Coronary Artery Aneurysm in Kawasaki Disease: Coronary CT Angiography through the Lens of Pathophysiology and Differential Diagnosis.

Kawasaki disease (KD) is an inflammatory autoimmune vasculitis affecting the coronary arteries of very young patients, which can result in coronary artery aneurysms (CAAs) with lifelong manifestations. Accurate identification and assessment of CAAs in the acute phase and sequentially during the chronic phase of KD is fundamental to the treatment plan for these patients. The differential diagnosis of CAA includes atherosclerosis, other vasculitic processes, connective tissue disorders, fistulas, mycotic aneurysms, and procedural sequelae. Understanding of the initial pathophysiology and evolutionary arterial changes is important to interpretation of imaging findings. There are multiple applicable imaging modalities, each with its own strengths, limitations, and role at various stages of the disease process. Coronary CT angiography is useful for evaluation of CAAs as it provides assessment of the entire coronary tree, CAA size, structure, wall, and lumen characteristics and visualization of other cardiothoracic vasculature. Knowledge of the natural history of KD, the spectrum of other conditions that can cause CAA, and the strengths and limitations of cardiovascular imaging are all important factors in imaging decisions and interpretation. Keywords: Pediatrics, Coronary Arteries, Angiography, Cardiac © RSNA, 2021.

Educating medical students about military health: Perspectives from a multidisciplinary lecture initiative.

BACKGROUND: Medical student education on military health topics is critical in ensuring optimal future care for military service members and their families. METHODS: Keck School of Medicine of the University of Southern California (Keck SOM) students were invited to participate in an anonymous, voluntary, online survey ("Pre") rating their level of interest, awareness, exposure and comfort with military health issues on a 5-point Likert scale. A student-organized program of four voluntary lectures discussing military health-related topics was then implemented. Students were invited to re-take the survey ("Post") and also indicate which, if any, lectures they had attended. RESULTS: 230 students completed the "Pre" survey. A statistically significant deviation in responses was observed in all four questions, showing high interest (mean: 3.19 ± 1.20, P = 0.002), low awareness (mean: 2.52 ± 1.15, P < 0.001), low comfort (mean: 2.66 ± 1.11, P < 0.001), and low exposure (mean: 1.80 ± 0.95, P < 0.001) to military health issues. 132 students completed the "Post" survey, including 37 lecture attendees and 95 non-attendees. A statistically significant difference in the level of interest (P < 0.05) and exposure (P < 0.05) was observed between these groups. DISCUSSION: Medical schools that lack military health curricula may underprepare students to care for military-affiliated patients. Student-led programs can help introduce this topic before formalized curricula are instituted.

Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia.

Cardiomyocyte T tubules are important for regulating ion flux. Bridging integrator 1 (BIN1) is a T-tubule protein associated with calcium channel trafficking that is downregulated in failing hearts. Here we find that cardiac T tubules normally contain dense protective inner membrane folds that are formed by a cardiac isoform of BIN1. In mice with cardiac Bin1 deletion, T-tubule folding is decreased, which does not change overall cardiomyocyte morphology but leads to free diffusion of local extracellular calcium and potassium ions, prolonging action-potential duration and increasing susceptibility to ventricular arrhythmias. We also found that T-tubule inner folds are rescued by expression of the BIN1 isoform BIN1+13+17, which promotes N-WASP-dependent actin polymerization to stabilize the T-tubule membrane at cardiac Z discs. BIN1+13+17 recruits actin to fold the T-tubule membrane, creating a 'fuzzy space' that protectively restricts ion flux. When the amount of the BIN1+13+17 isoform is decreased, as occurs in acquired cardiomyopathy, T-tubule morphology is altered, and arrhythmia can result.