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Introduction/Aims: Duchenne muscular dystrophy (DMD) is characterized by fibrofatty replacement of muscle. This has been documented in the ventricular myocardium of DMD patients, but there is limited description of atrial involvement. The purpose of this study is to examine the arrhythmia and ectopy burden in patients with DMD and non‐DMD dilated cardiomyopathy (DCM) and to characterize the cardiac histopathologic changes in DMD patients across the disease spectrum. Methods: This was a retrospective analysis of age‐matched patients with DMD and non‐DMD DCM who received a Holter monitor and cardiac imaging within 100 days of each other between 2010 and 2020. Twenty‐four‐hour Holter monitors were classified based on the most recent left ventricular ejection fraction at the time of monitoring. Cardiac histopathologic specimens from whole‐heart examinations at the time of autopsy from three DMD patients and one DCM patient were reviewed. Results: A total of 367 patients with 1299 Holter monitor recordings were included over the study period, with 94% representing DMD patients and 6% non‐DMD DCM. Patients with DMD had more atrial ectopy across the cardiac function spectrum (p < 0.05). There was no difference in ventricular ectopy. Four DMD patients developed symptomatic atrial arrhythmias. Autopsy specimens from DMD patients demonstrated fibrofatty infiltration of both atrial and ventricular myocardium. Discussion: The atrial myocardium in patients with DMD is unique. Autopsy specimens reveal fibofatty replacement of the atrial myocardium, which may be a nidus for both ectopy and arrhythmias in DMD patients. [ABSTRACT FROM AUTHOR]

Objectives/Hypothesis: To develop a reproducible and consistent chronic subglottic stenosis (SGS) in an endoscopic animal model. Study Design: Prospective study. Methods: We conducted a prospective study using New Zealand white rabbits. Chronic SGS was induced endoscopically by Bugbee electrocautery to 50% to 75% of the subglottic area's circumference, followed by 4‐hour endotracheal intubation. The rabbit airways were endoscopically assessed and sized with uncuffed endotracheal tubes (ETTs) before the injury, during follow‐up, and at the endpoints. There were four endpoints: 2, 4, 6, and 8 weeks post SGS induction. Animals were humanely euthanized for histopathological examination of the subglottic injury site and microscopic measurement of the cricoid lumen. Results: Twenty‐two rabbits reached the endpoints, and 18 rabbits developed chronic SGS. ETT size significantly decreased by 0.5 from preinjury to the endpoint in all groups, P <.001. Control median cricoid lumen measurements were 20.48 mm2, the median cricoid lumen measurement for the 2 weeks endpoint was 14.3 mm2, 4 weeks 11.69 mm2, 6 weeks 16.03 mm2, and 8 weeks endpoint median was 16.33 mm2. Histopathological examination showed chronic scar tissue and new cartilage formation at the cricoid level, mainly at the posterior subglottic injury site starting from 4 weeks postinjury. Collagen staining revealed substantial amounts of organized collagen and different collagen orientation starting 4 weeks postinjury lasting until 8 weeks postinjury. Conclusion: We developed an animal model to study chronic SGS. This model will be utilized to compare different endoscopic treatment interventions in acute SGS versus chronic SGS and further define the molecular basis of SGS. Level of Evidence: NA Laryngoscope, 132:1909–1915, 2022 [ABSTRACT FROM AUTHOR]

Background: Antithymocyte globulin (ATG) consists of polyclonal antibodies directed primarily against human T lymphocytes but may contain antibodies with affinity for other tissues in the transplanted organ, resulting in complement (C4d) deposition. This phenomenon has been demonstrated in endomyocardial biopsies (EMBs) of adult cardiac transplants. We examined the relationship of induction immunosuppression with ATG and C4d deposition in EMB of pediatric cardiac transplants. Methods: Results of C4d immunohistochemistry were available from all EMB of patients transplanted at our center between June 2012 and April 2018 (n = 48) who received induction immunosuppression with either ATG (n = 20) or basiliximab (n = 28) as the standard of care. Results: C4d deposition in the first year post–heart transplant was more commonly seen among patients who received ATG induction (20% of EMBs in ATG group vs 1% of EMBs in basiliximab group; p <.0001). C4d deposition related to ATG was observed early post‐transplant (50% ATG vs 0% basiliximab on first EMB; p <.0001 and 35% ATG vs 0% basiliximab on the second EMB; p =.0012). While this difference waned by the third EMB (5% ATG vs 0% basiliximab; p =.41), positive C4d staining persisted to the sixth EMB in the ATG group only (6%). Conclusion: C4d deposition is common on EMB up to 1 year post–pediatric cardiac transplant following ATG induction. This high rate of positive C4d staining in the absence of histologic AMR after ATG induction therapy must be accounted for in making clinical decisions regarding cardiac allograft rejection diagnosis and treatment. [ABSTRACT FROM AUTHOR]

The work Dr. Healy and his mentors had performed at that time were exceptional.[1] Our group described several methods for creating an endoscopic subglottic injury and found that cauterization with prolonged intubation achieved a reproducible and safe model,[2] which was sustainable during our study. Graded carbon dioxide laser-induced subglottic injury in the rabbit model. [Extracted from the article]

Chronic post-surgical lymphedema is common condition that afflicts nearly 2 million Americans. In the USA, it is most commonly encountered in the upper extremities of patients who have undergone axillary lymph node dissection for breast cancer. Lymphedema has a significant negative effect on cosmesis, limb function, and overall quality of life. Despite the impact of this condition, very little is known about how to effectively prevent or treat lymphedema. While therapeutic options for chronic extremity lymphedema remain limited, several surgical approaches have been suggested. These include techniques aimed at reducing limb volume, as well as techniques that aim to reconstitute disrupted lymphatic channels. Operations proposed to re-establish lymphatic continuity include lymphatico-venous anastomoses, lymphatico-lymphatico anastomoses, and tissue transfer. [ABSTRACT FROM AUTHOR]