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

Venovenous extracorporeal membrane oxygenation and late ductal stenting for infant with transposition of the great arteries, pulmonary stenosis and SARS, -CoV-2 pneumonia

Introduction: The SARS-CoV-2 pandemic has affected medical decision-making in all practice areas, including the pediatric cardiac intensive care unit (CICU), sometimes necessitating the use of innovative management strategies. Venovenous extracorporeal membrane oxygenation (VV-ECMO) and, particularly, late ductal stenting are infrequently applied interventions in the CICU. Here we present a critically ill infant with d-transposition of the great arteries (d-TGA), ventricular septal defect (VSD), pulmonary stenosis (PS), and patent ductus arteriosus (PDA), in which VV-ECMO and late ductal stenting were utilized successfully in the setting of active SARS-CoV-2 infection to treat worsening PS and pulmonary venous desaturation, thereby delaying surgical intervention and its associated risks during active infection. Case Description: A 3 month old male with d-TGA, VSD, and PS, initially managed with a balloon atrial septostomy at birth, was admitted to the CICU after presenting with respiratory distress and hypoxemia. He was found to be SARS-CoV-2 positive, requiring only nasal cannula initially. Admission echocardiogram demonstrated known d-TGA, VSD, severe pulmonary stenosis (peak gradient 95-110mmHg), unrestrictive atrial communication, and preserved systolic function. A tiny, hemodynamically insignificant PDA was also noted. While admitted, the patient exhibited intermittent, severe desaturations requiring escalating respiratory support. He was started on a prostaglandin infusion with aim to promote additional pulmonary blood flow through the PDA, thereby limiting the severity and frequency of desaturations. However, the patient ultimately became severely hypoxemic, despite multiple interventions to improve oxygenation. Echocardiogram at this time demonstrated preserved ventricular function, so the decision was made to escalate to VVECMO therapy. Following ECMO cannulation, the patient's hypoxemia quickly resolved, and he remained hemodynamically stable. Given the persistence of his PDA and the desire to avoid the risks of cardiac surgery in the setting of acute COVID infection, percutaneous intervention to augment pulmonary blood flow was attempted. Despite its diminutive size, his PDA was able to be successfully cannulated and stented the day after ECMO initiation. He was able to be quickly weaned from ECMO support and was decannulated the following day. He was subsequently extubated and ultimately discharged home with planning for definitive surgical intervention underway. Discussion(s): Here we present an interesting case of an infant with d-TGA, VSD, PS, and PDA in which VV-ECMO and PDA stenting were successfully applied to treat acute hypoxemia in the setting of SARS-CoV-2 infection and severe pulmonary stenosis. These therapies may be considered in appropriate patients for whom the risks of cardiac surgery are significant.

Pulmonary artery resection and reconstruction in locally advanced lung cancer with moderate hemoptysis

Lobectomy with pulmonary artery (PA) angioplasty in locally advanced lung cancer is an alternative to pneumonectomy. It is feasible, oncologically effective and the procedure of choice in patients with recurrent hemoptysis and limited pulmonary reserves. We present a case of a successful left upper lobectomy with PA resection and reconstruction by an autologous pericardial patch.Copyright © 2022 EDIZIONI MINERVA MEDICA.

Left atrial thrombus exclusion before atrial fibrillation ablation: Reconsidering the role of cardiac computed tomography

Objectives: Considering the risk of aerosolization during the COVID-19 pandemic associated with transesophageal echocardiography (TEE), we evaluated the diagnostic performance of cardiac computed tomography (CCT) before pulmonary vein isolation (PVI) in comparison to semi-invasive TEE in excluding left atrial (LA)/LA appendage (LAA) thrombus, limiting the need for TEE to only patients with possible thrombus on CCT. Material(s) and Method(s): We included a total of 145 consecutive patients with atrial fibrillation (AF) (age 52.4 +/- 10.3 years;63% males;89 paroxysmal AF) referred for radiofrequency ablation in National Cardiovascular Center Harapan Kita, Jakarta, Indonesia. All patients underwent preprocedural single-phase 128-slice multidetector CT and subsequent TEE as the reference standard with a mean time interval of 6.5 +/- 5.3 days between the two procedures. Result(s): CCT identified 30 patients (20.7%) with a filling defect in the LA/LAA, 8 of which were confirmed by TEE as thrombi (22 false positives and 8 true positives), whereas 9 true thrombi (6.2%) were detected by TEE (1 false negative by CCT). The sensitivity and specificity of CCT were 88.9% and 83.8%, respectively, with a positive predictive value of 26.8% and a negative predictive value of 99.1%. The overall accuracy was 84.1%. Conclusion(s): Apart from being a planned preparation modality before PVI, CCT is sufficient and could be used as an initial step to exclude the presence of LA/LAA thrombus, limiting the invasive TEE only for confirmation of the thrombus if detected by CCT.

Radiofrequency ablation of incessant atrial tachycardia after COVID-19 infection

Objectives: We present a case of a 38-year-old male with no known comorbidities who presented with incessant focal atrial tachycardia complicated by tachycardia-mediated cardiomyopathy and COVID-19 infection. He successfully underwent 3D Cardiac Mapping + radiofrequency ablation of the right superior pulmonary vein. Material(s) and Method(s): Results: A 38-year-old male presented with persistent palpitations and tachycardia associated with heart failure symptoms. On work up, 12 L-ECG showed sustained focal atrial tachycardia with heart rate (HR) ranges 170-190 bpm with positive p-wave axis in lead I, II, III, AVF and upright in lead V1. He was initially started on HR-lowering medications and given electrical synchronized cardioversion which were both unsuccessful. A week later, patient developed COVID-19 pneumonia and subsequently completed isolation as per local government protocol. During the course of admission, a POCUS echocardiogram was done which showed a newly depressed left ventricular ejection fraction (EF) of 22% compared to a previous 44% two weeks earlier. Hence, patient eventually underwent successful 3D-mapping and radiofrequency ablation of the right super pulmonary vein via transseptal approach. He was then successfully discharged with Metoprolol 200 mg twice daily alongside with other heart failure medications. Conclusion(s): Development of COVID-19 infection can run the risk of worsening and clinical decompensation among patients with incessant tachyarrhythmia and there are still no established data regarding the safety of doing radiofrequency ablation post-COVID-19 infection. This case report illustrates doing a successful radiofrequency frequency ablation post-COVID-19 infection in a patient who developed incessant atrial tachycardia.

Efficacy and Safety of Pulsed Field Ablation in Atrial Fibrillation: A Systematic Review.

BACKGROUND: Atrial fibrillation (AF) is the most common cardiac arrhythmia associated with high morbidity and mortality. AF treatment is guided by a patient-provider risk-benefit discussion regarding drug versus ablation or combination. Thermal ablation has a high rate of adverse events compared to pulsed field ablation (PFA). In this systematic review, we aimed to determine the safety and efficacy of PFA. METHODS: The electronic search for relevant articles in English was completed in PubMed, PubMed Central, Cochrane library, Scopus, and Embase databases till July 2022. The screening was completed via the use of Covidence software. The risk of bias assessment and data extraction from the included studies was performed, and the narrative synthesis was performed accordingly. RESULTS: A total of six studies were selected for review and 1897 patients receiving PFA were involved in these studies. Our review was focused on pulmonary vein isolation success, major adverse events, and arrhythmia recurrence. Successful pulmonary vein isolation (PVI) was completed in 100% of cases except in two studies. In one of them, six out of seven patients (86%) in the epicardial cohort had successful PVI. In the MANIFEST-PF survey, the acute PVI success rate was 99.9%. The major complications were rare and included pericardial tamponade, vascular complications requiring surgery, and stroke. The atrial arrhythmia recurrence was higher in the thermal group than in the PFA group (39% vs. 11%). CONCLUSIONS: The success rate of PVI by PFA is high, and major adverse events are low. PFA is found to decrease the recurrence of atrial arrhythmia compared to thermal ablation. Substantial randomized controlled trials (RCTs) are needed to validate the efficacy and safety of PFA over conventional methods.

Pulmonary Vein Thrombosis in the Setting of COVID-19 Infection: A Case Report.

The novel coronavirus SARS-CoV-2 (COVID-19) affects all three branches of Virchow's triad. It increases the risk of thrombosis and thromboembolic events. Pulmonary embolism and stroke are most commonly reported. However, there is an increasing number of cases demonstrating thrombosis in otherwise uncommon anatomical areas. In this presentation, we will explore the potential causes of pulmonary vein thrombosis secondary to COVID-19.

A RARE CASE OF HISTOPLASMA CAUSING OBLITERATION OF THE SUPERIOR VENA CAVA AND SUBSEQUENT DEVELOPMENT OF COLLATERAL CIRCULATION

SESSION TITLE: Critical Cardiovascular Disorders SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: Physicians are educated on the traditional pathways of sanguineous return of the head and neck through the superior vena cava (SVC). There are known causes of disruption of this system such as SVC syndrome and malignancy causing compression, delayed transit or invasion of these vessels. While compensatory angiogenesis is not a new concept, it has been primarily documented in cases involving coronary artery circulation or congenital heart defects. Here, we present a rare case of the development of left-sided collateral flow in lieu of a right sided SVC with connection to the IVC as a complication of histoplasma infection. CASE PRESENTATION: Our patient was a 67-year female with a past medical history of histoplasmosis, asthma and diabetes who presented with a chief complaint of shortness of breath. Shortly following admission, she was diagnosed with COVID19. In the course of her diagnostic evaluation, she was noted to have significant abnormalities of her thoracic vasculature. More specifically, she had developed calcified granulomas that included a large old calcified granuloma of her right hilum that caused a complete obliteration of her SVC and right middle lobe airways. Her right middle lobe airways had evidence of chronic scarring with development of left sided collateral circulation. Her collateral flow went through her innominate vein into her azygos system and from there into her inferior vena cava and back to her heart. DISCUSSION: It is well established in the literature that histoplasma can lead to scarring and granulomatous changes within lung parenchyma. Our case is unique in the location where the patient developed a granuloma. The close proximity to the SVC over time led to the complete obliteration of the vessel and as a compensatory mechanism her body developed collateral circulation to the left side via her azygous vein and IVC. While we were unable to find similar cases in the literature specifically caused by histoplasma, other phenomena have led to the development of collateral circulation within the lungs. Specifically, Genta et. al. published a case report of an acute pulmonary vein occlusion leading to the development of collateral circulation through the patients' bronchial veins and into the azygous & hemiazygos system similar to our patient. One of the clinical implications for this patient during her hospitalization was the severity of her illness with COVID19. She did require treatment in the intensive care unit. This prompted a discussion among the treatment team regarding developing a plan of action for central line placement should this patient have required vasopressor support. CONCLUSIONS: This case stresses the importance of understanding primary anatomy in order to comprehend potential variants and predict future consequences for patients. It also highlights how sequela of chronic conditions can impact treatment plans. Reference #1: Yu CH, Chen MR. Clinical investigation of systemic-pulmonary collateral arteries. Pediatr Cardiol. 2008 Mar;29(2):334-8. doi: 10.1007/s00246-007-9086-y. Epub 2007 Sep 18. PMID: 17876652. Reference #2: Schaper W. Development of the collateral circulation: History of an idea. Exp Clin Cardiol. 2002 Fall;7(2-3):60-3. PMID: 19649224;PMCID: PMC2719163. Reference #3: Genta PR, Ho N, Beyruti R, Takagaki TY, Terra-Filho M. Pulmonary vein thrombosis after bilobectomy and development of collateral circulation. Thorax. 2003 Jun;58(6):550-1. doi: 10.1136/thorax.58.6.550. PMID: 12775876;PMCID: PMC1746717. DISCLOSURES: No relevant relationships by Alessandra Carrillo No relevant relationships by Chetachi Odelugo No relevant relationships by Shil Punatar No relevant relationships by Ravi Sundaram

MANIFESTATIONS OF SCIMITAR SYNDROME IN AN ADULT

SESSION TITLE: Anatomical Cardiovascular Disease Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Scimitar Syndrome is a rare congenital disorder characterized by partial or complete anomalous pulmonary venous drainage to the inferior vena cava, right lung hypoplasia and displacement of the cardiac structures into the right hemi-thorax (1) The name Scimitar Syndrome is derived from the resemblance of the anomalous pulmonary vein to a curved Middle Eastern sword known as a scimitar (1). Some patients experience no symptoms while others may have severe pulmonary hypertension and dyspnea (2) (3). Cases may be discovered in infancy although some patients are not diagnosed until early adulthood. Here we present a case of a woman who was discovered to have symptomatic scimitar syndrome in her teenage years and opted to forego correction. CASE PRESENTATION: Patient was a 38 year old female with past medical history of Scimitar Syndrome who presented to the pulmonary clinic after a short hospitalization with mild COVID-19. Prior to contracting COVID-19 she had experienced worsening dyspnea over one year and now becomes short of breath after walking one half block. Open surgical correction was offered at diagnosis but was not pursued due to patient preference. A CT Angiogram of the chest was performed while she was hospitalized which showed an anomalous right pulmonary vein draining to the hepatic IVC, minimal bilateral patchy opacities and displacement of the heart into the right hemi-thorax. Echocardiography showed normal right ventricular size and function and did not show evidence of pulmonary hypertension. She was referred to the adult congenital heart disease clinic and continued to have severe dyspnea and fatigue. 6 months later, repeat echocardiography and cardiac MRI demonstrated borderline dilation of the right ventricle and atrium but no echocardiographic evidence of pulmonary hypertension. The patient remains hesitant to undergo invasive procedures or interventions. She has been offered a right heart catheterization to better characterize her volume status and obtain direct measurement of her pulmonary artery pressures. DISCUSSION: Although generally discovered in infancy and childhood, Scimitar syndrome may not be discovered until adulthood. Various treatments are available for correction of scimitar syndrome including open surgical approaches with direct implantation of the scimitar vein into the left atrium, trans-catheter occlusion of aorto-pulmonary collaterals and re-routing of the anomalous vein into the left atrium via endoscopic graft placement (4) (6) (7) (8). If left uncorrected worsening left to right shunting and pulmonary hypertension may occur (5). Our patient has developed borderline right ventricular dilation and has experienced severe functional limitation. A right heart catheterization is indicated to determine her pulmonary artery pressures. This case illustrates the potential consequences of deferring early treatment for Scimitar Syndrome CONCLUSIONS:. Reference #1: Frydrychowicz A, Landgraf B, Wieben O, François CJ. Images in Cardiovascular Medicine. Scimitar syndrome: added value by isotropic flow-sensitive four-dimensional magnetic resonance imaging with PC-VIPR (phase-contrast vastly undersampled isotropic projection reconstruction). Circulation. 2010 Jun 15;121(23):e434-6. doi: 10.1161/CIRCULATIONAHA.109.931857. PMID: 20547935 Reference #2: Abdullah A. Alghamdi, Mansour Al-Mutairi, Fahad Alhabshan, Scimitar syndrome: restoration of native pulmonary venous connection, European Heart Journal Supplements, Volume 16, Issue suppl_B, November 2014, Pages B41–B43, https://doi.org/10.1093/eurheartj/suu025 Reference #3: Khan A, Ring NJ, Hughes PD. Scimitar syndrome (congenital pulmonary venolobar syndrome). Postgrad Med J. 2005 Apr;81(954):216. doi: 10.1136/pgmj.2004.027813. PMID: 15811882;PMCID: PMC1743239 DISCLOSURES: No relevant relationships by John Prudenti No relevant relationships by Anthony Smith

HEPATO-PULMONARY SYNDROME: LOOK CLOSELY OR YOU MIGHT MISS IT

CASE: A Hispanic-speaking 63-year-old lady presented with left shoulder pain and dyspnea since two weeks. Past history was significant for cirrhosis due to autoimmune hepatitis and portal hypertension diagnosed 1.5 years prior. Upon further questioning, she revealed that she had exertional dyspnea for 2 years, which got progressively worse after her COVID-19 infection, 14 months prior. On initial exam, her hemoglobin levels were unchanged with previous. Troponin and BNP levels were unremarkable. CT Pulmonary Embolus scan and shoulder X-ray were negative. However, her SpO2 which was 90% on lying flat, fell to 84% on walking and she was admitted for further workup. On exam, she had a loud S2, spider angioma, and clubbing. ABG showed an alveolar-arterial oxygen gradient of 54.7 mm and PO2 of 61.7 mm. A contrastenhanced transthoracic echo with saline showed significant shunting with dilated pulmonary veins. Upon close inspection, she had a small right to left intracardiac shunt through an incidental PFO and a rather large intrapulmonary shunt. This was confirmed on trans-esophageal echo. Right heart catheterization showed a high cardiac index (5.3 L/min) suggestive of a high-output state, as typically seen with cirrhosis. It also revealed increased right-sided oxygen saturations, confirming the presence of a significant left to right shunt. Finally, pulmonary CT angiography was negative for AVMs. These findings were congruent with hepato-pulmonary syndrome (HPS) and based on her presenting symptoms she was referred to hepatology for consideration of liver transplantation. IMPACT/DISCUSSION: HPS is characterized by abnormal oxygenation due to intrapulmonary vascular dilations (IPVD) in the setting of advanced liver disease. Diagnosis needs an elevated A-a gradient (≥ 15mm or ≥ 20 mm if >64 years). IPVDs may not be seen on CT scans and are optimally detected on CE-TTE. The delayed appearance of injected microbubbles in the left heart, 3 or more cardiac cycles after visualization in the right heart signifies abnormally dilated pulmonary capillaries which don't trap the bubbles. TTE can help differentiate intracardiac and intrapulmonary shunts, by revealing the source of the microbubbles entering into the left atrium (across the atrial septum vs pulmonary veins). Shunting classically causes platypnea-orthodexia (worsening dyspnea on standing or sitting, alleviated by lying down). Alterations in lung parenchyma due to COVID-19 could have increased the flow through intrapulmonary AVMs and contributed to the worsening of symptoms. Management of HPS is supportive. Liver transplantation improves survival. CONCLUSION: Evaluation and management of HPS involves multiple modalities of testing and specialists in gastroenterology, cardiac imaging, interventional cardiology, interventional radiology, and transplant surgery. The diagnosis of HPS should escalate referral to a liver transplant center. Engaging medical interpreters can help elicit more detailed history and improve clinical outcomes.

Soluble Signals to Improve Endothelial Integrity in the Lung

Disorders in pulmonary vascular integrity are a prominent feature in many lung diseases, including acute respiratory distress syndrome (ARDS), capillary leak syndrome, and COVID19. Paracrine signals are enriched in the lung and are critically important in regulating the homeostasis of the functional pulmonary microvasculature. Here, we employed single-cell RNA-sequencing (scRNAseq) to study ligand and receptor interactions in the native human lung microvascular niche, and identified soluble factors that are critical in endothelial integrity. The scRNAseq data reveals a total of 47 cell populations consisting of five vascular endothelial subtypes in human lungs, including general capillary EC, aerocyte capillary EC (EC aCap), arterial EC, pulmonary venous EC, and systemic venous EC. Using EC aCap as a signal receiving core (Receptors) and the putative adjacent cell types (alveolar fibroblast, ATI, ATII, pericyte, plasma cell, etc.) in the EC aCap niche as senders (Ligands), we identified that SLIT2-ROBO4, ANGPT1-TIE1, ADM-RAMP2, VEGFD-KDR, and BMP5-BMPR2 are the top specific and abundant pairs in the niche. Immunostaining and ELISA assays confirmed their spatial information and secretion level. Furthermore, upon treatment with these ligands, real-time resistance recorded using an electric cell-substrate impedance sensing (ECIS) system revealed that VEGFD, ANGPT1 (angiopoietin 1), and ADM (adrenomedullin) could markedly increase the electrical resistance of human lung microvascular, arterial, and venous endothelial cells, suggesting their strong impact on the endothelial barrier function. Deciphering the cell-cell soluble signals that improve endothelial integrity in human lungs lays the foundation for uncovering the pathogenesis of pulmonary vascular disorders and the development of ex vivo functional lung vasculature.

Treatment of COVID-19 Pneumonia and Acute Respiratory Distress with Ramatroban, a Thromboxane A2 and Prostaglandin D2 Receptor Antagonist: A 4-Patient Case Series Report

Lungs in COVID-19 patients produce lipid mediators measured in bronchoalveolar lavage fluid (BALF), notably thromboxane B2 (TxB2) >> prostaglandin E2 > prostaglandin D2 (PGD2).1 High levels of TxA2 metabolites in BALF from COVID-19 associated ARDS,1 and systemically in non- ICU COVID-19 patients2,3 led us to propose a critical role for TxA2 prostanoid receptors (TPr) in COVID-19 respiratory distress. We hypothesized that TxA2/TPr signaling in airways, pulmonary microvasculature, and veins contributes to pulmonary edema and hypoxemia in COVID-19 pneumonia. TPr signaling contracts intrapulmonary veins with 10-fold higher potency than arteries.4 High concentrations of TxA2 impede pulmonary venous blood flow, increase microvascular pressure, and force fluid into alveoli.4 TPr signaling also activates platelets and triggers tissue factor expression on monocytes, which may contribute to thrombosis in COVID-19. A TPr antagonist was previously reported to decrease pulmonary capillary pressure by selectively reducing post-capillary resistance in patients with acute lung injury.5 PGD2 stimulation of Dprostanoid receptor 2 (DPr2, aka CRTH2) suppresses interferon lambda (IFN-λ) transcription in the upper respiratory tract in response to respiratory viruses. PGD2/DPr2 antagonism boosts local IFN- λ antiviral responses and limits viral replication.6 Antagonism of TxA2/TPr and PGD2/DPr2 signaling has been proposed for antiviral, antithrombotic and immunomodulatory action in COVID- 19.7 Ramatroban is an oral, dual receptor antagonist of TxA2/TPr and PGD2/DPr2 and a potential candidate for chemoprophylaxis and treatment of COVID-19.1,7 With well-established safety, ramatroban has been used since 2000 in Japan for the treatment of allergic rhinitis.8 We report here a small case series of four consecutive outpatients with COVID-19 with new onset or worsening respiratory distress and hypoxemia who were treated with oral ramatroban (Baynas®, Bayer Yakuhin, Japan). Summarized below, ramatroban afforded rapid improvement in respiratory distress and hypoxemia, followed by complete recovery, successfully avoiding hospitalization. Conclusion: Four consecutive outpatients with COVID-19 were treated with ramatroban. Improvement within hours was followed by gradual complete recovery, thereby avoiding hospitalization. As a safe, oral drug, ramatroban merits clinical trials for both outpatients and hospitalized patients with SARS-CoV-2 infection and COVID-19.

Deep sedation with dexmedetomidine administered by electrophysiologists during COVID-19 pandemic compared with propofol administered by anesthesiologists for ablation of atrial fibrillation

Background: COVID-19 pandemic, limiting the availability of anesthesiologists, has impacted heavily on the organization of invasive cardiac procedures such as transcatheter atrial fibrillation (AF) ablation. Purpose: We compared the safety and efficacy of deep sedation with dexmedetomidine administered by electrophysiologists without anesthesiologist supervision, against the standard protocol performed with propofol. Methods: We retrospectively included all AF ablation procedures performed in 2020: 23 patients sedated with 1% propofol (2 ml bolus followed by infusion starting at 1 mg/Kg/h), 26 patients with dexmedetomidine (infusion starting at 0.7 mcg/Kg/h). Both groups additionally received 1 mcg/Kg of midazolam as a single bolus and 0.05 mg single boluses of fentanyl prior to ablation on each pair of pulmonary veins (PV). Primary outcomes were oxygen desaturation (< 90%) or need for assisted ventilation/intubation, bradycardia (heart rate < 45 bpm) and persistent hypotension (systolic blood pressure < 90 mmHg). Results: Baseline characteristics and hemodynamic variables did not differ between the two groups (all p > 0.05). In 8/23 (35%) patients propofol infusion velocity reduction was necessary to maintain the hemodynamic values, compared to 7/26 (27%) with dexmedetomidine. Inter-group comparison of hemodynamic variables during the procedure showed no statistically significant difference, despite a trend in favor of dexmedetomidine (3 respiratory depressions and 3 persistent hypotension episodes with propofol vs. 0 with dexmedetomidine;p = 0.057). Conclusion: Deep sedation with dexmedetomidine administered by electrophysiologists without anesthesiologist supervision is safe and effective for AF transcatheter ablation. A trend towards a lower incidence of hypotension and respiratory depression was noted when compared to propofol.

Perspective: The Case for Acute Large Vessel Ischemic Stroke in COVID-19 Originating Within Thrombosed Pulmonary Venules.

The main burden of SARS-CoV-2 falls on the lungs but neurological manifestations, the most disabling of which are strokes and which correlate with disease severity, are common. We proffer a novel mechanism for acute COVID-19 stroke whereby pulmonary vein clots developing within the characteristic pulmonary intravascular thrombotic lesions can embolize to the brain. Appreciation of this mechanism requires an understanding of the tricompartmental model of lung parenchyma oxygenation (the alveolus, the bronchial artery, and the pulmonary artery), all of which are compromised in COVID-19. Of these 3 sources, the bronchial artery plays a crucial role in COVID-19 stroke because the unique collaterals from bronchial artery to pulmonary vein which exist under normal physiological conditions (and which maintain venous patency when the pulmonary artery is blocked by embolus) are occluded, thus leading to venular thrombosis in the presence of hypercoagulability. Dislodgement of clots from this source translocates the pathology to the brain and is a disease mechanism, formerly rare, which may account for many cases of large vessel occlusion stroke in COVID-19. This mechanism extends the concept of cardioembolic stroke from endocardium retrogradely into the pulmonary circulation with which the left cardiac chambers lie in direct continuity, and which is an accepted stroke mechanism under other circumstances such as lung lobectomy, where surgical ligation of the pulmonary vein creates a blind sac from which thrombi can embolize. The proposed model is supported by postmortem studies which have demonstrated venular thrombosis and by case reports of pulmonary vein thrombosis in COVID-19. This concept provides a more plausible cause for COVID-19 associated large vessel occlusion stroke than other putative mechanisms, such as cerebral endotheliitis, cytokine storm, and hypercoagulopathy, although it is acknowledged that the latter mechanism contributes to the genesis of pulmonary vein clots. Recognizing that extrapulmonary manifestations including stroke arise within thrombosed pulmonary veins is key to understanding of neurological manifestations of SARS-CoV-2 infection.

Longitudinal Tracking of Cardiac Alterations Among Young Adults with SARS-CoV2

Background The novel SARS-CoV-2 virus inflicts far-reaching health decrements, both directly and through secondary inflammatory stimulation. To date, there is little information regarding the effects of COVID-19 on the heart after infection, especially among young healthy adults. Purpose We sought to determine whether contracting SARS-CoV-2 affects cardiac function in young, otherwise healthy adults and whether these alterations recede after testing positive for SARS-CoV-2. Methods Transthoracic echocardiography was performed on 7 subjects with SARS-CoV-2 (3F/4M, 21±1y, 24±2 kg m ) who tested positive 3-4 weeks prior to baseline testing followed by 1- month and 2-month follow-up testing. A parasternal long-axis view was utilized to measure septal and left ventricular posterior wall thickness, left ventricular volume, and left ventricular outflow tract dimensions. A four-chamber view was utilized to measure mitral and tricuspid valve, left ventricular, and pulmonary vein function. Data are mean±SD. Results Stroke volume (Baseline: 44±11ml, 1-month: 42±13ml, 2-month: 54±12ml) and stroke index (Baseline: 24±6ml/m

DON'T BLAME THE VACCINE

Background: The mRNA COVID vaccine is a rare cause of myocarditis in young patients. We describe a case of cardiogenic shock with extensive workup ruling out COVID vaccine induced myocarditis. Case: 42-year-old female who drinks 5 Monster energy drinks and 3-4 cups of coffee daily presented to the hospital with palpitations two weeks following her mRNA COVID vaccine. EKG showed atrial tachycardia with heart rates of 160 beats per minute. Adenosine and Lopressor were administered resulting in hemodynamic instability requiring norepinephrine. An echocardiogram showed dilated cardiomyopathy with ejection fraction of 15%. Right heart catheterization was performed, and the cardiac index was 1.22 L/min/m², systemic vascular resistance was 1918 dynes*sec*cm-5 and wedge pressure was 31 mm Hg. The patient was started on nitroprusside, furosemide, and milrinone drips and she began to improve. The patient was adamant the vaccine is what triggered her heart failure and extensive testing was performed to rule out COVID vaccine induced myocarditis. Workup showed normal coronary arteries and no evidence of infiltrative disease or myocarditis on cardiac MRI. The etiology was from tachycardia induced cardiomyopathy triggered by excessive stimulants and the patient had successful atrial tachycardia ablation of the right superior pulmonary vein. She was discharged on medical therapy for heart failure and advised to stop drinking energy drinks. Decision-making: Once the patient did not respond to the rate controlling agents an echocardiogram showed reduced ejection fraction. Right heart catheterization confirmed cardiogenic shock and nitroprusside and milrinone were started to help reduce afterload and improve contractility. Workup to exclude COVID induced myocarditis lead to the diagnosis of tachycardia induced cardiomyopathy and atrial tachycardia ablation was performed. Conclusion: We report a case of cardiogenic shock with workup diagnosing tachycardia induced cardiomyopathy induced from a combination of excessive monster energy drinks and coffee. She was treated successfully with afterload reduction, inotrope support, and atrial tachycardia ablation.

Diagnosis and robotic-assisted, minimally invasive, autologous pericardial patch repair of a sinus venosus atrial septal defect (ASD) with repair of partial anomalous pulmonary venous connection

Case Report Sinus venosus ASDs are usually associated with one or more anomalous right sided pulmonary veins. Diagnosis by transthoracic echocardiogram (TTE) and confirmation with transesophageal echocardiogram (TEE) and right heart catherization can lead to a multidisciplinary approach for appropriate surgical correction. Case A 21-year-old male with no PMH presented to clinic for a routine physical to return to collegiate athletics post COVID-19 infection. His only complaint during this time was residual dyspnea (NYHA Class 1). An ECG was obtained and showed an incomplete right bundle branch block and TTE revealed an ASD with moderate RV dilation. Repeat TTE at our institution showed an interatrial shunt on injection of agitated saline via the right arm within three beats after injection. Subsequent right heart catheterization with shunt series revealed a step in oxygen saturation from 75% in the superior vena cava (SVC) to 88% in the right atrium. Additional imaging obtained with TEE confirmed a sinus venosus ASD. Cardiovascular surgery was engaged and further imaging with computed tomography angiography (CTA) of the chest confirmed a large superior sinus venosus ASD measuring 16 mm in diameter as well as partial anomalous right pulmonary venous drainage into the SVC. The heart team decided on a minimally invasive robotic approach and performed an autologous pericardial patch repair of the ASD with redirection of the right and superior pulmonary veins into the left atrium. Intra-op TEE showed no residual shunt across the interatrial septum. The patient had an uncomplicated post-operative course and was discharged home on day 4. Decision-Making Sinus venosus ASDs and associated anomalous pulmonary veins are often missed on TTE. In our patient, TEE and CTA assisted in the detection of anomalous pulmonary venous connection. A multidisciplinary heart team approach helped determine and tailor the best option for surgical correction in our patient's case. Conclusion Sinus venosus defects account for up to 10% of ASDs and can lead to pulmonary hypertension if left uncorrected. TTE remains the first imaging modality in assessing for ASDs, but TEE, RHC, and CTA can assist in comprehensive diagnosis and planning for procedural correction. Surgical closure in patients less than 25 years old without pulmonary hypertension is associated with low postoperative mortality, and a multidisciplinary approach can help ensure the most optimal method of surgical correction. (Figure Presented).

Pulmonary venous thrombosis in a patient with COVID-19 infection.

OBJECTIVES: Infection with the SARS-COV2 virus (COVID-19) may be complicated by thrombotic diathesis. This complication often involves the pulmonary microcirculation. While macrovascular thrombotic complications of the lung may include pulmonary artery embolism, pulmonary artery thrombus in situ has also been hypothesized. Pulmonary vein thrombosis has not been described in this context. METHODS/RESULTS: Herein, we provide a case of an otherwise healthy male who developed an ischemic stroke with left internal carotid thrombus. Further imaging revealed pulmonary emboli with propagation through the pulmonary veins into the left atrium. This left atrial thrombus provides a source of atypical "paradoxic arterial embolism". CONCLUSIONS: Thrombotic outcomes in the setting of severe COVID 19 pneumonia may include macrovascular venous thromboembolism, microvascular pulmonary vascular thrombosis and arterial thromboembolism. Pulmonary vein, herein described, provides further mechanistic pathway for potential arterial embolic phenomenon.