Report of the Association Between Multisystem Inflammatory Syndrome and Severe Myocarditis

Introduction: The people worldwide have been affected by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection since its appearance in December, 2019. Kawasaki disease-like hyperinflammatory shock associated with SARS-CoV-2 infection in previously healthy children has been reported in the literature, which is now referred to as a multisystem inflammatory syndrome in children (MIS-C). Some aspects of MIS-C are similar to those of Kawasaki disease, toxic shock syndrome, secondary hemophagocytic syndrome, and macrophage activation syndrome. Case Presentation: This study reported an 11-year-old boy with MIS-C presented with periorbital and peripheral edema, abdominal pain, elevated liver enzymes, severe right pleural effusion, moderate ascites, and severe failure of right and left ventricles. Conclusion(s): Due to the increasing number of reported cases of critically ill patients afflicted with MIS-C and its life-threatening complications, it was recommended that further studies should be carried out in order to provide screening tests for myocardial dysfunction. Adopting a multidisciplinary approach was found inevitable.Copyright © 2023, Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

The impact of covid-19 on amiodarone use in nottingham university hospitals dc cardioversion service, 1 year follow up

106 Table 13 MonthsRhythmAmiodarone (n=159)No Amiodarone (n=223)SR126141AF3382 106 Table 212 MonthsRhythmAmiodarone (n=113)No Amiodarone (n=125)SR5934AF5491Conflict of InterestNil

Variable radiographic and histologic presentations of amiodarone-related interstitial lung disease and the importance of avoiding re-exposure.

Amiodarone is a commonly used antiarrhythmic agent but exhibits potential pulmonary toxicity. In this case series, we describe the clinical, radiographic, and histologic manifestations of three patients who developed interstitial lung disease (ILD) following amiodarone treatment for variable lengths of time with different dosages. The presentations on computed tomographic images and in pulmonary pathology differed among the three patients. All three had immediate discontinuation of amiodarone and received treatment with systemic corticosteroids. One patient eventually died from ventilator-associated pneumonia after an initial improvement. The other two patients recovered well but later experienced ILD recurrence following brief re-exposure to amiodarone. Through this case series, we aim to demonstrate the variable features of amiodarone-related ILD, and highlight the importance of timely amiodarone cessation and avoiding re-exposure to prevent the progression and recurrence of ILD.

Atrial Torsades De Pointes Post Covid Myocarditis

Background: Among patients with COVID-19 infection, the risk of adverse cardiovascular outcome, particularly myocarditis and dysrhythmias remain elevated at least up to one year after infection. We present a case of atrial tachycardia and atrial Torsades de Pointes from COVID myocarditis, persisted 6 months after infection, which was successfully managed by ablation. Objective(s): A 25-year-old female presented with mild COVID-19 infection, Omicron variant, in May 2022. One month after, her Covid infection resolved;she presented with symptomatic atrial tachycardia, paroxysmal atrial fibrillation and flutter. ECG showed multiple blocked premature atrial contractions (PAC) (Figure 1A). Holter monitor showed PAC triggered atrial tachycardia degenerating to paroxysmal atrial fibrillation, atrial Torsades de Pointes. She has mild persistent troponin elevation. Echocardiography was normal. Cardiac MRI showed evidence of mild myocarditis with subepicardial late Gadolinium enhancement (LEG) along the lateral mid-apical left ventricular wall and edema. (Figure 1B). She was treated with Colchicine for 2 months. Repeat cardiac MRI 4 months after COVID infection showed resolution of edema and LGE. However, her symptomatic PAC and atrial tachycardia did not respond to betablocker and amiodarone. She underwent electrophysiology study. Activation mapping of PAC using CARTO revealed earliest activation at the right anterior atrial wall, with close proximity to tricuspid valve;unipolar signal showed QS pattern, bipolar signal showed 16 msec pre-PAC (Figure 1C and 1D). Mechanical pressure from ThermoCool SmartTouch ablation catheter (Biosense Webster Inc.) at this site suppressed the PAC. Radiofrequency ablation resulted with an initial acceleration and then disappearance of the PAC. We did not isolate pulmonary veins or ablate cavotricuspid isthmus. Post ablation, PAC and atrial fibrillation were not inducible on Isoproterenol. Method(s): N/A Results: Covid myocarditis can result in dysrhythmia that lingers long after Covid myocarditis has resolved. Covid myocarditis can be caused by direct viral invasion of myocytes or more commonly is inflammatory related to cytokine release and edema. Our case demonstrates that dysrhythmias can persist despite resolution of myocarditis. Catheter ablation can successfully to treat these arrhythmias. Conclusion(s): This case highlights the importance of recognizing cardiac dysrhythmia as possible the long-term cardiac complications of COVID-19, requiring specific treatment such as catheter ablation. [Formula presented]Copyright © 2023

Thyroiditis Post COVID-19 mRNA Booster Dose Vaccination

Introduction: SARS-CoV-2 vaccines have been associated with thyroid dysfunction including thyroiditis and Graves' disease. We report a patient who developed thyrotoxicosis secondary to thyroiditis after COVID-19 mRNA booster dose vaccination. Case Description: A 74-year-old man with no known personal or family history of thyroid disorders went to his primary care physician with symptoms of palpitations. Of note, he had the first booster (third dose) of the Pfizer/BioNTech vaccine about 1 week before. He did not recall any similar symptoms after the first two doses of the same vaccine. There were no other symptoms of thyrotoxicosis such as hand tremors, weight loss or mood change. There was no family history of thyroid disorders. He was not on any medications such as amiodarone and was not taking any herbal supplements. He did not have any symptoms of upper respiratory tract infection. There was no neck pain. Physical examination was unremarkable with no goiter or thyroid eye manifestations. Thyroid function: free T4 elevated at 46.7 pmol/L (11.5-22.7) and TSH suppressed at 0.01 mIU/L (0.5-4.5). Thyroid stimulating immunoglobulin was positive at 200% (50-179). He was initially started on carbimazole 15mg daily. However, the patient became rapidly hypothyroid despite dose reduction and subsequent discontinuation of carbimazole with free T4 of 8 pmol/L and TSH of 36.4 mIU/L. An ultrasound of the thyroid gland showed vascularity with no discrete nodules. No thyroid uptake scan was done. The diagnosis was revised to thyroiditis post vaccination. Hypothyroidism persisted despite discontinuation of carbimazole before recovery 8 months later. Patient was well and did not require any thyroxine supplementation. Discussion(s): It is postulated that COVID-19 vaccines triggered thyroiditis via an autoimmune inflammatory syndrome caused by the vaccine adjuvants. A high index of suspicion is necessary and a thyroid uptake scan may be useful in making the diagnosis. Thyroiditis is a self-limiting condition and recognising it is important as no specific thyroid treatment is necessary in most patients. Patients should not be deterred from subsequent vaccination as COVID-19 infection has higher mortality risk than thyroiditis.Copyright © 2023

Amiodarone-Induced Lung Toxicity: A Case Initially Not Correctly Framed.

Amiodarone-induced pulmonary toxicity (AIPT) is one of the most serious adverse effects of amiodarone and is one of the leading causes of death associated with its use. The onset of AIPT depends on dosage, patient's age, and pre-existing pulmonary pathologies; typically, the adverse effects stop progressing when a cumulative dose higher than 150 mg is reached. The risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dosage and duration of administration. In this case report, the effect of a prolonged overdose of amiodarone taken at doses of 200 mg/day for two years is reported, with symptoms and instrumental evidence of respiratory pathology induced by amiodarone drug toxicity. Comorbidities, oxygen therapy, invasive procedures, and surgical interventions can trigger pulmonary symptoms. Despite significant advances in understanding AIPT, its etiology and pathogenesis remain poorly understood. The role of steroids in the treatment of AIPT is still under debate as most reports of improvement after amiodarone withdrawal differ little from those in which concomitant steroid therapy was used. In clinical practice, therapeutic doses of corticosteroids may be indicated for patients with AIPT; usually, a starting dose of prednisone from 40 to 60 mg daily, which is then gradually reduced, is prescribed. The pharmacodynamics of amiodarone determines a treatment period of four to 12 months. The patient with AIPT in this case report, who markedly improved after treatment with prednisone at a starting dose of 50 mg/day, which was then gradually tapered. At the end of the therapy, the computed tomography (CT) scan revealed the disappearance of most of the scattered ground-glass opacities and of the thickening indicating bi-apical pulmonary fibrosis. The case report is unique because: 1) Bronchoalveolar lavage (BAL)/transbronchial biopsy was not used for diagnosis. 2) The case was framed based on the patient's laboratory and clinical data. 3) The pathology is normally prevalent in men rather than women.

Intentional Taxus Baccata Ingestion Presenting with Cardiogenic Shock and Ventricular Tachycardia

Background The prevalence of anxiety and depression has increased following the COVID pandemic. Young women are disproportionally at risk of suicidal behaviors. Ingestion of Taxus baccata (English Yew) may lead to cardiotoxicity and death. Intoxication is known to be resistant to standard treatments with no effective antidotes. Case A 20-year-old female with a history of major depressive disorder presented to our emergency department unresponsive in pulseless ventricular tachycardia (VT) (figure 1A). She underwent CPR and achieved ROSC, however, was persistently hypotensive despite multiple pressors and was subsequently placed on VA ECMO. Review of a home journal revealed a plan to ingest 50 grams of Yew with suicidal intent. Decision-making Taxoids have been reported to have similar properties to digoxin and therefore digoxin-specific FAB antibodies were administered. She was also started on amiodarone and lidocaine for management of VT. After 3 hours she converted into sinus rhythm and had no further episodes of VT. Her clinical course was complicated by severe LV dysfunction and dilation while on VA-ECMO necessitating placement of an LV impella. By day three, all mechanical support was weaned off and she had normalization of her EF. Patient was discharged to an inpatient psychiatry facility on day 7 of hospitalization. Conclusion Ingestion of English Yew with suicidal intent is rare but may cause cardiogenic shock and VT requiring aggressive hemodynamic support until the toxin is metabolized. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Successful Use of Biventricular Assist Devices in Fulminant Myocarditis

Background Fulminant myocarditis can cause biventricular dysfunction with a mortality rate over 40%. We report a case with severe biventricular failure due to fulminant myocarditis that was successfully supported by left and right ventricular assist devices. Case A 65-year-old woman presented with chest pain, abdominal pain and diarrhea. She was hypotensive and labs revealed elevated troponin-T of 13.5 ng/mL and lactate of 4.3 mmol/L. She was positive for COVID by antigen testing. She was started on multiple vasopressor infusions and admitted to the intensive care unit. Echocardiogram revealed a severely reduced left ventricular ejection fraction of 15% and severe global hypokinesis. The following day, she developed a wide complex tachycardia that was refractory to amiodarone, lidocaine and multiple defibrillation attempts. She was transferred emergently to the cardiac cath lab where coronary angiography revealed an isolated 70% stenosis of the distal left circumflex artery. A Swan-Ganz catheter was placed that yielded a cardiac index by Fick of 1.2 L/min/m2, systemic vascular resistance of 1270 dynesseccm-5 and mixed venous oxygen saturation of 35%. Decision was made to emergently insert an Impella CP device. That evening, she developed complete heart block and transvenous pacing wire was inserted. Due to frequent suction alarms, decision was made to insert ProtekDuo device, which resulted in hemodynamic stabilization. A temporary coronary sinus pacing lead for atrial capture was inserted to improve atrioventricular synchrony. After several days of monitoring, repeat echocardiogram showed complete recovery of biventricular function and Impella CP and ProtekDuo devices were removed. Decision-making The decision of early implantation of ProtekDuo device was made to provide adequate blood flow to the left ventricular assist device for hemodynamic support. In addition, increased atrioventricular synchrony via insertion of temporary coronary sinus pacing wire improved cardiac output. Conclusion Fulminant myocarditis involving biventricular dysfunction can be supported by the use of simultaneous left and right ventricular assist devices.Copyright © 2023 American College of Cardiology Foundation

Legionella Myocarditis Masquerading as Dual Chamber Cardiac Arrhythmia

Background Legionella pneumonia is a rare cause of myocarditis. Case 64-y.o male with CAD and PCI to LAD, DM and HTN presented to ER with mental status changes. On exam he was febrile and hypoxic.Presenting rhythm was Afib with frequent bouts of sustained and non-sustained stable posteroseptal VT treated with amiodarone and mexilitene. With right lung infiltrate on CXR and elevated WBC count, antibiotics were initiated for pneumonia. SARS COV-2 Ag and Influenza A & B was negative. Urine Ag for legionella was positive and was promptly treated with Levofloxacin. Coronary angiogram prior to discharge showed non-obstructive CAD. Decision-making Legionnaires' disease with myocarditis was suspected. Patient underwent CMR with late gadolinium enhancement (LGE) and Rest 82Rb perfusion and 18F-FDG PET/CT with high-fat dietary preparation scan for evaluation of legionella myocarditis. CMR revealed LVEF of 46%, with LGE and PET findings as described in the Figure. He was initiated on solumedrol for ongoing inflammation after completion of antibiotic therapy for Legionella pneumonia. Conclusion Our case highlights a systematic approach to differential diagnosis and use of multimodality imaging in legionella myocarditis presenting with dual chamber arrhythmia. There was good correlation between LGE inflammation/scar location and origin of VT, as well as active inflammation demonstrated by FDG PET imaging. The patient was successfully treated with antibiotics, steroids and anti-arrhythmic drugs. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

Amiodarone for the Treatment of Arrhythmias in COVID-19 Patients Does Not Increase the Risk of Pulmonary Fibrosis: A Retrospective Cohort Study.

Amiodarone is a class III antiarrhythmic medication used to treat atrial and ventricular tachyarrhythmias. Pulmonary fibrosis from amiodarone use is a well-documented side effect. Pre-COVID-19 pandemic studies have shown that amiodarone-induced pulmonary fibrosis occurs in 1%-5% of patients and usually occurs between 12 to 60 months after initiation. The risk factors associated with amiodarone-induced pulmonary fibrosis include a high total cumulative dose (treatment longer than two months) and high maintenance dose (>400 mg/day). COVID-19 infection is also a known risk factor for developing pulmonary fibrosis and occurs in approximately 2%-6% of patients after a moderate illness. This study aims to assess the incidence of amiodarone in COVID-19 pulmonary fibrosis (ACPF). This is a retrospective cohort study with 420 patients with COVID-19 diagnoses between March 2020 and March 2022, comparing two populations, COVID-19 patients with exposure to amiodarone (N=210) and COVID-19 patients without amiodarone exposure (N=210). In our study, pulmonary fibrosis occurred in 12.9% of patients in the amiodarone exposure group compared to 10.5% of patients in the COVID-19 control group (p=0.543). In multivariate logistic analysis, which controlled for clinical covariates, amiodarone use in COVID-19 patients did not increase the odds of developing pulmonary fibrosis (odds ratio (OR): 1.02, 95% confidence interval (CI): 0.52-2.00). The clinical factors associated with the development of pulmonary fibrosis in both groups included a history of preexisting interstitial lung disease (ILD) (p=0.001), exposure to prior radiation therapy (p=0.021), and higher severity of COVID-19 illness (p<0.001). In conclusion, our study found no evidence that amiodarone use in COVID-19 patients increased the odds of developing pulmonary fibrosis at six-month follow-up. However, long-term amiodarone usage in the COVID-19 population should be based on the physician's discretion.

Treating Supraventricular Tachycardia With Amiodarone in a Patient With Ebstein's Anomaly.

Ebstein's anomaly is a congenital deformity marked by disease of the tricuspid valve and right cardiac hypertrophy. The severity, morphology, and appearance of Ebstein's anomaly cases might vary greatly. We discuss a case of an eight-year-old child with Ebstein's anomaly who presented with supraventricular tachycardia and was effectively treated with amiodarone after initial treatment with adenosine failed to reduce the heart rate.

Antiviral Activity of Amiodarone in SARS-CoV-2 Disease

Amiodarone seems to exhibit some antiviral activity in the disease caused by SARS-CoV-2. Here we have examined the SARS-CoV-2 disease course in the entire population of the Czech Republic and compared it with the course of the disease in patients treated with amiodarone in two major Prague's hospitals. In the whole population of the Czech Republic SARS-CoV-2 infected 1665070 persons (15.6 %) out of 10694000 (100 %) between 1 April 2020 and 30 June 2021. In the same time period only 35 patients (3.4 %) treated with amiodarone were infected with SARS-CoV-2 virus out of 1032 patients (100 %) who received amiodarone. It appears that amiodarone can prevent SARS-CoV-2 virus infection by multiple mechanisms. In in-vitro experiments it exhibits SARS-CoV-2 virus replication inhibitions. Due to its anti-inflammatory and antioxidant properties, it may have beneficial effect on the complications caused by SARS-CoV-2 as well. Additionally, inorganic iodine released from amiodarone can be converted to hypoiodite (IO-), which has antiviral and antibacterial activity, and thus can affect the life cycle of the virus.

Hidden in plain sight: A case of arrhythmia and sudden cardiac failure masked by COVID-19 positivity

Background and Aim: Whilst most commonly recognised as a res-piratory pathogen, COVID-19 can also result in a variety of extrapulmonary manifestations including myocardial dysfunction and arrhythmia. We report a case of a 15 year old girl with repaired atrioventricular septal defect, presenting with arrhythmia and sud-den severe cardiac failure masked by COVID-19 positivity. Method(s): A 15 year old girl with repaired atrioventricular septal defect and tetralogy of Fallot, under regular follow up with asymp-tomatic moderate to severe atrioventricular valve dysfunction, pre-sented with one month's history of progressive breathlessness to her local hospital. Onset of illness coincided with typical COVID-19 symptoms;her family, attributing her deterioration to this, delayed seeking medical help. She was rapidly referred to our unit. The heart failure severity, which included diffuse dependent oedema, large pleural effusion and severe biventricular dysfunc-tion, could not be attributed to major valve function change. Moreover, deterioration had occurred rapidly without apparent ongoing cause, after extensive diagnostics. Tachyarrhythmia was suspected;initial adenosine challenge via peripheral vein was inconclusive. Diuretics, inotrope and empirical administration of amiodarone provided limited response;the patient was therefore ventilated, enabling further adenosine challenge via central line, which revealed atrial flutter. Shortly after conversion to sinus rhythm and pleural drainage, her biventricular function improved to near normal. Result(s): Redo surgery was undertaken. Firstly, this included mechanical valve replacement of left and right atrioventricular valves and ablation of the isthmus. Secondly, a permanent pace-maker was inserted a few days later. The patient made a quick and uneventful recovery and was discharged on day 10 with good biventricular function on minimal medical therapy and no symptoms. Conclusion(s): Our case highlights delayed presentation as a hidden effect of the COVID-19 pandemic, and that sudden deterioration in stable children with repaired congenital heart disease should prompt the clinician to exclude all reversible causes of de-stabili-sation, and in particular to maintain high suspicion of arrhythmia.

Life-threatening rhythm and conduction disorders by a child with MIS-C

Background and Aim: Cardiac involvement is seen in the majority of cases with multisystem inflammatory syndrome in children (MIS-C). Various rhythm and conduction disturbances, as well as repolarization abnormalities, have been described by more than 50% of the patients, while there are few cases with complete heart block or with asystole. Method(s): Case report Results: 8-year old girl presented with a 5-day history of fever, cough, headache, and abdominal pain. Because of the critical con-dition, with respiratory insufficiency and heart failure symptoms, the child was intubated and started on inotropic support. ECG showed complete AV-block with a ventricular rate of 75/min and with ST-T changes;echocardiography revealed dilated left ventricle with reduced contractility, CT-scan of the lungs showed bilateral pneumonia, the inflammatory markers were elevated, in combination with high troponin levels, and positive SARS-CoV2-IgG antibodies. The diagnosis MIS-C was made and treatment with immunoglobulins, antibiotics, corticosteroids, and anticoagulants was initiated. During the next 2 days, the cardiac function deteriorated further, and while still on mechanical ventilation and inotropic support, extreme bradycardia with a ventricular rate of 35/min was regis-tered, and the patient was indicated for temporary emergency pac-ing. Upon induction of anesthesia, the child became asystolic, requiring extensive resuscitation. After circulation recovery, the ECG showed nodal tachycardia with a heart rate of 140-170/min. A temporary transvenous pacemaker (PM) was inserted, and the patient was started on intravenous amiodarone which resulted in a slower ventricular rate of 70/min. 3 days later sinus rhythm was restored, with first-degree AV-block, which allowed removal of the PM 5 days after its insertion. Left ventricular dimensions were normalized and contractility remained low-normal (EF 56%). During the 6-month follow-up, the ECG and the Holter-monitoring showed sinus rhythm with first-degree AV-block. Magnetic resonance imaging (MRI) on day 15 of the hospital stay demonstrated scattered areas of myocarditis and ischemia predominantly in the left ventricle, as well as thickening of the basal septum. Six months later the MRI changes were reduced but still persistent. Conclusion(s): MIS-C can present with serious and life-threatening rhythm and conduction disturbances in children;this is why extensive cardiac monitoring is obligatory by all patients.

DISSEMINATED INVASIVE ASPERGILLUS MASQUERADING AS AMIODARONE-INDUCED THYROTOXICOSIS

SESSION TITLE: Rare Pulmonary Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Aspergillus is a group of opportunistic endemic fungal species that causes pathology within the respiratory tract and sinuses of individuals with predisposing factors, such as immunosuppression. While less frequently discussed, aspergillosis thyroiditis represents the most common fungal thyroiditis. We present a case of this condition that was misdiagnosed as amiodarone induced thyrotoxicosis. CASE PRESENTATION: A 54-year-old male was evaluated in outpatient pulmonary clinic after a chest CT revealed new upper lobe mass-like pleural based infiltrates with accompanying symptoms of dyspnea on exertion and fevers. His medical history was significant for orthotopic heart transplant 6 months ago due to a combination of non-ischemic cardiomyopathy with further decompensation from COVID-19 infection. After transplant, he was diagnosed with thyrotoxicosis secondary to amiodarone that was being treated with prednisone and methimazole. Given the concern for infection on imaging, he was admitted to the hospital and underwent urgent bronchoscopic evaluation. During the procedure, he was noted to have severe extrinsic tracheal compression. His neck imaging was consistent with a nodular goiter. The BAL revealed Aspergillosis fumigatus and he was subsequently treated with isavuconazium. Given the compression on the trachea and persistent dyspnea, the decision was to pursue total thyroidectomy. Surgery occurred 2 months after treatment was initiated for the Aspergillosis and with improvement on serial chest CTs. Pathologic examination of the thyroid tissue revealed extensive invasive aspergillus with abscesses involving both lobes. DISCUSSION: Aspergillus infection leading to disseminated disease typically occurs in individuals that have a compromised immune system such as seen in malignancy, solid organ transplant, chronic steroid use, and poorly controlled diabetes mellitus. Recently, it has been cited that up to 15% of hospitalized COVID-19 patients requiring intensive care develop aspergillus infection. After initial aspergillosis infection has been established, the thyroid gland is a site for dissemination due to its rich vascular supply. In addition, due to the angioinvasive properties of the pathogen, the fungus can breakdown tissue planes and easily travel from its site of origin. Thereby a primary infection in the respiratory tract can lead to dissemination to the neck structures due to its proximity. When thyroid invasion occurs, the common complaints are neck pain and swelling. Thyroid laboratory findings encompass the full spectrum including hyperthyroidism, hypothyroidism, and euthyroid. Given these non-specific findings, clinicians need to be conscious of this disease entity. CONCLUSIONS: In patients with immunocompromising conditions, findings of neck pain, swelling, and abnormal thyroid laboratory values should broaden the differential for clinicians to include aspergillosis thyroiditis. Reference #1: Alvi, Madiha M et al. "Aspergillus thyroiditis: a complication of respiratory tract infection in an immunocompromised patient.” Case reports in endocrinology vol. 2013 (2013): 741041. doi:10.1155/2013/741041 Reference #2: Marui, Suemi, et al. "Suppurative thyroiditis due to aspergillosis: a case report.” Journal of Medical Case Reports 8.1 (2014): 1-3. Reference #3: Kuehn, Bridget M. "Aspergillosis Is Common Among COVID-19 Patients in the ICU.” JAMA 326.16 (2021): 1573-1573. DISCLOSURES: No relevant relationships by A. Whitney Brown, value=Honoraria Removed 04/03/2022 by A. Whitney Brown No relevant relationships by A. Whitney Brown, value=Honoraria Removed 04/03/2022 by A. Whitney Brown No relevant relationships by A. Whitney Brown, value=Consulting fee Removed 04/03/2022 by A. Whitney Brown No relevant relationships by Kristen Bussa Advisory Committee Member relationship with Boehringer Ingelheim Please note: 2019-2021 Added 04/03/2022 by Christopher King, value=Consulting f e Advisory Committee Member relationship with Actelion Please note: 2019-2022 Added 04/03/2022 by Christopher King, value=Consulting fee Advisory Committee Member relationship with United Therapeutics Please note: 2019-2022 Added 04/03/2022 by Christopher King, value=Consulting fee Speaker/Speaker's Bureau relationship with Actelion Please note: 2019-2022 Added 04/03/2022 by Christopher King, value=Consulting fee Speaker/Speaker's Bureau relationship with United Therapeutics Please note: 2020-22 Added 04/03/2022 by Christopher King, value=Consulting fee No relevant relationships by Haresh Mani No relevant relationships by Mary Beth Maydosz No relevant relationships by Alan Nyquist No relevant relationships by Anju Singhal No relevant relationships by Amy Thatcher

A CASE REPORT OF AMIODARONE PULMONARY TOXICITY MIMICKING AS COVID-19 PNEUMONIA

SESSION TITLE: Drug-Induced Lung Injury Pathology Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: The most dangerous complication of amiodarone use is amiodarone-induced pulmonary toxicity (AIPT) (1). AIPT has no pathognomonic findings & is therefore diagnosed based on clinical suspicion & exclusion of other possible pulmonary diseases (2) CASE PRESENTATION: A 91-year-old female with history of CHF & atrial fibrillation on amiodarone 200mg once daily for approximately 10 years, presented for worsening shortness of breath for 3 days. On admission vitals were stable & pulse oximetry revealed a SpO2 of 89% on room air which increased to 96% on 4 litres oxygen. Examination revealed decreased breath sounds at bases, bilateral rales right>left. No clinical signs of fluid overload. Chest x-ray (fig 1) showed increased bilateral airspace opacities and computed tomography (CT) of chest (fig 3) revealed diffuse airspace opacities, right > left. Initial lab work was within normal limits. She was admitted with a working diagnosis of acute hypoxemic respiratory failure due to community acquired pneumonia (CAP) versus COVID-19 pneumonia due to high suspicion based on her clinical picture. She received remdesvir, empiric antibiotics and amiodarone was discontinued. COVID-19 PCR was negative, patient did not spike fevers or had any leukocytosis & pneumonia workup was negative. Therefore we now considered AIPT. Gallium scan for AIPT revealed abnormal uptake involving lungs bilaterally consistent with AIPT. Patient was continued on dexamethasone, after which patient's oxygen requirement subsequently decreased & repeat chest x-ray (fig 2 ) showed a significant decrease in bilateral infiltrates on steroids. She was discharged home on 2 litres oxygen & prednisone taper for 4 months. DISCUSSION: The advent of the highly contagious SARS-CoV-2 has made it further essential to diagnose AIPT correctly & to differentiate between these two entities. They have similar & non-specific features which makes this an even a greater challenge. Our elderly patient on long-term amiodarone use represents an at-risk group for AIPT (1). Her clinical picture was non-specific, initially suggesting CAP versus COVID-19 pneumonia. In our case, the consistent gallium scan findings confirmed the diagnosis of AIPT & enabled prompt anti-inflammatory treatment along with cessation of amiodarone which resulted in improved prognosis & outcome. AIPT should be suspected in patients taking amiodarone who have new or worsening symptoms with an insidious onset &/or new infiltrates on chest x-ray. Greater parenchymal activity on gallium scintigraphy scanning & the presence of lung biopsy findings can help further confirm the diagnosis (1) CONCLUSIONS: In the era of the COVID-19 pandemic, it becomes even more challenging to diagnose and differentiate AIPT from SARS-CoV-2 pneumonia, which can have a similar presentation (3). Early recognition of AIPT is critical to prevent or minimize its potentially devastating pulmonary effects. Reference #1: Martin, W. J., & Howard, D. M. (1985). Amiodarone-induced lung toxicity: In vitro evidence for the direct toxicity of the drug. American Journal of Pathology, 120(3), 344–350. Reference #2: Benassi, F., Molardi, A., Righi, E. et al. ECMO for pulmonary rescue in an adult with amiodarone-induced toxicity. Heart Vessels 30, 410–415 (2015). Reference #3: Macera M, De Angelis G, Sagnelli C, Coppola N, Vanvitelli Covid-Group. Clinical Presentation of COVID-19: Case Series and Review of the Literature. Int J Environ Res Public Health. 2020 Jul 14;17(14):5062. DISCLOSURES: No relevant relationships by Nayaab Bakshi No relevant relationships by Navjot Kaur Grewal No relevant relationships by Talha Munir No relevant relationships by Anusha Singhania

COVID-19: A CONFOUNDING MIMICKER OF HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS

SESSION TITLE: Challenging Cases of Hemophagocytic Lymphohistiocytosis SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) is a rare syndrome involving pathologic immune activation that is often fatal. The link between the cytokine storm related to COVID-19 and development of HLH has been reported since the onset of the pandemic, but little is known about clinical manifestations of HLH, thereby delaying treatment. CASE PRESENTATION: A 50 year-old male presented with a several day history of progressive weakness in the setting of missed dialysis session. Medical history was significant for ESRD on dialysis and diastolic heart failure (EF 35%). Initial vitals were unremarkable. Physical exam was notable for peripheral edema bilaterally. Laboratory studies were consistent with hyperkalemia, elevated ferritin (28,383) and elevated liver function tests. COVID-19 PCR was positive upon admission. Chest x-ray, CTA chest and a right upper quadrant ultrasound were unremarkable. He was admitted to the medical ICU for emergent dialysis. Soon after arrival to the ICU, he became lethargic and confused with increasing oxygen requirements and a subsequent a code blue was called. Cardiopulmonary resuscitation was immediately initiated, with a first rhythm consistent with ventricular fibrillation. He was shocked and placed on an amiodarone infusion with return of spontaneous circulation. TTE revealed a severely reduced EF <10%. Despite initiation of advanced COVID-19 therapies with Solu-Medrol and tocilizumab he remained ventilator dependent. Due to hemodynamic instability and persistent metabolic acidosis, he was transitioned to continuous renal replacement. Further blood work showed worsening inflammatory markers (ferritin 33,500, LDH 6981). Because of the significantly elevated ferritin, there were concerns for possible HLH. Triglycerides and IL-2 receptor were 395 mg/dL and 9300 pg/mL respectively. Total NK cells were decreased to 1.2%. He remained persistently unstable despite aggressive measures. He suffered a second cardiopulmonary arrest, which was unable to achieve return of spontaneous circulation and he ultimately passed away. DISCUSSION: HLH is characterized by uncontrolled activation and proliferation of benign macrophages in reticuloendothelial organs. This results in histiocytic hemophagocytosis, worsening peripheral blood cytopenia(s), cytokine storm, and cytokine mediated biochemical alteration ultimately culminating in multiorgan dysfunction and disseminated intravascular coagulation. Although a distinctive constellation of features has been described for HLH, diagnosis remains challenging as patients have diverse presentations associated with a variety of triggers. CONCLUSIONS: As HLH is a medical emergency with poor prognosis, prompt recognition and early treatment is crucial for improving clinical outcomes. We hope this case will create increased awareness and timely diagnosis of cytokine storm syndromes in patients with severe COVID-19 infection. Reference #1: Meazza Prina M, Martini F, Bracchi F, Di Mauro D, Fargnoli A, Motta M, Giussani C, Gobbin G, Taverna M, D'Alessio A. Hemophagocytic syndrome secondary to SARS-Cov-2 infection: a case report. BMC Infect Dis. 2021 Aug 13;21(1):811. doi: 10.1186/s12879-021-06532-7. PMID: 34388982;PMCID: PMC8361241. Reference #2: Schnaubelt, Sebastian MDa,*;Tihanyi, Daniel MDb;Strassl, Robert MDc;Schmidt, Ralf MDc;Anders, Sonja MDb;Laggner, Anton N. MDa;Agis, Hermine MDd;Domanovits, Hans MDa Hemophagocytic lymphohistiocytosis in COVID-19, Medicine: March 26, 2021 - Volume 100 - Issue 12 - p e25170 doi: 10.1097/MD.0000000000025170 DISCLOSURES: No relevant relationships by Garrett Fiscus No relevant relationships by Niala Moallem No relevant relationships by Resham Pawar

A FEBRILE CRISIS: MONOMORPHIC VENTRICULAR TACHYCARDIA IN A STRUCTURALLY INTACT HEART

SESSION TITLE: Cardiovascular Complications in Patients with COVID-19 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: COVID-19 infection has been shown to exhibit an array of deleterious cardiac effects specifically arrhythmias. While arrhythmias of ventricular origin are less common, direct insult to the myocardium is cited as the most common etiology [1]. Here we present a unique case of hyperthermia induced monomorphic ventricular tachycardia (VT) in the setting of COVID-19 infection. CASE PRESENTATION: A 65-year-old male with medical history of dyslipidemia and hypertension presented with cough, dyspnea and subsequently diagnosed with COVID-19 pneumonia and was noted to be persistently febrile with a peak temperature of 40.1° C, which coincided with the onset of sustained monomorphic VT for approximately 40 minutes. He was treated with amiodarone. He did not have chest pain and troponin levels were normal. Cooling measures were initiated in the ICU. While normothermic, he did not have episodes of VT until the following day when his temperature again peaked at 40.6° C. A lidocaine drip was started to maintain sinus rhythm. However, due to multi-system organ failure, the family decided to proceed with comfort care. DISCUSSION: COVID-19 infection associated with fatal VT has been documented in the literature mainly attributed to ischemia and myocarditis. [1,2]. COVID-19 virus has the potential to trigger a massive inflammatory response causing systemic illness. Classically, the prototypical patient has a scar from previous ischemic heart disease that allows reentry to occur. Our patient had no prior history of structural heart disease, evidence of acute coronary syndrome or myocarditis. Other known causes of VT were ruled out. It became clear that the patient’s induction of VT had a temporal association with hyperthermia. Once the patient’s temperature was above 40° C, VT would ensue and only terminate with resolution of the fever. Temperature has been shown to affect the transmembrane gradient and the flow velocity of ions through myocardial ion gated channels [3]. These physiological changes could lead to increased automaticity or triggered events that induce VT. Therefore, hyperthermia should not be neglected as a potential trigger for VT in an otherwise intact myocardium. CONCLUSIONS: A systemic illness like COVID-19 associated with cytokine storm can drastically influence the thermal regulation of the body. This can cause a shift in the transmembrane gradient and resting membrane potential, which could in turn alter automaticity. Therefore, hyperthermia could be a possible trigger for monomorphic VT in an otherwise intact myocardium. Early recognition and rapid external cooling are crucial to minimize the risk of ventricular dysrhythmias. Reference #1: Manolis, Antonis S et al. "COVID-19 infection and cardiac arrhythmias.” Trends in cardiovascular medicine vol. 30,8 (2020): 451-460. doi:10.1016/j.tcm.2020.08.002 Reference #2: Bhatla, A., Mayer, M., Adusumalli, S., Hyman, M., Oh, E., Tierney, A., Moss, J., Chahal, A., Anesi, G., Denduluri, S., Domenico, C., Arkles, J., Abella, B., Bullinga, J., Callans, D., Dixit, S., Epstein, A., Frankel, D., Garcia, F., Kumareswaram, R., Nazarian, S., Riley, M., Santangeli, P., Schaller, R., Supple, G., Lin, D., Marchlinski, F. and Deo, R., 2020. COVID-19 and cardiac arrhythmias. Heart Rhythm, 17(9), pp.1439-1444. Reference #3: Huckell, V F et al. "Cardiac Manifestations Of Malignant Hyperthermia Susceptibility.". Circulation, vol 58, no. 5, 1978, pp. 916-925. Ovid Technologies (Wolters Kluwer Health), doi:10.1161/01.cir.58.5.916. Accessed 1 June 2021. DISCLOSURES: No relevant relationships by Robert Cacdac No relevant relationships by Nami Moradi

I will never forget the day

Introduction: I would like to present a poem I have written about my experience of being part of the multidisciplinary team at a remote district general hospital on the day that a COVID-19 patient was retrieved for ECMO. Main Body: I will never forget the day It was late in the month of May It started in the usual way A handover with our patient lists We gathered, doctors, nurses, therapists And discussed a patient with COVID-19 infection And his clinical deterioration. He was a man of about fifty Usually well and pretty healthy Brought in by ambulance to A&E With oxygen saturations of eighty And quickly escalated to NIV. Three days alternating CPAP and high flow But progress was extremely slow And by the morning of day four He couldn't cope any more Sixty was his respiratory rate So the decision was made to intubate. He was given every treatment known Antimicrobials, paralysis and prone Epoprostenol and dexamethasone So brittle was his gas exchange with any small position change And even on APRV His FiO2 reached seventy. His only chance of salvation Was extracorporeal membrane oxygenation As the retrieval team began their journey ICU and theatre staff worked closely Nurse, consultant and operating department practitioner Helped move the patient into theatre Still proned, too unstable To even transfer to the table We waited in personal protective gear For the ECMO team to appear. From London arrived the ECMO specialist Her registrar and perfusionist A quick briefing, roles allocated, The patient was swiftly cannulated, With the largest lines I'd ever seen! And established on the ECMO machine It was a truly inspiring scene. Switching infusions, monitoring, ventilation, Ready for patient transportation But during the preparation He went into fast atrial fibrillation Requiring electrical cardioversion Amiodarone and magnesium. Sinus rhythm was restored But it was an insult he couldn't afford Increasingly hypotensive he became Chest compressions, adrenaline, all in vein, And to a difficult decision we came All agreed as a team Time to switch off the machine. I will never forget that day It was late in the month of May A life lost in a tragic way But something I can honestly say Never prouder have I been Of every person in that team We gave our all, we did our best In peace may our patient rest. Conclusion: I would like to dedicate this poem to all my ICU and theatre colleagues who shared this experience with me and, if given the opportunity, present it alongside pictures of them in their PPE as they were that day.