Background Treatment options for patients with recurrent ventricular arrhythmias refractory to pharmacotherapy and ablation are minimal. Although left cardiac sympathetic denervation (LCSD) is well established in long-QT syndrome, its role in non-long-QT syndrome arrhythmogenic channelopathies and cardiomyopathies is less clear. Here, we report our single-center experience in performing LCSD in this setting. Methods and Results In this institutional review board-approved study, we retrospectively reviewed the electronic medical records of all patients (N=91) who had videoscopic LCSD at our institution from 2005 to 2011. Data were analyzed for the subset (n=27) who were denervated for an underlying diagnosis other than autosomal dominant or sporadic long-QT syndrome. The spectrum of arrhythmogenic disease included catecholaminergic polymorphic ventricular tachycardia (n=13), Jervell and Lange-Nielsen syndrome (n=5), idiopathic ventricular fibrillation (n=4), left ventricular noncompaction (n=2), hypertrophic cardiomyopathy (n=1), ischemic cardiomyopathy (n=1), and arrhythmogenic right ventricular cardiomyopathy (n=1). Five patients had LCSD because of high-risk assessment and β-blocker intolerance, none of whom had a sentinel breakthrough cardiac event at early follow-up. Among the remaining 22 previously symptomatic patients who had LCSD as secondary prevention, all had an attenuation in cardiac events, with 18 having no breakthrough cardiac events so far and 4 having experienced ≥1 post-LCSD breakthrough cardiac event. Conclusions LCSD may represent a substrate-independent antifibrillatory treatment option for patients with life-threatening ventricular arrhythmia syndromes other than long-QT syndrome. The early follow-up seems promising, with a marked reduction in the frequency of cardiac events postdenervation.

Langerhans cell histiocytosis (LCH) is a rare histiocytic disorder with an unpredictable clinical course and highly varied clinical presentation ranging from single system to multisystem involvement. Although head and neck involvement is common in LCH, isolated bilateral temporal bone involvement is exceedingly rare. Furthermore, LCH is commonly misinterpreted as mastoiditis, otitis media and otitis externa, delaying diagnosis and appropriate therapeutic management. To improve detection and time to treatment, it is imperative to have LCH in the differential diagnosis for unusual presentations of the aforementioned infectious head and neck etiologies. Any lytic lesion of the temporal bone identified by radiology should raise suspicion for LCH. We hereby describe the radiologic findings of a case of bilateral temporal bone LCH, originally misdiagnosed as mastoiditis.

Repeated imaging of the surface of Mars by orbiting spacecraft over the last two decades has revealed more than one thousand impact sites formed in this time period (Daubar et al., 2013(Daubar et al., , 2019(Daubar et al., , 2022. These observations provide important constraints on the current rate of small impacts on Mars, which are valuable for calibrating crater production models (Daubar et al., 2013;Williams et al., 2014), assessing the impact hazard to spacecraft on Mars, and determining the ratio of primary to secondary crater production rates (Hartmann et al., 2018).Among the known recent impact sites, fewer than half are single craters; the majority are fields of craters, known as crater clusters (Daubar et al., 2013(Daubar et al., , 2019(Daubar et al., , 2022Neidhart et al., 2021). The size and separation of individual craters within these clusters suggest that they are formed due to atmospheric break up of the primary meteoroid into a collection of fragments that separate and strike the ground almost simultaneously (Artemieva & Shuvalov, 2001;Popova et al., 2003Popova et al., , 2007. The diversity of crater clusters, in terms of the spatial distributions and size-frequency distributions of their craters, provide a unique opportunity to interrogate the processes of atmospheric entry and fragmentation, and potentially constrain properties of the impactor population (Daubar Abstract The current rate of small impacts on Mars is informed by more than one thousand impact sites formed in the last 20 years, detected in images of the martian surface. More than half of these impacts produced a cluster of small craters formed by fragmentation of the meteoroid in the martian atmosphere. The spatial distributions, number and sizes of craters in these clusters provide valuable constraints on the properties of the impacting meteoroid population as well as the meteoroid fragmentation process. In this paper, we use a recently compiled database of crater cluster observations to calibrate a model of meteoroid fragmentation in Mars' atmosphere and constrain key model parameters, including the lift coefficient and fragment separation velocity, as well as meteoroid property distributions. The model distribution of dynamic meteoroid strength that produces the best match to observations has a minimum strength of 10-90 kPa, a maximum strength of 3-6 MPa and a median strength of 0.2-0.5 MPa. An important feature of the model is that individual fragmentation events are able to produce fragments with a wide range of dynamic strengths as much as 10 times stronger or weaker than the parent fragment. The calibrated model suggests that the rate of small impacts on Mars is 1.5-4 times higher than recent observation-based estimates. It also shows how impactor properties relevant to seismic wave generation, such as the total impact momentum, can be inferred from cluster characteristics.Plain Language Summary Over a thousand meteorite impacts have been detected in spacecraft images of the surface of Mars in the last two decades. In more t...

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Distinguishing congenital long QT syndrome from QT prolongation caused by drugs or a different underlying disease process is essential for selecting the proper treatment. Herein, we present a case of a patient referred for left cardiac sympathetic denervation as a last resort treatment option for her 19-year standing diagnosis of long QT syndrome with malignant ventricular fibrillation. However, based on her atypical clinical course and additional imaging studies, a diagnosis of left ventricular noncompaction, rather than long QT syndrome, was made. She left the clinic with a drastically different treatment plan and an improved quality of life. Because many cardiac and noncardiac diseases can demonstrate QT prolongation on electrocardiogram, all possible diagnoses should be considered before diagnosing a patient with congenital long QT syndrome especially with regard to the profound treatment implications and genetic follow-up in family members.