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Anti-arrhythmics can be useful for ventricular arrhythmias in cardiac sarcoidosis (CS) that are refractory to immunosuppression. However, there is conflicting evidence on the efficacy of immunosuppression for treating arrhythmias in CS patients and a lack of data to support using immunosuppression alone as an initial strategy. The objective of this study was to assess for differences in arrhythmia burden over time with currently used immunosuppression and anti-arrhythmic regimens. Patients with CS and implanted cardiac devices were identified from a single-center registry. Study participants were retrospectively classified based on the medication regimen as follows: control (no therapy), immunosuppression, anti-arrhythmics, or dual therapy. Device interrogations were reviewed for premature ventricular contractions (PVCs), non-sustained ventricular tachycardia (NSVT), and device firings over time. Interrogations for 42 patients were reviewed over a mean period of 31 months. Regression analysis showed a significant decrease in the frequencies of PVCs (slope, -1.47

Background: Immunosuppression and antiarrhythmics can be useful for the treatment of arrhythmias in cardiac sarcoidosis (CS). The current evidence on the efficacy of corticosteroid sparing agents for arrhythmias is limited, and the optimal timing for initiation of antiarrhythmic therapy is unknown. Objective: To assess the impact of corticosteroid sparing immunosuppression with and without antiarrhythmics on arrhythmia burdens in CS. Methods: Patients with CS and implanted cardiac devices were identified from a single center sarcoidosis registry. The patients' medical regimens were grouped as no therapy, immunosuppression alone, antiarrhythmic alone, or dual therapy. Device interrogations were reviewed for premature ventricular contractions (PVCs), nonsustained ventricular tachycardia (NSVT), and appropriate device firing. Results: Interrogations for 42 patients were reviewed over a mean of 31 months. Regression analysis showed a significant decrease in the PVC (slope -1.47, p=0.04) and NSVT frequency (slope -0.05, p=.01) for patients on dual therapy compared to an increase or no change in the other groups. Across all patients, there was no difference between groups in the percentage of patients experiencing device firing. In a subset analysis of patients with ICDs for primary prevention, 6% on dual therapy required device firing compared to 43% and 40% on single or no therapy (P=.049, Chi Sq=6.02). Conclusions: Patients on both immunosuppression and antiarrhythmics had a reduction in PVCs and NSVT over time. Those with devices placed for primary prevention experienced fewer device firings while on dual therapy.

Introduction Sexsomnia is a NREM parasomnia under the subtype of Confusional Arousals, defined as abnormal sexual behaviors emerging from partial arousals during slow-wave sleep. Case reports suggest that is more common in men. Precipitating factors include Obstructive Sleep Apnea, insufficient sleep, alcohol and fatigue/stress and history of NREM parasomnias. Report of case(s) A 37-year-old male with bruxism (using mouth guard) and anxiety for 7 years, who presented to the sleep clinic for a second opinion to discuss concerns around the safety of his children due to his sleep related sexual behavior. Sexsomnia was first noted with the stressors related to becoming a parent (fostering children and having biological children). Sexual behavior reported by the couple was mostly provoked with spouse’s touch during sleep. Behaviors ranging from fondling to aggressive sexual intercourse were reported to occur 1 to 3 times/week. There were no injuries during episodes which only occurred in the bedroom with the spouse and the patient was amnestic of his behavior. Due to marital discord provoked by other stressors, he began to sleep alone in the basement. A video-polysomnogram revealed no parasomnia, sleep apnea, or other sleep arousal disorders. Normal REM with atonia was observed. The patient was treated with Duloxetine 20mg for anxiety after the initial sleep visit. His condition contributed to marital separation. In the divorce proceedings, the spouse argued for denial of visitation rights related to his sleep-sexual behaviors noting that the children may be at risk. After separation, his anxiety and stress levels lowered in conjunction with therapy and medication. Follow up after 2 months found the patient asymptomatic. He placed an alarm on his bedroom door, to alert him and others during sleep. There are no published reports to provide a prediction as to whether his condition would-be supporting restrictions in overnight visitation by the foster and biological children. Conclusion In this case, there was a precedent condition (bruxism) and precipitating stress and anxiety, known to provoke NREM parasomnia. The absence of polysomnographic evidence is not unusual. Forensic repercussions, in particular prospective calculations of risk, are poorly described in the literature. Support (if any)

The pathophysiology of cerebral vasospasm is complex and multifactorial. The present study sought to identify the degree of correlation between cerebral vasospasm as observed angiographically and clinical evaluation of an animal's neurologic status in the canine model following a single and double experimental subarachnoid hemorrhage (SAH) protocol. Nineteen mongrel dogs underwent single or double experimental SAH by percutaneous needle puncture of the cisterna magna and placement of a subarachnoid blood clot in the basal cistern on day 1 and day 4, respectively. At 72 h after each experimental SAH, vertebral angiography was performed and compared to control angiography. Basilar artery diameter measured at multiple positions was expressed as percentage of control diameter. Clinical evaluation of the animals was performed every day throughout the experiments. To assess the degree of neurologic impairment we developed a coma scale that efficiently estimated motor ability, eye response and eating habits of the animals. Vasoconstriction after experimental SAH reduced mean basilar artery diameter to 79.1% (+/- 5.4) of control diameter following single SAH and to 69.0% (+/- 2.1) of control diameter following double SAH. No changes were observed in the neurologic behavior of the animals throughout the experiment. Since a principal characteristic of human cerebral vasospasm is the close correlation between arterial constriction and neurological deficit, we believe that the canine model of SAH, although good in creating cerebral arterial vasoconstriction, does not fully represent the best model of human cerebral vasospasm.

✓ Vasodilation of rabbit carotid arteries induced by a pulsed-eye laser was studied in vitro to clarify the underlying mechanism. Artery segments were double cannulated in a pressure-perfusion apparatus which, under physiological conditions, allows for differential application of various solutions, pharmacological agents, and pulsed-dye laser light. Vaso-constriction was activated using both pharmacological and nonpharmacological agonists. Laser energy at a wavelength of either 480 or 575 nm was applied intraluminally in 1-µsec pulses, which caused dilation of the arteries if hemoglobin was present in the lumen at sufficient concentration. Induced vasodilation did not specifically require the presence of hemoglobin; the same phenomenon could be repeated using an inert dye such as Evans blue as an optical absorber of laser energy. The optical density of the absorber, the number of applied laser pulses, and total amount of applied energy directly influenced the vasodilatory response. Laser-induced vasodilation was possible in both normal vessels and vessels denuded of endothelium. Pulsed-dye laser-induced vasodilation is therefore not a phenomenon mediated through chemical processes, but is rather a purely physical process initiated by the optical absorption of laser energy by the intraluminal medium, which probably induces cavitation bubble formation and collapse, resulting in the vasodilatory response of the vessel.

A causal or supportive relationship between 1,2-diacylglycerol (DAG) content and the maintenance of tonic vasoconstriction was sought in carbine basilar arteries treated in vitro with various agents reported to increase DAG levels in other tissues (platelet-derived growth factor, vasopressin, angiotensin II, and endothelin-1) and, conversely, with agents known to activate sustained constriction (high K + , phorbol ester,hemolysate, and endothelin-1). Multiple segments from individual isolated arteries were prepared. Some segments were immediately frozen as controls and others incubated in physiological saline solution at 37 o C for either 5 minutes or 30 minutes in the presence or absence of different concentrations of the test materials. Segments were then quickly frozen until homogenized for lipid extraction and DAG assay. The DAG content of samples incubated up to 2 hours in physiological saline solution alone did not significantly differ from that of immediately frozen control samples. Resting DAG content expressed relative to total protein measured in each sample averaged 3.82±0.26 (standard error of the mean) pmol DAG/μg of protein (74 samples from 37 arteries). Endothelin at 2×10 -7 mol/L led to a statistically significant increase in DAG content of approximately 40% of basal content at 5 and 30 minutes. A smaller increase in DAG attributable to hemolysate (∼25%) was statistically significant at 30 minutes, whereas vasopressin provoked a notable decrease in DAG content. The other agents had no effect. No differences in these results were noted between normal canine basilar arteries and arteries constricted in vivo by subarachnoid blood clot before isolation. The observed increases in DAG content with endothelin and hemolysate may be large enough to play a role in promoting sustained vasoconstriction