Ventricular Fibrillation Arrest Research Articles

Long-term Rate of Ventricular Arrhythmia in Autoimmune Disease.

Although selected autoimmune diseases (AIDs) have been linked to an increased risk of ventricular arrhythmias (VAs), data on the long-term rate of VAs across the spectrum of AIDs are lacking. The aim of our study was to investigate the long-term rate of VAs (a composite of ventricular tachycardia, ventricular fibrillation, ventricular flutter, or cardiac arrest) in individuals with a history of 28 different AIDs. Individuals diagnosed with an AID (2005-2018) were identified through Danish nationwide registries. Each patient with AID was matched with four individuals from the background population by age and sex. Multivariable Cox regression was used to compare the rate of VAs between the AIDs and background population, overall and according to individual AIDs. In total, 186,733 patients diagnosed with AIDs were matched with 746,932 individuals without AIDs (median age 55 years; 63% female; median follow-up 6.0 years). The 5-year cumulative incidence of VAs was 0.5% for patients with AIDs and 0.3% for matched individuals. Patients with any AIDs had a higher associated rate of VAs than matched individuals (HR 1.39 [95% CI, 1.29-1.49]). The highest HR was observed in patients with systemic sclerosis (3.86 [95% CI, 1.92-7.75]). The higher rate of VAs in patients with AIDs, compared with individuals from the background population, was more pronounced in patients without ischemic heart disease or heart failure/cardiomyopathy compared to those with these conditions (Pinteraction < 0.05). Despite a low cumulative incidence, patients with a history of AIDs had a higher relative rate of VAs than matched individuals.

Emergency transvenous temporary pacing during rotational atherectomy.

Rotational atherectomy (RA) during percutaneous coronary intervention may cause transient bradycardia or a higher-degree heart block. Traditionally, some operators use prophylactic transvenous pacing wire (TPW) to avoid haemodynamic complications associated with bradycardia. We sought to establish the frequency of bail-out need for emergency TPW insertion in patients undergoing RA that have received no upfront TPW insertion. We performed a single-centre retrospective study of all patients undergoing RA between October 2009 and October 2022. Patient characteristics, procedural variables, and in-hospital complications were registered. A total of 331 patients who underwent RA procedure were analysed. No patients underwent prophylactic TPW insertion. The mean age was 73.3 ± 9.1 years, 71.6% (n = 237) were male, while nearly half of the patients were diabetic [N = 158 (47.7%)]. The right coronary artery was the most common target for RA (40.8%), followed by the left anterior descending (34.1%), left circumflex (14.8%), and left main stem artery (10.3%). Altogether 20 (6%) patients required intraprocedural atropine therapy. Emergency TPW insertion was needed in one (0.3%) patient only. Eight (2.4%) patients died, although only one (0.3%) was adjudicated as being possibly related to RA-induced bradycardia. Five patients (1.5%) had ventricular fibrillation arrest, while nine (2.7%) required cardiopulmonary resuscitation. Six (1.8%) procedures were complicated by coronary perforation, two (0.6%) were complicated by tamponade, while 17 (5.1%) patients experienced vascular access complications. Bail-out transvenous temporary pacing is very rarely required during RA. A standby temporary pacing strategy seems reasonable and may avoid unnecessary TPW complications compared with routine use.

Neuromuscular and cardiovascular phenotypes in paediatric titinopathies: a multisite retrospective study

BackgroundPathogenic variants in TTN cause a spectrum of autosomal dominant and recessive cardiovascular, skeletal muscle and cardioskeletal disease with symptom onset across the lifespan. The aim of this study was...

Risk differences between atrial fibrillation patients with different clinical phenotypes: insights from the French population

Abstract Background Atrial fibrillation (AF) patients represent a clinically complex, heterogeneous population comprising multiple homogeneous cohorts. Purpose We aimed to identify the common clinical phenotypes of AF patients and compare clinical outcomes between these subgroups. Methods A 1% representative sample of all AF patients hospitalized between 2010 and 2019 was identified from the French national database. Agglomerative hierarchical cluster analysis was performed using Ward’s method and squared Euclidian distance , to derive 4 distinct clusters of patients (Figure 1) using 31 clinical variables. Cox regression analyses were used to evaluate outcomes including all-cause death, cardiovascular death, non-cardiovascular death, ischaemic stroke, hospitalisation for heart failure (HF) and composite of ventricular tachycardia, ventricular fibrillation and cardiac arrest (VT/VF/CA). Results Four clusters were generated from the 12,688 patients included. Cluster 1 (n=2375) was younger, with a low risk of cardiovascular disease (CVD) and risk factors such as hypertension, dyslipidaemia and diabetes, but had the highest cancer prevalence. Clusters 2 (n=6441) and 3 (n=1639) depicted moderate-risk groups for CVD, with the female majority and high rates of lung conditions being the distinct features respectively. Cluster 3 also had the highest degree of frailty, with clusters 2 and 4 following closely. Cluster 4 (n=2233) represented a high-risk cohort for CVD with a high prevalence of coronary artery and vascular disease. Over a follow-up period of 2.0±2.3 years (median 1.1, interquartile range 0.1-3.4), cluster 3 had the highest cumulative incidence of all outcomes except for cardiovascular death which was highest in cluster 4. Compared to cluster 1, cluster 3 had the highest risk for all-cause death, HR 1.24 (1.09-1.41), cardiovascular death, HR 1.56 (1.19-2.06), non-cardiovascular death, HR 1.20 (1.04-1.38), hospitalisation for HF, HR 2.07 (1.71-2.50) and VT/VF/CA, HR 1.74 (1.20-2.53). Conclusion Four main clusters of AF patients were identified, discriminated by the differential presence of comorbidities. Our findings suggest that AF patients with moderate CVD-risk may have a poorer prognosis compared to AF patients with high CVD-risk in the presence of lung pathology. Therefore, this subgroup of patients may require more stringent management of existing comorbidities such as chronic obstructive pulmonary disease and sleep apnoea, alongside their AF.

Abstract 218: Effect of Airway Pressure and Localized Sternal Compression Upon Hemodynamics During Cardiopulmonary Resuscitation

Background: During cardiopulmonary resuscitation (CPR), chest compression (CC) and mechanical ventilation are cyclic in nature and each modulate the intrathoracic pressure (ITP). ITP is increased during the compression phase of CC, causing an increase in aortic pressure (AoP) and right atrial pressure (RAP) to drive forward blood flow. Similarly, positive pressure ventilation increases ITP during the inspiratory phase as pressure is transmitted through the lungs, which also has an impact on hemodynamics. The purpose of this analysis was to examine differences in hemodynamics during ventricular fibrillation (VF) arrest due to ventilation alone and during localized sternal CC of varying depths in a porcine model of cardiac arrest. Methods: Domestic swine (n = 8) underwent electrically induced VF with ten-minute downtime, followed by resuscitation with mechanical ventilation and CC with active lift to neutral chest position. Mechanical ventilation was delivered using pressure-controlled synchronized intermittent mandatory ventilation (SIMV) mode (Vt 10 mL/kg, 10 bpm, trigger -6 cmH 2 O, PEEP 5 cmH 2 O, FiO 2 100). CPR was initiated with three minutes of ventilation only, followed by one minute of break-in CC at 1.0 in and 1.5 in prior to increase to depth of 2.0 in. AoP, RAP, esophageal pressure (Pes), and airway pressure (Paw) were examined over the ventilation cycle to determine the effect of each treatment upon parameters. Results: Positive pressure ventilation caused similar changes to the Pes, RAP, and AoP values (3-5 mmHg). CC caused similar changes to Pes (3-5 mmHg), but much larger changes to the RAP and AoP (10-130 mmHg) depending on compression depth. Conclusions: The ITP is not uniform during CC, creating only modest changes to Pes. This suggests that CC generate blood pressures, and presumably flows, through mechanisms other than ITP modulation. Understanding this interaction could improve our understanding of blood flow during CPR.

Abstract 16003: A Case of Ventricular Fibrillation Arrest in a Healthy Young Female With Newly Discovered Mitral Annular Disjunction

Introduction: Mitral annular disjunction (MAD) is an under-recognized cause of ventricular arrhythmias. Case Presentation: A previously healthy, athletic 43-year-old female suddenly collapsed during a staff meeting at a medical center. Cardiopulmonary resuscitation was initiated and she was found to be in ventricular fibrillation, requiring three defibrillation shocks to achieve ROSC. EKG was notable for prolonged QTc without signs of pre-excitation or Brugada syndrome. Patient denied any personal or family cardiac history but endorsed frequent palpitations in the past. No electrolyte derangements were identified. Coronary angiography revealed normal origins of the coronary arteries and no evidence of obstructive disease. Transthoracic echocardiogram demonstrated normal left ventricular systolic function, normal wall thickness, and no regional wall motion abnormalities. There was mild bileaflet mitral valve prolapse with mild mitral regurgitation and mitral annular disjunction measuring 0.7 cm. Cardiac MRI was obtained and demonstrated biventricular dilation (consistent with athlete’s heart) with evidence of MAD. The myocardium was normal with no evidence of late enhancement. She underwent dual-chamber cardioverter-defibrillator implantation for secondary prevention. Discussion: Mitral annular disjunction is a structural abnormality involving atrial displacement of the mitral annulus, leading to an abnormal separation between the posterior mitral valve leaflet and basal ventricular myocardium during systole. Etiology of MAD remains unclear. It is estimated to be present in 8.7% of the general population and in over 30% of individuals with mitral valve prolapse. This case presents an example of a previously healthy patient with sudden cardiac arrest. After extensive workup, MAD was identified as the most likely trigger for her new onset arrhythmia. This case highlights the severe, and potentially fatal, arrhythmias that can arise from MAD. It is important to recognize MAD seen on echocardiograms and counsel patients on potential complications. Patients with MAD and increased risk factors should undergo further evaluation with cardiac MRI and/or electrophysiology studies.

Ventricular Fibrillation Arrest after Blunt Chest Trauma in a 33-year-old Male, Commotio Cords?

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Atrioventricular Nodal Ablation Is Not an Effective Treatment Strategy in Catecholaminergic Polymorphic Ventricular Tachycardia.

Catecholaminergic polymorphic ventricular tachycardia is a rare but lethal heritable arrhythmia syndrome associated with both atrial and ventricular arrhythmias. Treatment includes antiarrhythmics, sympathetic denervation, and implantable cardioverter-defibrillators. The use of atrioventricular nodal ablation as a treatment strategy to prevent ventricular arrhythmias in catecholaminergic polymorphic ventricular tachycardia was not found in the literature. This report describes a teenager with a presenting rhythm of atrial and ventricular fibrillation and cardiac arrest. Her clinical arrhythmia was predominantly atrial dysrhythmias, which delayed her diagnosis of catecholaminergic polymorphic ventricular tachycardia. Before her diagnosis, she underwent atrioventricular nodal ablation in an effort to prevent ventricular arrhythmias, which was ultimately ineffective. This report highlights the importance of recognizing atrial arrhythmias in catecholaminergic polymorphic ventricular tachycardia and provides evidence that atrioventricular nodal ablation is not an effective treatment strategy for this disease.

Robotic totally endoscopic mitral valve surgery with moderate hypothermic ventricular fibrillatory arrest

Robotic totally endoscopic mitral valve surgery with moderate hypothermic ventricular fibrillatory arrest

High-Dose Levetiracetam: A Novel Post-Arrest Anti-Arrhythmic Medication? (P8-7.005)

<h3>Objective:</h3> To describe a case of post-cardiac arrest refractory myoclonus and ventricular tachycardia responsive to high-dose levetiracetam. <h3>Background:</h3> Levetiracetam is a first-line agent for anoxic myoclonus. However, levetiracetam is not known to have anti-arrhythmia properties, particularly in persistent arrhythmias following cardiac arrest. <h3>Design/Methods: Case Description:</h3> A 17-month-old female presented in ventricular fibrillation arrest thought to be secondary to methamphetamine toxicity and a mitochondrial genetic mutation (discovered and confirmed later in her hospitalization). Return of spontaneous circulation was achieved after prolonged resuscitation. Seven days later, she demonstrated frequent (&gt;40/minute), large-amplitude, non-stereotyped, brief movements involing the neck and all extremities consistent with myoclonus. Elecetroencephalogram (EEG) determined movements to be non-epileptic. Magnetic resonance imaging (MRI) on day 8 post-arrest was without evidence of diffusion restriction or T2-flair abnormalities and was thought to represent pseudonormalization in setting of hypoxic injury. Her movements were refractory to: ketamine, morphine, midazolam, dexmedetomidine, and cisatracurium. She developed frequent ectopy and intermittent ventricular tachycardia refractory to esmolol, sotalol, and lidocaine. After receiving 60 milligrams/kilogram (mg/kg) of intravenous levetiracetam, both the myoclonus and arrhythmia temporarily normalized, but returned on maintenance dosing of 30 mg/kg twice a day (BID). After increasing the maintenance dosing to 50 mg/kg BID, her myoclonus and arrhythmia both improved again with sustained benefit with higher dosing. <h3>Results:</h3> NA <h3>Conclusions:</h3> A sustained improvement in post-cardiac arrest refractory myoclonus and tachyarrhythmia was achieved with high-dose levetiracetam. Peripheral overactive N-type calcium currents from sympathetic hyperactivation have been implicated in ventricular arrhythmogenesis. Hypoxic injury to the brainstem could cause a brainstem reticular reflex myoclonus as well as damage to the autonomic relay nuclei. Temporal lobe injury could cause subcortical myoclonus as well as increased sympathetic outflow. Levetiracetam’s blockade of calcium currents at any of these sites could be an explanation for its beneficial effect on both myoclonus and tachyarrhythmia in this patient. <b>Disclosure:</b> Dr. Stulberg has nothing to disclose. Dr. O’Connor has nothing to disclose. Dr. Swartwood has nothing to disclose.

A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts

Ventricular fibrillation (VF) is a fatal arrhythmia with a high incidence in cardiac patients, but VF arrest under perfusion is a neglected method of intraoperative arrest in the field of cardiac surgery. With recent advances in cardiac surgery, the demand for prolonged VF studies under perfusion has increased. However, the field lacks simple, reliable, and reproducible animal models of chronic ventricular fibrillation. This protocol induces long-term VF through alternating current (AC) electrical stimulation of the epicardium. Different conditions were used to induce VF, including continuous stimulation with a low or high voltage to induce long-term VF and stimulation for 5 min with a low or high voltage to induce spontaneous long-term VF. The success rates of the different conditions, as well as the rates of myocardial injury and recovery of cardiac function, were compared. The results showed that continuous low-voltage stimulation induced long-term VF and that 5 min of low-voltage stimulation induced spontaneous long-term VF with mild myocardial injury and a high rate of recovery of cardiac function. However, the low-voltage, continuously stimulated long-term VF model had a higher success rate. High-voltage stimulation provided a higher rate of VF induction but showed a low defibrillation success rate, poor recovery of cardiac function, and severe myocardial injury. On the basis of these results, continuous low-voltage epicardial AC stimulation is recommended for its high success rate, stability, reliability, reproducibility, low impact on cardiac function, and mild myocardial injury.

Old Meets New: Cold Ventricular Fibrillatory Arrest and Robotic Cardiac Surgery

Old Meets New: Cold Ventricular Fibrillatory Arrest and Robotic Cardiac Surgery

Abnormal kinetics of contraction caused by an α-actinin 2 missense variant in the EF-3-4 hand domain in human myocardium.

ACTN2 gene encodes α-actinin 2 protein, which binds actin. In cardiac muscle, α-actinin 2 is located in the Z-disc of the sarcomere, where it anchors myofibrillar actin filaments. A 48-years old female presented with out-of-hospital ventricular fibrillation arrest. Echocardiogram showed stage II diastolic dysfunction, elevated RVSP, and abnormal global longitudinal strain consistent with early LV systolic dysfunction. Cardiopulmonary testing indicated AHA functional class IV HF. Genetic testing identified a missense heterozygous variant of unknown significance in ACTN2 (gene previously associated with HCM and DCM), and SCNB2 (β-2 subunit of type II voltage-gated sodium channel). Histopathology demonstrated mild interstitial fibrosis of the LV free wall. We investigated the effects of the heterozygous A868T variant in α-actinin 2 on cardiac muscle mechanics. LV free wall samples were obtained from the patient's explanted heart at the time of cardiac transplantation. Permeabilized cardiac muscle preparations (CMPs) containing A868T and WT proteins displayed increased myofilament Ca2+-sensitivity of isometric force and lower maximal isometric specific force when compared to human donor samples. Sinusoidal stiffness was decreased at all levels of Ca2+-activation in A8686T CMPs. The rate of tension redevelopment (kTR) was faster at all levels of Ca2+-activation in A8686T CMPs. Computational modeling suggests that faster kTR in A868T CMPs is mainly due to faster cross-bridge detachment (g). The kinetic changes are consistent with decreased force generation by A868T CMPs being due to abnormalities in the cross-bridge interaction. Molecular dynamics simulation did not find significant differences in the interaction of A868T variant with titin and α-actinin. This project establishes the importance of α-actinin 2 variant in the Z-disc mechanosensitive interaction of thin- and thick-filament distal from its structural role in the sarcomere.

Successful percutaneous coronary intervention with extracorporeal membrane oxygenation in a patient with acute inferior wall myocardial infarction complicated by electrical storm, cardiogenic shock, and cardiac arrest: a case report

BackgroundHigh-risk patients with coronary heart disease who develop acute myocardial infarction (AMI) have severe coronary lesions. If severe complications occur, such as malignant ventricular arrhythmia, cardiogenic shock, and cardiac arrest, implementation of emergency percutaneous coronary intervention (PCI) may be hindered, leading to a higher perioperative mortality rate. Extracorporeal membrane oxygenation (ECMO) can pave the way for rapid myocardial reperfusion therapy. When cardiac arrest occurs, hemodynamic support with ECMO can facilitate revascularization with PCI, which can increase the time available for further salvage and treatment and reduce intraoperative risk during PCI.Case presentationHerein, we report a case of a 61-year-old man with AMI who suffered electrical storm of sustained malignant ventricular fibrillation, cardiogenic shock, and cardiac arrest and was successfully treated with PCI with ECMO support. During PCI, repeated aspiration and removal of the right coronary artery thrombus were performed, and blood flow was restored after right coronary artery balloon dilation. One episode of defibrillation was delivered to restore sinus rhythm. Then, stents were implanted in the distal and proximal right coronary artery lesions to achieve revascularization. After PCI with ECMO support, irreversible malignant arrhythmia returned to sinus rhythm through coronary perfusion, which prevented death following unsuccessful cardiopulmonary resuscitation. After applying active treatments, including anti-shock, mechanical ventilation, anti-inflammation, and organ support, the patient was discharged after his condition and vital signs stabilized. The patient was followed up once a week after hospital discharge, and his cardiopulmonary function recovered well.ConclusionsWith ECMO support, PCI should be performed immediately in patients with inferior wall AMI complicated by electrical storm of sustained ventricular fibrillation, cardiogenic shock, and cardiac arrest to facilitate stent placement, achieve complete revascularization, restore coronary perfusion, and avoid death

Ventricular Fibrillatory Arrest: A Safe Option in Robotic Totally Endoscopic Intracardiac Surgery

BackgroundModerate hypothermic ventricular fibrillatory arrest during heart surgery is an alternative to cardioplegic arrest in selected patients. We reviewed our experience using a ventricular fibrillatory arrest technique in robotic totally endoscopic intracardiac surgery. MethodsFrom February 2014 through July 2022, 128 patients who underwent robotic totally endoscopic intracardiac surgical procedures performed using moderate hypothermic ventricular fibrillatory arrest were reviewed. Patients were chosen based on the risk of aortic manipulation, complexity of the procedure, grade of aortic valve insufficiency and comorbidities, including history of prior cardiac surgery and peripheral vascular disease. ResultsPatients were a mean age of 65 ± 14 years, and the mean The Society of Thoracic Surgeons score was 2.7 ± 2.9. Fourteen patients (11%) had a history of previous cardiac surgery. The intracardiac procedures were mitral valve surgery in 84 patients (66%), isolated cryomaze procedure in 27 (21%), and other in 17 (13%). The mean ventricular fibrillatory arrest time was 79 ± 26 minutes, and the mean cardiopulmonary bypass time was 174 ± 49 minutes. There was no conversion to sternotomy. Seven patients (5.5%) required inotropic support, and 2 patients (1.6%) needed an intra-aortic balloon pump. There was no incidence of postoperative stroke or clinical myocardial infarction. The mean hospital and intensive care unit lengths of stay were 3.1 ± 1.7 and 1.4 ± 0.7 days, respectively. One death (0.78%) occurred due to respiratory failure. ConclusionsModerate hypothermic ventricular fibrillatory arrest in robotic intracardiac surgery may be a safe and effective alternative in selected patients.

The Heart as a Target of Vasopressin and Other Cardiovascular Peptides in Health and Cardiovascular Diseases.

The automatism of cardiac pacemaker cells, which is tuned, is regulated by the autonomic nervous system (ANS) and multiple endocrine and paracrine factors, including cardiovascular peptides. The cardiovascular peptides (CPs) form a group of essential paracrine factors affecting the function of the heart and vessels. They may also be produced in other organs and penetrate to the heart via systemic circulation. The present review draws attention to the role of vasopressin (AVP) and some other cardiovascular peptides (angiotensins, oxytocin, cytokines) in the regulation of the cardiovascular system in health and cardiovascular diseases, especially in post-infarct heart failure, hypertension and cerebrovascular strokes. Vasopressin is synthesized mostly by the neuroendocrine cells of the hypothalamus. There is also evidence that it may be produced in the heart and lungs. The secretion of AVP and other CPs is markedly influenced by changes in blood volume and pressure, as well as by other disturbances, frequently occurring in cardiovascular diseases (hypoxia, pain, stress, inflammation). Myocardial infarction, hypertension and cardiovascular shock are associated with an increased secretion of AVP and altered responsiveness of the cardiovascular system to its action. The majority of experimental studies show that the administration of vasopressin during ventricular fibrillation and cardiac arrest improves resuscitation, however, the clinical studies do not present consisting results. Vasopressin cooperates with the autonomic nervous system (ANS), angiotensins, oxytocin and cytokines in the regulation of the cardiovascular system and its interaction with these regulators is altered during heart failure and hypertension. It is likely that the differences in interactions of AVP with ANS and other CPs have a significant impact on the responsiveness of the cardiovascular system to vasopressin in specific cardiovascular disorders.

Abstract 11589: Total Artificial Heart Placement in a Case of Recurrent Ventricular Tachycardia Storm

Background: Electrical storm is defined as three or more episodes of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) within a 24-hour period requiring termination by cardioversion, anti-tachycardia pacing (ATP) or defibrillation. It can be a particularly challenging syndrome to treat when refractory to standard of care therapies, which include antiarrhythmics, sedation, and ablation. We present a case of refractory electrical storm requiring total artificial heart placement (TAH) as a bridge to transplant. Case: A 65-year-old male with a history of idiopathic non-ischemic cardiomyopathy presented with VF arrest. After return of spontaneous circulation, he was admitted to the cardiac intensive care unit. Implantable cardioverter defibrillator (ICD) interrogation showed 38 shocks delivered over the prior two-week period. Coronary angiography showed no obstructive coronary disease and an intraaortic balloon pump (IABP) was placed for cardiogenic shock. He was intubated and sedated on fentanyl and propofol. He continued to have episodes of VT despite treatment with lidocaine, procainamide, and amiodarone drips. Further trials of paralysis and left stellate ganglion nerve block did not suppress his VT. Since the patient was refractory to all prior interventions, was deemed too unstable for VT ablation, and had a prolonged anticipated wait time for heart transplant, he underwent TAH placement as a bridge to heart transplant. He recovered well and eventually underwent successful heart transplant. Discussion: Management of electrical storm requires a stepwise approach including administration of antiarrhythmics, sedation, mechanical hemodynamic support, and catheter ablation. Our patient had incessant VT despite exhaustive medical and supportive therapies, but was too unstable to undergo VT ablation. In cases of refractory VT storm, definitive treatment with heart transplantation must be considered, but bridging patients to transplant poses a challenge. Our patient underwent TAH placement and was successfully stabilized prior to transplant. In centers with this capability, TAH should be recognized as a legitimate option in the pathway for VT, particularly with a long anticipated wait time for heart transplant.

Abstract 11307: Longer Outflow Tract Conduction Time by Magnetocardiography as a Novel Non-Invasive Maker for Predicting Lethal Events in Patients With Brugada Syndrome Without Ventricular Fibrillation

Introduction: Many of the Brugada syndrome (BrS) patients have no symptom or only syncope without ventricular fibrillation (VF)/sudden cardiac death (SCD), thus to whom we should recommend implantable cardioverter defibrillator (ICD) for primary prevention of SCD is still the biggest concern in the BrS. Here we investigated whether a high spatial resolution magnetocardiography (MCG) could predict lethal events of the BrS without history of VF/SCD. Methods: This study retrospectively enrolled 157 BrS patients without VF or cardiopulmonary arrest (CPA) (150 male, 42±13 years old, 118 spontaneous and 39 drug-induced type-1 ECG). Outflow tract conduction time (OT-CT) from 2-D current map of MCG was measured in all patients as well as the standard 12-lead ECG and signal-averaged ECG (SAECG). Programmed electrical stimulation (PES) for VF induction was performed in 47 patients. Results: Patients with spontaneous type-1 ECG had longer OT-CT compared with type-2 BrS patients. Na channel blocker, pilsicainide (25-50mg) unmasked type-1 ECG as well as increased OT-CT (54±18 to 127±62 ms; p&lt;0.05), whereas additional isoproterenol (1ug/kg/min) reversed the pilsicainide-induced delayed OT-CT, thus normalized the ST elevation of ECG. During follow-up (mean 72 [6-147] months), 10 (6%) patients suffered VF/CPA, and those had a higher incidence of previous syncope (50% vs. 14.4%, p=0.01) and longer baseline OT-CT (83±31ms vs. 55±24ms, p=0.01) compared with event-free patients. Receiver operating curve (ROC) revealed OT-CT=65ms was a cut-off value of VF/CPA (AUC=0.78), whereas, spontaneous type-1 ECG, late potential of SAECG, family history, and VF inducibility by PES were not associated with VF/CPA events during follow-up. Multivariate Cox proportional analysis revealed that previous syncope (HR=1.70, 95%CI:1.01-3.05, p=0.04) and OT-CT≥65ms (HR=1.72, 95%CI=1.16-2.62) were the independent predictor for lethal events in the BrS without VF/CPA. Among asymptomatic BrS patients (n=131), OT-CT≥65ms was also an independent predictor for VF/CPA (HR=1.69, 95%CI=1.04-2.79, p=0.03). Conclusion: Longer OT-CT in the MCG may noninvasively demonstrate substrate of VF in BrS and stratify the risk of lethal events in patients with BrS without history of VF or CPA.

Abstract 15244: Rapid Recognition and Implementation of Mechanical Circulatory Support in Rare Fulminant Lymphocytic Myocarditis

Case Presentation: A 65 year-old woman with heart failure, nonischemic cardiomyopathy, atrial fibrillation, hypertension, prior stroke presented with chest pain and shortness of breath for three days. She was ill-appearing, hypotensive and tachypneic, with troponins reaching greater than 125,000 ng/L. Initial ECG demonstrated sinus rhythm with inferior ST elevations and lateral T wave inversions, however emergent catheterization revealed angiographically normal coronary arteries. Repeat 2D echocardiography showed sharp decline to ejection fraction (EF) 5-10%. Patient subsequently developed cardiogenic shock and despite inotropes, vasopressors and intra-aortic balloon pump, she suffered ventricular fibrillation arrest requiring defibrillation. This prompted escalation with emergent veno-arterial extracorporeal membrane oxygenation. Endomyocardial biopsy findings taken at that time were consistent with lymphocytic myocarditis with negative viral panel. Her hospital course was also complicated by acute renal injury, respiratory failure requiring intubation, metabolic acidosis and shock liver. With treatment with high dose steroids and mechanical circulatory support, the patient's severely diminished EF improved to 20% and she is undergoing placement of a left ventricular assist device. Discussion: Fulminant lymphocytic myocarditis is a rare disease that has clinically and pathologically distinct features from subacute or acute lymphocytic myocarditis particularly in its timeline of onset and features of hemodynamic compromise. It most frequently affects young and pediatric individuals and can result in significant mortality and morbidity. This case with an older patient with severe fulminant lymphocytic myocarditis confirmed on biopsy highlights: 1) the importance of early recognition affecting survival outcome, 2) golden standard for diagnosis with endomyocardial biopsy and immunohistochemical analysis for subtype-specific evidence-based treatment, and 3) integrated medical and surgical management, including mechanical circulatory support as an essential life-saving tool.

S2431 A Rare Case of Esophageal Kaposi Sarcoma Causing Dysphagia

Introduction: Kaposi sarcoma (KS) is an angioproliferative disorder(low grade vascular tumor) caused by human herpesvirus-8 in immunocompromised patients. The disease is multifocal, ranging from indolent skin manifestations to extensive visceral involvement. We are describing a rare case of esophageal KS causing dysphagia. Case Description/Methods: A 57-year-old bisexual male with a medical history of hypertension, syphilis and recent diagnosis of HIV (untreated) admitted for hypotension, tachycardia, nausea, vomiting,hemoptysis and dysphagia to soilds. He was noted to have oropharyngeal lesions and biopsy of the lesions were obtained. An EGD performed for evaluation of dysphagia (denied odynophagia) showed circumferential erythema, purplish plaques and friability of the esophagus. Biopsies were obtained from esophagus. Pathology from tongue, gingiva, proximal and distal esophagus returned positive for Kaposi sarcoma with positive staining for HHV-8 and CD31. CD4 count was 31/uL and HSV8 PCR showed 1,000,000 copies. Patient was treated with Bictegravir, emtricitabine and tenofovir alafenamide. Hematology was consulted for potential pulmonary KS and patient was started on liposomal doxorubicin. He developed Ventricular fibrillation and cardiac arrest. He was revived and intubated. Patient improved initially but developed neutropenic fever. Infectious disease treated him with empirical antibiotics and antivirals. Patient further developed Castleman’s disease, respiratory failure, acute kidney failure requiring CRRT, and altered mental status. Despite aggressive measures patient did not survive (Figure). Discussion: AIDS-related KS varies in clinical progression and occurs in 20% of patients with AIDS. The CD4 count will typically be less than 150 cells per cubic millimeter with a high viral load ranging from greater than 10,000 copies per millimeter. Gastrointestinal manifestation is the most common extra-cutaneous site of KS in AIDS-related cases though rarely does it occur without cutaneous involvement. The majority of the patients are asymptomatic, roughly 75%. Symptomatic patients present with nonspecific findings such as abdominal discomfort, cramps, nausea, vomiting, diarrhea, and upper or lower GI bleed. KS lesions causing dysphagia are extremely rare. The mainstay of therapy is combined antiretroviral therapy (ART). Local intralesional chemotherapy can be utilized to manage limited lesions. Systemic therapy with liposomal anthracyclines is recommended for patients with advanced or rapidly progressive disease.Figure 1.: Kaposi Sarcoma Lesions.