Cytokine elimination in suspected COVID-19 perymyocarditis

Background: Only recently studies have been able to demonstrate the safety and efficacy of purification therapies in inflammatory diseases. Here we present the management of a young (21y) male patient in severe cardiogenic shock due to COVID-19 perymyocarditis admitted to the ICU at Bolzano Central Hospital. November 30th 2020 the patient developed high fever (>40 C) and diarrhea. After unsuccessfully being treated orally with a macrolide he was admitted to a peripheral hospital the 4th of December. The day after he deteriorated, required transfer to the ICU, endotracheal intubation and pharmacological cardiovascular support (Norepinephrine, Levosimendan). Antimicrobial treatment was started with piperacillin/tazobactam, linezolid and metronidazole. Despite multiple radiological and microbiological diagnostic attempts the origin of this severe septic shock remained unclear. December 6th the patient was transferred to Bolzano Central Hospital for VA-ECMO evaluation. Method(s): The transesophageal echocardiography revealed 15-20% of EF, lactate (5,2 mmol/l), cardiac enzymes (TropT 1400 mcg/l) and inflammatory parameters (PCT 35 ng/ml, IL-6 685 pg/ml) were elevated. We performed cardiac monitoring via Swan-Ganz catheter. The cardiac index was 1,6 l/min/m2. The peak dosage for Norepinephrine reached 7,5mg/h (1,47 mcg/kg/min). At Bolzano ICU we facilitate the pharmacological therapy with milrinone, vasopressin and low dose epinephrine. Furthermore, we impost continuous hemodiafiltration with CytoSorb filter. Result(s): Only hours after the start of filtration therapy the patient improved and we were able to gradually reduce catecholamine therapy, lactate values decreased. A VA-ECMO implantation was no more necessary. December 10th, we saw a stable patient without ventilatory or cardiovascular support, at echocardiography we revealed a normal EF. Conclusion(s): Clinically we saw a young patient in severe septic/cardiogenic shock due to perimyocarditis. Yet diagnostic attempts (CT-scan, multiple blood/urinary/liquor cultures) remained negative. Despite multiple negative PCR tests for SARS-CoV2 infection we performed specific immunoglobulin analysis and received a positive result for IgM. We therefore conclude on a COVID-19 associated perymyocarditis. Furthermore, this case illustrates the potential benefit of cytokine filtration and elimination in COVID-19 patients with altered IL6 levels.

Clinical observation of Suhexiang Pills in treatment of patients with tachycardia after SARS-CoV-2 infection.

Objective To explore the clinical effect and safety of Suhexiang Pills () in the treatment of patients with tachycardia after severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. Methods A total of 138 patients with tachycardia after SARS-CoV-2 infection admitted to eight hospitals such as 971st Hospital of the PLA Navy, Changzhou Second People's Hospital, Xuzhou First People's Hospital, Henan Provincial People's Hospital, Henan Chest Hospital from February 2023 to March 2023 were randomly divided into control group and treatment group, with 87 patients in the treatment group and 51 in the control group. Patients in the control group were po administered with betaloc, once a day, and the initial dose was 23.75 mg, adjusted in time according to the patient's heart rate. Patients in the treatment group were po administered with Suhexiang Pills, 1 pill/time, twice daily. Patients in two groups were treated for 7 d. The clinical efficacy of the two groups was observed, and the heart rate and cardiac function indexes, RR interval, blood oxygen saturation and adverse reactions were compared between the two groups before and after treatment. Results After treatment, the total effective rate of the treatment group was 98.85%, and the total effective rate of the control group was 90.20%, and the difference between the two groups was statistically significant (P < 0.05). After treatment, heart rates were significantly decreased in both groups (P < 0.05), and the heart rates of the treatment group were significantly better than those of the control group (P < 0.05) on the 7th day of treatment. After treatment, the level of left ventricular ejection fraction (LVEF) in both groups was significantly higher than that before treatment (P < 0.05), and there was statistical difference between the treatment group and the control group (P < 0.05). The levels of left ventricular end diastolic dimension (LVEDD) and left ventricular end-systolic diameter (LVESD) in the treatment group significantly decreased than that before treatment (P < 0.05), and there was no statistical difference compared with the control group (P > 0.05). After treatment, the maximum RR interval in both groups reached the normal range on the third day, and the treatment group was significantly better than the control group (P < 0.05). Blood oxygen saturation of the treatment group was significantly increased on the 7th day of treatment compared with before treatment (P < 0.05), but there was no statistical significance between the two groups (P > 0.05). There was no significant difference in the total incidence of adverse events between the two groups (P > 0.05). Conclusion Suhexiang Pills decrease heart rates in patients with tachycardia after SARS-CoV-2 infection, which was equivalent to the effect of western medicine, and can protect heart, improve heart function to a certain extent.Copyright © 2023 Editorial Office of Chinese Traditional and Herbal Drugs. All rights reserved.

Hemodynamic Effects of Awake Prone Positioning With COVID-19 Acute Respiratory Failure.

INTRODUCTION: Awake prone positioning (PP) reduces need for intubation for patients with COVID-19 with acute respiratory failure. We investigated the hemodynamic effects of awake PP in non-ventilated subjects with COVID-19 acute respiratory failure. METHODS: We conducted a single-center prospective cohort study. Adult hypoxemic subjects with COVID-19 not requiring invasive mechanical ventilation receiving at least one PP session were included. Hemodynamic assessment was done with transthoracic echocardiography before, during, and after a PP session. RESULTS: Twenty-six subjects were included. We observed a significant and reversible increase in cardiac index (CI) during PP compared to supine position (SP): 3.0 ± 0.8 L/min/m2 in PP, 2.5 ± 0.6 L/min/m2 before PP (SP1), and 2.6 ± 0.5 L/min/m2 after PP (SP2, P < .001). A significant improvement in right ventricular (RV) systolic function was also evidenced during PP: The RV fractional area change was 36 ± 10% in SP1, 46 ± 10% during PP, and 35 ± 8% in SP2 (P < .001). There was no significant difference in PaO2 /FIO2 and breathing frequency. CONCLUSION: CI and RV systolic function are improved by awake PP in non-ventilated subjects with COVID-19 with acute respiratory failure.

A Rare Case Of Eosinophilic Myocarditis Due To Subacute Sars-cov-2 Illness

Background: Eosinophilic myocarditis is a rare inflammatory cardiomyopathy with a poor prognosis. SARS-CoV-2 (COVID-19) illness has been associated with myocarditis, particularly of lymphocytic etiology. Although there have been cases of eosinophilic myocarditis associated with COVID-19 vaccination, there have been few reported cases secondary to COVID-19 illness, with the majority being diagnosed via post-mortem autopsy. Case: A 44-year-old woman with no significant medical history other than recent COVID-19 illness 6 weeks prior presented with progressive dyspnea. Patient developed acute dyspnea and diffuse pruritic rash after taking hydroxyzine. Labs were significant for mild eosinophilia. Echocardiography showed biventricular systolic dysfunction with left ventricular ejection fraction of 40%, and a moderate pericardial effusion that was drained percutaneously. She underwent left heart and right heart catheterization showing elevated biventricular filling pressures, Fick cardiac index of 1.6 L/min/m2, and no coronary disease. She was started on intravenous diuretics and transferred to our facility for further management. Her course was complicated by cardiogenic shock requiring intra-aortic balloon pump (IABP) support. Mixed venous saturations continued to decline and the patient was placed on veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support. The patient underwent endomyocardial biopsy (EMB) showing marked interstitial infiltration of eosinophils and macrophages with myocyte injury (see image). She was intubated with mechanical ventilation as well due to worsening pulmonary edema and hypoxemia. She was started on intravenous steroids with improvement of hemodynamics and myocardial function and eventually VA- ECMO was decannulated to low-dose inotropic support which in turn was ultimately weaned after 3 days of mechanical support. Conclusion(s): Eosinophilic myocarditis is a rare and under-recognized sequela of acute COVID-19 infection associated with high mortality rates. It requires prompt diagnosis and aggressive supportive care, including temporary mechanical circulatory support. There are few literature-reported cases of COVID-19 myocarditis requiring use of both IABP and VA-ECMO, none of which were used in biopsy-proven eosinophilic myocarditis, with most of these cases resulting in either fatal or unreported outcomes. Most cases of covid myocarditis required IV glucocorticoids therapy in conjunction with IVIG or interferon therapy. Here, we present a rare case of cardiogenic shock secondary to biopsy-proven eosinophilic myocarditis associated with recent COVID-19 illness with a survival outcome after temporary use of IABP and VA-ECMO support, as well as aggressive immunosuppressive therapy.Copyright © 2022

An Unusual Case of Cardiogenic Shock in a Cardio-Oncologic Patient

Background Graft versus host disease (GVHD) most often occurs 100-365 days after hematopoietic stem cell transplant (HSCT). Manifestations most often are dermatologic, hepatic or pulmonic, and are rarely cardiac. We present a unique case of GVHD inducing cardiogenic shock necessitating advanced heart failure therapies. Case This is a 34 year-old male with a history of acute lymphoblastic leukemia who completed chemoradiation and HSCT from an HLA perfect sibling in 1992. In May 2020, he presented with dyspnea for 6 weeks. An echocardiogram at that time showed an EF of 10% and severe biventricular dilatation. He was originally hospitalized at an outside institution for hypoxia where a left heart catheterization showed normal coronaries and goal directed therapy was initiated. After 2 negative COVID tests, he was discharged with a LifeVest. One month later, despite medication compliance, he returned in cardiogenic shock after his LifeVest was activated for ventricular tachycardia (VT). Decision-making He was started on inotropic therapy and an intra-aortic balloon pump (IABP) was placed 1:1 prior to transfer to our tertiary center. After support was started, a right heart catheterization showed a right atrial pressure of 13 mmHg, a wedge of 17, and a cardiac index of 2.6. His course was complicated by VT storm. Differentials for his non-ischemic cardiomyopathy (NICMO) included myocarditis (viral vs. giant cell) with a possible component of chemotherapy/radiation induced NICMO. Immediate AHFT work-up was started. He was unable to be weaned off his IABP or inotropic support. The decision was made to pursue emergent left ventricular assist device placement (LVAD) and achieve a definitive diagnosis with a core biopsy. Pathology resulted with myocyte hypertrophy, chronic inflammation with eosinophils concerning for chronic GVHD. Conclusion There have only been a handful of case reports describing cardiac manifestations of GVHD, and none with NICMO and cardiogenic shock requiring an LVAD. Despite this, suspicion should remain present for GVHD in HSCT patients regardless of time frame from oncologic therapies or specificity of HLA match when presenting in cardiogenic shock.Copyright © 2023 American College of Cardiology Foundation

Influenza a Myocarditis Vs Multisystem Inflammatory Syndrome Causing Cardiogenic Shock in a 34-Year-Old

Background Cardiogenic shock is a rare complication of influenza myocarditis and multisystem inflammatory syndrome. We present the case of a 32-year-old female in cardiogenic shock who met criteria for both entities. Case A 34-year-old female with hypothyroidism presented after being found down and covered in feces. She had cough and weakness the preceding days. She was febrile and hypotensive. Point of care ultrasound showed severe biventricular dysfunction and she was started on norepinephrine. She was influenza A positive with a lactate of 5.1. Right heart catheterization on 2ug/kg/min of norepinephrine showed a cardiac index (CI) of 2.82 L/min/m2 and a systemic vascular resistance (SVR) of 300 dynes/sec/cm-5. She was started on vasopressin, stress dose steroids, and oseltamivir. She received 6 amps of bicarbonate with aggressive electrolyte repletion. CI as per the Fick equation was within normal limits but lactate continued to rise. Thermodilution showed a CI of 1.6 L/min/m2 and an SVR of 2200 dynes/sec/cm-5, indicating mixed cardiogenic and distributive shock. The patient developed severe abdominal pain and was found to have elevated COVID-19 spike domain and nucleocapsid antibodies, meeting criteria for multisystem inflammatory syndrome (MIS-A). Decision-making The patient was started on dobutamine after thermodilution showed decreased CI. Intravenous immunoglobulin was started after meeting criteria for MIS-A. Her pressor requirements were weaned and then her dobutamine requirements. Follow up cardiac MRI showed mild global hypokinesis of the left ventricle and subtle hypokinesis of the right ventricular inferior wall. Left ventricular ejection fraction was 51%. The patient's cardiac MRI findings were not specific. However, her rapid improvement was suggestive of MIS-A. Additionally, consistent discordance between Fick and thermodilution resulted in confusion regarding optimization of pressors and inotropes. Conclusion The patient responded to dobutamine and MIS-A treatment after an initial impression of myocarditis. Infectious processes should be considered in any patient with new onset heart failure.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

Effusive Constrictive Pericarditis, a Heart Failure Mimicker

Background Effusive constrictive pericarditis can initially mimic heart failure and ultimately result in cardiogenic shock. Case Patient is a 57-year-old female with history of recent massive pulmonary embolism status post systemic alteplase, chronic diastolic heart failure, and history of COVID-19 infection presenting with increasing dyspnea on exertion and weakness despite compliance to outpatient diuretics. Patient was noted to be hypotensive, and fluid overloaded on exam. Decision-making Due to concern for constriction right heart catheterization (RHC) was completed and showed cardiac index of 1.1 with elevated filling pressures, discordant variation of right ventricle (RV) and left ventricle (LV) pressure tracings, diastolic equalization of pressure, and dip and plateau pattern of RV and LV diastolic tracing suggestive of constrictive physiology. Transesophageal echocardiogram showed no pericardial effusion with increased echo-density of the pericardium. Cardiac MRI showed mild diffuse thickening and subtle enhancement of the pericardium with septal bounce and no significant pericardial effusion consistent with constrictive pericarditis. Due to persistent hypotension requiring milrinone infusion, the patient underwent pericardiectomy with improvement of hemodynamics and symptoms. Conclusion Effusive constrictive pericarditis can mimic heart failure and should be ruled out in those with evidence of low cardiac output to avoid cardiovascular morbidity and mortality. [Formula presented]Copyright © 2023 American College of Cardiology Foundation

2022 Annual World Congress of the Pulmonary Vascular Research Institute

Pulmonary hypertension (PH) is a severe disease that can progress to clinical decompensation, risk of hospitalization and death owing to disease-related or other diseases. In the context of coronavirus disease 2019 (COVID-19), PH was considered a risk factor for complications. The purpose of the study was to assess the mortality rate of COVID-19 in PH patients from a PH Center in Brazil. We conducted a telephone survey between June and August 2021 among all patients or relatives from the PH referral center who were followed after the first case of COVID- 19 in Brazil. Only patients with a confirmed diagnosis of PH were included in the analysis. Of the 426 patients followed in the first 18 months of the pandemic, 115 patients were excluded (lost to follow-up, post-acute PE or unconfirmed PH). Among 311 patients included, 39 had a confirmed diagnosis of COVID-19 (COVID-19 + ), and 38.5% of patients were hospitalized. The estimated incidence rate was 12.5%. Comparing the COVID-19+ versus patients without infection (COVID-19 - ) in the period, the mean age was similar (55 +/- 17 vs. 54 +/- 16 years) and the majority in the COVID-19+ group were female (85% vs. 69%, p = 0.039), respectively. There was no difference in the proportion of patients diagnosed with pulmonary arterial hypertension (PAH;49% and 42%) and chronic thromboembolic pulmonary hypertension (CTEPH;24% and 33%) between groups. All PAH patients and the majority of CTEPH patients were treated on specific therapy (combination/triple therapy, 70%). The case fatality rate in the PH-COVID-19+ group was 23%. Considering only PAH and CTEPH, the case fatality rate was 21,9%, while COVID-19 mortality was 2.9% and overall lethality in Brazil was 2.8%. In the COVID-19+ group, the mean pulmonary artery pressure was 48 +/- 14 mmHg, cardiac index 2.7 +/- 0.6 L/min/m2 and pulmonary vascular resistance 730 +/- 424 dyn.s/cm5. In conclusion, among PH patients there was high incidence and mortality from COVID-19, even in those with PHspecific therapy. Further studies are needed to evaluate the prognostic predictors in PH-COVID-19 patients.

2022 Annual World Congress of the Pulmonary Vascular Research Institute

Pulmonary hypertension (PH) is a severe disease that can progress to clinical decompensation, risk of hospitalization and death owing to disease-related or other diseases. In the context of coronavirus disease 2019 (COVID-19), PH was considered a risk factor for complications. The purpose of the study was to assess the mortality rate of COVID-19 in PH patients from a PH Center in Brazil. We conducted a telephone survey between June and August 2021 among all patients or relatives from the PH referral center who were followed after the first case of COVID- 19 in Brazil. Only patients with a confirmed diagnosis of PH were included in the analysis. Of the 426 patients followed in the first 18 months of the pandemic, 115 patients were excluded (lost to follow-up, post-acute PE or unconfirmed PH). Among 311 patients included, 39 had a confirmed diagnosis of COVID-19 (COVID-19 + ), and 38.5% of patients were hospitalized. The estimated incidence rate was 12.5%. Comparing the COVID-19+ versus patients without infection (COVID-19 - ) in the period, the mean age was similar (55 +/- 17 vs. 54 +/- 16 years) and the majority in the COVID-19+ group were female (85% vs. 69%, p = 0.039), respectively. There was no difference in the proportion of patients diagnosed with pulmonary arterial hypertension (PAH;49% and 42%) and chronic thromboembolic pulmonary hypertension (CTEPH;24% and 33%) between groups. All PAH patients and the majority of CTEPH patients were treated on specific therapy (combination/triple therapy, 70%). The case fatality rate in the PH-COVID-19+ group was 23%. Considering only PAH and CTEPH, the case fatality rate was 21,9%, while COVID-19 mortality was 2.9% and overall lethality in Brazil was 2.8%. In the COVID-19+ group, the mean pulmonary artery pressure was 48 +/- 14 mmHg, cardiac index 2.7 +/- 0.6 L/min/m2 and pulmonary vascular resistance 730 +/- 424 dyn.s/cm5. In conclusion, among PH patients there was high incidence and mortality from COVID-19, even in those with PHspecific therapy. Further studies are needed to evaluate the prognostic predictors in PH-COVID-19 patients.

Right Ventricular Hemodynamics in COVID Patients With Shock

Introduction: Patients with serious COVID infections frequently develop shock. Their right-sided hemodynamic profiles have not been well characterized. Method(s): In a prospectively collected database including 1997 patients hospitalized for COVID pneumonia from March 2020 to March 2021, 368 had shock requiring vasopressors. 327 had echocardiography to assess ventricular function and stroke volume based on clinical indications. LVEF (LV ejection fraction) and RVFAC (RV fractional area change) were measured using Simpson's rule, stroke volume (SV) by aortic Doppler, and RVSP (RV systolic pressure) from tricuspid regurgitation velocity;187 had evaluable data on all parameters. Patients were divided into groups with low or preserved RVFAC (RVFAC or RVFAC , cutoff <e35%), and low or normal cardiac index, (CI, CI or CI cutoff <e2.2 L/min/m2 ). Result(s): Mean age: 65+/-12, LVEF 59.5+/-12.8, RVFAC 35.3+/-10.6, CI 2.41+/-0.89. Overall hospital mortality in this cohort with shock was 80%. Mean RVSP was 38.8+/-12.2, PEEP 11.0+/-3.7. 43% of patients had low RVFAC (<35%), and RVFAC correlated with other measures of RV function such as tricuspid annular peak systolic excursion (TAPSE) and lateral tricuspid annulus peak systolic velocity (S'). Higher RVSP correlated with lower CI (r=0.134, p= 0.016) but not with PEEP (r=0.03, p=0.70). Mortality did not differ significantly among groups, (p=0.19 by ANOVA) but was highest in the group with low RVFAC and low CI. (Figure) Conclusion(s): RV dysfunction is common in patients with severe COVID-19 and shock. Although RV dysfunction is probably associated with a worse prognosis, outcome in COVID may be tied to pulmonary recovery. Whether treatment targeted at RV dysfunction will improve outcome remains uncertain.

HYDROXYCHLOROQUINE CAN BREAK YOUR HEART

SESSION TITLE: The Cardiac Intensivist 2 SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Hydroxychloroquine and chloroquine are medications derived from aminoquinoline. They are disease-modifying antirheumatic drugs used in the treatment of systemic lupus erythematosus (SLE). Although well tolerated, they do have side effects such as retinopathy, vacuolar myopathy, neuropathy, and as seen in our patient, cardiotoxicity. CASE PRESENTATION: Patient is a 48 year old female with a past medical history significant for chronic kidney disease secondary to autosomal dominant polycystic kidney disease, SLE on hydroxychloroquine who presented to the emergency department complaining of weakness. On arrival the patient was found to be in cardiogenic shock. Her transthoracic echocardiogram revealed a reduced ejection fraction of 37% and a large pericardial effusion concerning for tamponade physiology. Her COVID-19 PCR test was positive. She was taken for emergent pericardiocentesis which revealed 300cc of exudative fluid. Patient’s right heart catheterization revealed mean pulmonary capillary wedge pressure of 23 mmHg, pulmonary artery pressures of 44 mmHg/24 mmHg, mean 31mmHg, cardiac index 1.1L/min/m² by thermodilution, 1.7 L/min/m² by Fick. Following right heart catheterization and intra aortic balloon pump placement, the patient was admitted to the medical intensive care unit (MICU) and placed on intravenous inotropic and vasopressor support. Shortly after arrival to the MICU, patient had an increase in vasopressor requirements. Bedside ultrasound revealed cardiac tamponade. Patient had approximately 400cc of bloody pericardial fluid removed from her pericardial drain. The decision was made for emergent venoarterial extracorporeal membrane oxygenation (ECMO) to be initiated. Endomyocardial biopsy was performed which revealed vacuolization in the cytoplasm of several myocytes as well as lymphocytes in the interstitium of the endocardium. The vacuoles found in the cardiac myocytes were PAS positive. These biopsy results are consistent with hydroxychloroquine cardiotoxicity. The patient’s hydroxychloroquine was discontinued. In addition to hemodynamic support, she also received intravenous immunoglobuluin and systemic steroids. After a prolonged hospitalization she was successfully discharged. DISCUSSION: Cardiotoxicity is a rare adverse reaction seen with hydroxychloroquine. A 2018 systematic review revealed 127 cases of cardiac toxicity associated with the use of hydroxychloroquine or chloroquine. Most patients had been treated with the medication for a prolonged period of time and the toxicity is dose dependent. The mechanism behind hydroxychloroquine and chloroquine induced cardiomyopathy is believed to be secondary to lysosomal dysfunction as a result of toxic phospholipid accumulation in cardiomyocytes. CONCLUSIONS: In patients with new onset cardiomyopathy, a detailed medication reconciliation should be conducted to evaluate for toxins such as hydroxychloroquine and chloroquine. Reference #1: Della Porta, A., Bornstein, K., Coye, A., Montrief, T., Long, B., & Parris, M. A. (2020). Acute chloroquine and hydroxychloroquine toxicity: A review for emergency clinicians. The American Journal of Emergency Medicine. Reference #2: Abbi, B., Patel, S., Kumthekar, A., Schwartz, D., & Blanco, I. (2020). A Case of Cardiomyopathy With Long-term Hydroxychloroquine Use. JCR: Journal of Clinical Rheumatology, 26(8), e300. Reference #3: Chatre, C., Roubille, F., Vernhet, H., Jorgensen, C., & Pers, Y. M. (2018). Cardiac complications attributed to chloroquine and hydroxychloroquine: a systematic review of the literature. Drug safety, 41(10), 919-931. DISCLOSURES: no disclosure on file for Joseph Adams;no disclosure on file for Suliman Alradawi;No relevant relationships by George Kalapurakal No relevant relationships by Mohammed Siddiqui

COVID-19 MULTISYSTEM INFLAMMATORY SYNDROME IN A YOUNG ADULT: RAPID REVERSAL OF CARDIOGENIC SHOCK WITH IVIG AND STEROIDS

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: Multisystem inflammatory syndrome in adults (MIS-A) is a hyperinflammatory condition characterized by fever, elevated inflammatory markers, and multi-organ dysfunction, including severe cardiac illness, neurological and gastrointestinal symptoms, mucocutaneous involvement, and thrombocytopenia usually 2-5 weeks after COVID-19 infection (1). There are currently no guidelines for the management of this novel syndrome. CASE PRESENTATION: A 20-year-old obese male presented for 3 days of fatigue, fever, dyspnea, diarrhea, and worsening encephalopathy. He tested positive for COVID-19 3 weeks prior and experienced 4 days of mild symptoms. He had received 2 doses of Moderna mRNA vaccine 9 months prior. On presentation, he had a GCS of 3. He was febrile, hypotensive, tachycardic, not hypoxic, and found to have non-purulent conjunctivitis but no rash. He was intubated for airway protection and started on norepinephrine (NE) shortly after arrival. Labs revealed positive COVID-19 PCR, lactate of 5.6 mmol/L, elevated hs-troponin which peaked at 11,300 ng/L, D-Dimer 12,574 ng/ml, ferritin >16,500 ng/ml, CRP 224 mg/L, platelet count 18 x109/L. EKG showed sinus tachycardia without ST changes. CT chest/abdomen/pelvis was unremarkable. The patient was given broad-spectrum antibiotics and admitted to ICU. An echocardiogram (echo) showed global hypokinesis with an ejection fraction of 10-15%. Right heart catheterization found a wedge pressure of 23 mmHg, and a cardiac index of 1.4 L/min/m2. NE was weaned, and dobutamine and bumetanide drips were started. Infectious disease was consulted and diagnosed the patient with MIS-A. Treatment was started with methylprednisolone 2mg/kg/day and IVIG (2 g/kg x2 days). 48 hours later, dobutamine was able to be discontinued and follow-up echo showed normalization of biventricular systolic function. Steroids were continued for 7 days before tapering off. The patient’s presenting symptoms, platelets, and inflammatory markers rapidly improved, and he was ultimately able to be discharged home. DISCUSSION: MIS-A is a rare but serious extrapulmonary sequela of COVID-19 which can cause critical illness including cardiogenic shock. The long-term consequences of MIS-A are not known, but fortunately, as demonstrated by our case, severe cardiac dysfunction can be effectively reversed with timely diagnosis and initiation of immunosuppressive treatment. This recovery was achieved without immunomodulators (eg tocilizumab) which have been used in other MIS-A cases (2). MIS-A should be considered in patients with severe cardiac dysfunction and evidence of systemic inflammation even with no known history of COVID as this can develop after mild or even asymptomatic COVID-19 infections. CONCLUSIONS: Immunosuppressive therapies can rapidly reverse severe multiorgan dysfunction in MIS-A. Still, further study is needed to identify at-risk patients and create definitive treatment guidelines. Reference #1: Vogel TP, Top KA, Karatzios C, et al. Multisystem inflammatory syndrome in children and adults (MIS-C/A): Case definition & guidelines for data collection, analysis, and presentation of immunization safety data. Vaccine. 2021;39(22):3037-3049. doi:10.1016/j.vaccine.2021.01.054 Reference #2: Patel P, DeCuir J, Abrams J, Campbell AP, Godfred-Cato S, Belay ED. Clinical Characteristics of Multisystem Inflammatory Syndrome in Adults: A Systematic Review. JAMA Netw Open. 2021;4(9):e2126456. doi:10.1001/jamanetworkopen.2021.26456 DISCLOSURES: No relevant relationships by Christopher Allison no disclosure on file for Sandeep Arepally;No relevant relationships by Amad Chohan No relevant relationships by Albert Manudhane No relevant relationships by Griffin Reed

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.

CONTINUOUS REMOTE PATIENT MONITORING SHOWS EARLY CARDIOVASCULAR CHANGES IN COVID-19 PATIENTS

Objective: COVID-19 exerts deleterious cardiopulmonary effects, leading to a worse prognosis in the most affected. This study aimed to analyze the trajectories of key vitals amongst hospitalized COVID-19 patients using a chest-patch wearable medical-grade monitor providing continuous remote patient monitoring of numerous vital signs. Design and method: This retrospective multicenter observational cohort study was conducted in five COVID-19 isolation units. 492 COVID-19 patients were included in the final analysis. Physiological parameters were measured every 15 minutes. Results: More than 3 million measurements were collected including heart rate, systolic and diastolic blood pressure, cardiac output, cardiac index, systemic vascular resistance, respiratory rate, blood oxygen saturation, and body temperature. Cardiovascular deterioration appeared early after admission and in parallel with changes in the respiratory parameters, showing a significant difference in trajectories within sub-populations at high risk. Conclusions: Early detection of cardiovascular deterioration of COVID-19 patients is achievable when using frequent remote patient monitoring.

Defer Thy Diuresis

With the spread of the novel coronavirus disease 2019 (COVID-19) pandemic, an alarming number of patients now present with acute respiratory distress syndrome (ARDS). Conservative fluid management with diuresis in the ARDS patients improves lung function and decreases ventilator-dependent days. Several cardiac manifestations have been reported in COVID-19 patients including rhythm disorders, myocarditis, Takotsubo cardiomyopathy and myocardial infarction. A 65-year-old Asian female with a history of hypertension presented to the emergency department with cough, worsening dyspnea and palpitations of one-week duration. Investigations at admission were significant for a positive COVID-19 polymerase chain reaction test with an electrocardiogram (EKG) (Figure 1 Panel-A) revealing inferior ST-elevations. Troponin-T was elevated to 1162 ng/L with bedside echocardiogram revealing inferior hypokinesis. Due to concerns for acute ST-elevation myocardial infarction (STEMI), the patient underwent cardiac catheterization with no obvious coronary artery occlusion. A ventriculogram revealed apical ballooning and the patient was treated for COVID-19 induced Takotsubo cardiomyopathy. The patient developed worsening respiratory distress on hospitalization day 3 requiring oxygen supplementation with a high-flow nasal cannula. Conservative fluid regimen and diuretic therapy were being administered when the patient developed ventricular fibrillation and suffered a cardiac arrest. After successful resuscitation, a repeat EKG (Figure 1 Panel-B) demonstrated new anterior and inferior ST-elevations. The patient required increasing vasopressor support, and a repeat cardiac catheterization to rule out coronary artery thromboembolism induced STEMI was negative. A right heart catheterization revealed elevated SVR with decreased cardiac index. The patient clinically deteriorated despite negative fluid balance with recurrent malignant arrhythmias. A bedside echocardiogram performed revealed persistent apical hypokinesis and systolic anterior motion of anterior mitral leaflet (Figure 1 Panel-C) with flow acceleration at left ventricular outflow tract (LVOT) (Figure 1 Panel-D). Due to concerns of cardiogenic shock secondary to Takotsubo cardiomyopathy with dynamic LVOT obstruction physiology, the patient was treated with liberal intravenous fluid resuscitation and successfully weaned from vasopressor therapy. Although she was successfully extubated 2 days later, the patient, unfortunately, passed away later from a thromboembolic stroke. Severe COVID-19 infections are associated with catecholamine surge which may precipitate Takotsubo cardiomyopathy in the susceptible patient population. Female patients with Takotsubo cardiomyopathy are at increased risk of developing dynamic LVOT obstruction. In these patients, management of shock and ARDS can be challenging as the use of inotropic agents may result in hemodynamic instability. Our patient was successfully hemodynamically stabilized using fluid resuscitation once the inotropic support was withdrawn after identifying dynamic LVOT obstruction.

A MULTIMODALITY IMAGING DIAGNOSIS OF A CHALLENGING CASE OF CONCOMITANT GROUP 1 PULMONARY HYPERTENSION AND PARADOXICALLY LOW- FLOW, LOW-GRADIENTAORTIC STENOSIS

A 76 year old woman was admitted to our hospital for self-limiting dyspnoea (NYHA class III) in oxygen dependence and frequent lipothymia following Valsalva manoeuvres. She was previously admitted to a Spoke Centre for heart failure (HF) with preserved ejection fraction (EF) and a new diagnosis of “pre-capillary pulmonary hypertension (PH)”. Despite a diagnosis of PH of unclear aetiology, she was started on macitentan without being reassessed for functional capacity due to Covid emergency;because of worsening symptoms, she was admitted to our Hub Centre. Resting ECG showed right axis deviation, right ventricle (RV) hypertrophy, first-degree atrioventricular block and right bundle branch block. Transthoracic echocardiography (TTE) showed reduced left ventricular (LV) volume with preserved EF (diastolic volume= 37 ml, EF=88%), severe right atrial and RV dilation with flattening of the interventricular septum, estimated pulmonary artery systolic pressure (PASP) of 124 mmHg, and moderate calcific aortic stenosis (peak aortic velocity 3.3 m/s, mean gradient 25 mmHg, valve area 1.1 cm2). Right and left heart catheterization showed severe pre-capillary PH (mean pulmonary pressure 60 mmHg, mean wedge 11 mmHg, pulmonary vascular resistance 14.41 WU), a severe aortic valve stenosis (aortic valve area 0.68 cmq and peak-to-peak gradient 25 mmHg, slight reduction of cardiac index 2.04 l/min/mq) and no significant coronary artery disease. The degree of aortic stenosis was considered as moderate-severe by integrating data of transesophageal echocardiography (planimetric area 1cm2) and assessment of calcium score (1615 Agatson units). Pneumological causes, chronic thromboembolic PH, rheumatologic diseases, HIV infection, paraneoplastic origin and veno-occlusive disease were all ruled out as potential PH causes and a diagnosis of Idiopathic pulmonary arterial hypertension (IPAH) was finally made. The Heart Team established the best therapeutic option was a transcatheter aortic valve replacement (TAVI) allowing better haemodynamic tolerability of PH therapy. The patient underwent TAVI and was started on PH therapy;a complete atrio-ventricular block developed after the procedure, requiring permanent pacemaker (PM) implantation. Unfortunately, few days later, the patient died following pacemaker's lead dislocation. Conclusion: PH has a diverse aetiology, and prognosis is generally poor, especially in patients with severe comorbidities. (Figure Presented).

THE ELDEST HEART TRANSPLANTED PATIENT IN EUROPE: 36 YEARS SURVIVAL AND STILL GOING ON

Development of endomyocardial biopsy for acute rejection monitoring in the early Seventies, and above all use of cyclosporine in the clinical practice starting from 1980, introduced the modern era of heart transplantation. Following the initial positive outcomes, the first Italian transplant was performed in Padua by V.Gallucci on November 15th 1985. This pioneering success was rapidly repeated in Pavia, where M.Viganò performed the second transplant on Novembre 17th. Recipient was 20 years old man, suffering from dilated cardiomyopathy, on urgent transplant list. Cardiac index was 1.38 l/min/m2 and pulmonary vascular resistance 1.6 WU. Donor was a 14 years old boy died of brain injury. Total ischemic time was 125 minutes. Induction immunosuppression consisted of horse anti-lymphocyte immunoglobulins, whereas maintenance therapy included cyclosporine, azathioprine and steroids. Postoperative course was complicated by pericardial effusion and cholestatic jaundice. Later pulmonary aspergillosis occurred and due to the profound immunodepression was complicated by fungal localization at L2 vertebral body. The infection was treated with surgical removal of the secondary localization and amphotericin B administration. On December 6th severe acute rejection was found at biopsy and treated with i.v. steroid pulse. Length of ICU and hospital stay was 28 and 72 days, respectively. In 1998 HCV infection was detected and eradicated in 2017 with elbasvir/grazoprevir therapy. Complications of long term immunosuppressive treatment included dyslipidemia, myeloma and basal cell carcinoma. Due to long-term calcineurin inhibitors therapy progressive chronic renal failure occurred, leading to replacement therapy in 2015 and kidney transplantation in 2016. In 2015 the patient underwent percutaneous coronary intervention with stents implantation in two marginal branches and in the anterior descending artery in 2021. Everolimus was introduced to slow down progression of cardiac allograft vasculopathy. In 2020 he suffered from Covid-19, but the course of infection was uneventful being cough the only symptom. We report the eldest survivor after heart transplant in Europe. Our case demonstrates that despite early and long-term complications of immunosuppressive therapy, a careful and patient tailored management allowed an amazing outcome. Nowadays heart transplant remains the best treatment for end stage heart failure and allows to resume a nearly normal quality of life.

ECHO, ECHO AGAIN: PROSTHETIC MITRAL REGURGITATION PRESENTING AS B-TYPE SYMPTOMS

Background: Prosthetic valve dehiscence is a manifestation of endocarditis which may be difficult to diagnose based on imaging. Case: A 68-year-old female with mechanical mitral valve replacement (MVR) complicated by recurrent endocarditis requiring two redo MVR presented with subacute chills, nausea, fatigue and dyspnea. Evaluation revealed leukocytosis, elevated NT-proBNP, acute kidney injury, negative blood cultures, and negative SARS-CoV2. Transthoracic echocardiography (TTE) showed normal prosthetic valve function. She was managed for acute decompensated heart failure and placed on empiric antibiotics. She continued to have chills, night sweats and developed hypotension. Blood cultures remained negative, and no source of infection was identified on imaging. Decision-making: To aid in differentiation shock, patient underwent right heart catheterization. This revealed severe cardiogenic shock, with cardiac index of 1.3 L/min/m2. Repeat TTE demonstrated dehiscence of the prosthetic mitral valve, which was confirmed on transesophageal echocardiogram (Figure 1). An intra-aortic balloon pump was placed, and inotropic support provided. Patient underwent successful redo MVR using a bioprosthetic valve. Tissue microbiology was positive for coagulase negative staph. Conclusion: Unmasking the etiology of vague clinical presentations may pose a challenge. Our case highlights the importance of a high index of suspicion and serial imaging when patients present with B-type symptoms. [Formula presented]

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.