 adult lung and 4,128 adult heart-lung transplants performed through June 30, 2018 and reported to the International Thoracic Organ Transplant Registry. With each year's report, we now provide more detailed analyses on a particular focus theme important to patient outcomes. Since 2013, these have been donor and recipient age; retransplantation; early graft failure; indication for transplant; allograft ischemic time; and multiorgan transplantation. Although widely accepted as critical to decision making at the time of receipt of an organ donor offer, there is surprisingly little literature outlining current practice and the impact of size (mis-)matching on outcomes. Hence, this year's report focuses on an overall theme of donor and recipient size matching. In addition to reporting donor and recipient height and weight difference for all adult lung and heart-lung transplant recipients stratified by transplant type (bilateral or single) and indication, we report historical trends and associations between size match and survival. The Registry's online slide sets include results from additional analyses and complementary information not included in this publication (see https:// ishltregistries.org/registries/slides.asp).

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Antibody-mediated rejection (AMR) is a recognized cause of allograft dysfunction in lung transplant recipients. Unlike AMR in other solid-organ transplant recipients, there are no standardized diagnostic criteria or an agreed-upon definition. Hence, a working group was created by the International Society for Heart and Lung Transplantation with the aim of determining criteria for pulmonary AMR and establishing a definition. Diagnostic criteria and a working consensus definition were established. Key diagnostic criteria include the presence of antibodies directed toward donor human leukocyte antigens and characteristic lung histology with or without evidence of complement 4d within the graft. Exclusion of other causes of allograft dysfunction increases confidence in the diagnosis but is not essential. Pulmonary AMR may be clinical (allograft dysfunction which can be asymptomatic) or sub-clinical (normal allograft function). This consensus definition will have clinical, therapeutic and research implications.

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SUMMARY In human pathophysiology, the clash between microbial infection and host immunity contributes to multiple diseases. Cystic fibrosis (CF) is a classical example of this phenomenon, wherein a dysfunctional, hyperinflammatory immune response combined with chronic pulmonary infections wreak havoc upon the airway, leading to a disease course of substantial morbidity and shortened life span. Pseudomonas aeruginosa is an opportunistic pathogen that commonly infects the CF lung, promoting an accelerated decline of pulmonary function. Importantly, P. aeruginosa exhibits significant resistance to innate immune effectors and to antibiotics, in part, by expressing specific virulence factors (e.g., antioxidants and exopolysaccharides) and by acquiring adaptive mutations during chronic infection. In an effort to review our current understanding of the host-pathogen interface driving CF pulmonary disease, we discuss (i) the progression of disease within the primitive CF lung, specifically focusing on the role of host versus bacterial factors; (ii) critical, neutrophil-derived innate immune effectors that are implicated in CF pulmonary disease, including reactive oxygen species (ROS) and antimicrobial peptides (e.g., LL-37); (iii) P. aeruginosa virulence factors and adaptive mutations that enable evasion of the host response; and (iv) ongoing work examining the distribution and colocalization of host and bacterial factors within distinct anatomical niches of the CF lung.

This continues to be an exciting time for pediatric heart transplantation. Since the first orthotopic heart transplantation a little over 50 years ago, the field has grown tremendously, including many advancements in the application of this therapy to children. Today, heart transplantation is performed routinely in many pediatric centers throughout the world with over 100 centers reporting to the International Thoracic Transplant Registry (Figure 1, eSlide H(p) 4). The Registry is the largest source of worldwide data on pediatric heart transplantation with over 14,000 transplants reported in children. The focus theme for this year's report is donor and recipient size match. Statistical methods Data collection, conventions, and statistical methods National and multinational organ and data exchange organizations and individual centers submit data to the International Society for Heart and Lung Transplantation (ISHLT)

These data provide evidence that azithromycin affects the inflammatory process at the level of the macrophage and shifts macrophage polarization towards the alternatively activated phenotype. This recently defined M2 phenotype has been described in conditions in which pulmonary inflammation and fibrosis are major determinants of clinical outcome, but the concept of antibiotics altering macrophage phenotype has not yet been critically evaluated.