Fulminant myocarditis following SARS-CoV-2 mRNA vaccination rescued with venoarterial ECMO: A report of two cases

Objectives: Cases of fulminant myocarditis after mRNA COVID-19 vaccination have been reported. The most severe may need venoarterial extracorporeal membrane oxygenation (V-A ECMO) support. Here we report two cases successfully rescued with V-A ECMO. Method(s): We included all the cases supported with V-A ECMO for refractory cardiogenic shock due to myocarditis secondary to a mRNA SARS-COV2 vaccine in the high-volume adult ECMO Program in Vall Hebron University Hospital since January 2020. Result(s): We identified two cases (table). One of them was admitted for out-of-hospital cardiac arrest. In both, a peripheral V-A ECMO was implanted in the cath lab. An intra-aortic balloon pump was needed in one case for left ventricle unloading. Support could be successfully withdrawn in a mean of five days. No major bleeding or thrombosis complications occurred. Definite microscopic diagnosis could be reached in one case (Image, 3). Treatment was the same, using 1000mg of methylprednisolone/day for 3 days. A cardiac magnetic resonance 10 days after admission showed a significant improvement in systolic function and diffuse oedema and subepicardial contrast intake in different segments (Image, 1-2). Both patients were discharged fully recovered. Conclusion(s): V-A ECMO should be established in cases of COVID-19 vaccine-associated myocarditis with refractory cardiogenic shock during the acute phase. (Table Presented).

ECMO in acute fulminant myocarditis in pediatrics

Objectives: To describe our experience in ECMO for acute myocarditis Methods: Descriptive, retrospective study (2018-2022) of a cohort of 8 patients < 16 years with acute myocarditis who were assisted on ECMO. Result(s): 8 patients were collected, (6 females), with a mean age 7;8 years [range 0;1-13;8]. In 7/8, the reason for cannulation was hemodynamic instability refractory to medical treatment, with a mean inotropic score of 70 [range 10-122]. Sixty-two percent presented cardiorespiratory arrest prior to cannulation and 2 of them needed ECRP. The mean precannulation troponin level was 1498 ng/ml [range 89-6212]. Primary transport was performed in 4 patients. ECMO was peripheral veno-arterial in 100%, jugulo-carotid in 2/8 and femoro-femoral in 6/8. All patients underwent atrioseptostomy. They received treatment with levosimendan, immunoglobulins, corticoids and carnitine. In 4 acute infectious etiology was confirmed (parvovirus, influenza and SARSCoV2), another one was due to PIMS-TS and in 3 no etiology was found. Six patients underwent myocardial biopsy and 5 of them showed inflammatory infiltrates. The mean time on ECMO was 8 days [range 3-14], 2 of them requiring 2 ECMO courses. The mean length of PICU stay was 21 days [range 10-50]. Two were transferred to a heart transplant center. The main complications were arterial hypertension (88%), bleeding (63%), neurological (50%), arrhythmias (38%), coagulopathy (38%) and infectious (38%). One patient required renal replacement therapy. 1 patient died, 2 had moderate neurological sequels. Conclusion(s): ECMO is a therapeutic option in patients with fulminant myocarditis refractory to medical treatment and may help improve their prognosis.

The impact that myocarditis for post-acute COVID-19 syndrome may be dermatomyositis-like myocarditis: A case report.

Myocarditis is often reported as a complication of COVID-19 infection or post-vaccination, but there are few reports of "myocarditis for Post-acute COVID-19 syndrome", and many unknowns still remain. Apart from that, an association between COVID-19 infection and dermatomyositis has also been reported. We describe the clinical presentation of acute myocarditis in a patient who had developed COVID-19 syndrome one-month earlier. A healthy 49-year-old man experienced typical COVID-19 symptoms. Thirty-two days later, he was admitted because of fever and severe fatigue, chest pain and bradycardia. Blood tests showed major inflammation. PCR for SARS-CoV-2 on nasopharyngeal swab (ID NOW™) was positive, but diagnosed as a previous infection due to a high CT value. Because of haemodynamic worsening with both an increase in cardiac troponin I and NT-pro BNP levels and reduced wall motion on echocardiography, acute myocarditis was suspected. Myocardial biopsy revealed severe lymphocytic infiltration and interstitial edema between myocardial fibers. These findings led to the diagnosis of fulminant myocarditis. Interestingly, myocardium was also stained with human myxovirus resistance protein 1 (MxA). We consider that there may be an aspect of "dermatomyositis-like myocarditis with SARS-CoV-2" in our case. This is the first case of fulminant myocarditis for Post-acute COVID-19 syndrome in which diagnosis of active myocarditis was proven by pathological examination following myocardial biopsy and strong association with dermatomyositis was suggested pathologically.

On-Site Whole-Genome Sequencing of Sars-Cov-2 Reveals C3037t Mutation in Patient with Atrioventricular Nodal Reentry Tachycardia (Avnrt)

Intro: The spike protein of the SARS-CoV-2 virus targets the human cell receptor of angiotensin-converting enzyme (ACE2), including the myocardium and heart's conduction system. Patients diagnosed with COVID-19 have also been found to exhibit cardiac arrhythmia. Here, a whole-genome sequencing analysis using long-read sequencing was proposed to evaluate the virus genome in a patient who presented with AVNRT as a main presentation of COVID-19. Method(s): The sample was recovered from nasopharyngeal and oropharyngeal swab specimens of a 46-year-old female with no comorbidities who presented with palpitation, and ECG showed typical AVNRT features. The RT-qPCR of SARS- CoV-2 was confirmed positive with a CT-value of 15.82. The total RNAs were extracted and proceeded for RT-qPCR and proceeded with Oxford Nanopore Flongle sequencing. The genomics data of the virus was deposited in GISAID (EPI_ISL_3241561) and further analysed using online bioinformatics tools such as Nextclade CLI 2.3.0. Ethical approval (IREC 2021-080) for the study was obtained from IIUM Research Ethics Committee. Finding(s): Here, we reported a total of 29,775 bp near-complete whole-genome belonging to clade 21J (Delta) of AY.79 lineage (also known as B.1.617.2.79), which formed a dominant variant in Malaysia during the time of sampling. Discussion(s): While a previous study showed an association between Delta variant infection with fulminant myocarditis, the present study reported the benign AVNRT as the main presentation of SARS-CoV-2 infection. Furthermore, we observed the presence of the C3037T mutation previously described in the endomyocardial biopsy of a patient with persistent arrhythmia. Conclusion(s): Even though SARS-CoV-2 targets the respiratory tract, the present study supports the evidence that the ACE2 receptors are present in the heart. In addition, COVID19 is causing more and more damage to heart tissue, and viral transcription has been confirmed on cardiomyocytes. Further functional studies are needed to explore the associated mutations and their relation to cardiac manifestation.Copyright © 2023

COVID-19 fulminant myocarditis recovered with veno-arterial extracorporeal membrane oxygenation and Impella CP.

A 38-year-old man without a history of coronavirus disease 2019 (COVID-19) vaccination presented with dyspnea and fever. Polymerase chain reaction nasopharyngeal swab for severe acute respiratory syndrome coronavirus 2 was positive. Electrocardiogram showed diffuse ST-segment elevation, and chest radiography showed mild pulmonary congestion. The left ventricular (LV) function was markedly impaired. Vital signs were unstable, and serum lactate level was elevated. The patient was diagnosed with cardiogenic shock due to COVID-19 fulminant myocarditis and received veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and Impella CP (Abiomed, Inc., Danvers, MA, USA). Remdesivir and intravenous immunoglobulin were also administered. Corticosteroids were not administered because of the absence of pneumonia. On admission, endomyocardial biopsy showed a small direct inflammatory infiltrate of the myocardium. During mechanical support, the cardiac function improved, the patient was weaned off VA-ECMO on day 6, and Impella CP on day 7. Cardiac magnetic resonance imaging implied recent myocardial damage. The patient was discharged on day 30, and the LV function fully recovered. Since the treatment and prognosis of COVID-19 fulminant myocarditis remain unclear, we report the course of COVID-19 fulminant myocarditis with favorable outcomes. Mechanical circulatory support might be an important factor in determining the prognosis of COVID-19 fulminant myocarditis. Learning objective: Coronavirus disease 2019 fulminant myocarditis sometimes requires mechanical circulatory support. The prognosis and treatment have not yet been adequately established. The prognosis is favorable if adequate hemodynamic support is provided.

Post COVID-19 cardiac magnetic resonance findings among inpatients vs outpatients

Background: Myocardial injury and myopericarditis constitute an important complication after viral infection. The prevalence of myocardial injury among patients that survived COVID - 19 infections and its causes are still not clear. The purpose of this study is to estimate whether there is a difference in the prevalence of cardiac magnetic findings between patients treated in a hospital vs patients treated at an outpatient clinic. Method(s): We evaluated 360 cardiac magnetic resonance examinations, performed from 1st of June 2020 until the 31st of August, 2021. Out of them, 141 patients (39%) underwent cardiac magnetic resonance due to persistent symptoms after a SARS-CoV-2 infection. A conventional CMR protocol was performed to rule out myocarditis. Revised 2018 Lake Louise Criteria were used to diagnose myocarditis. All scans were performed by Phillips Medical Systems Ingenia 1.5T. T1 native values were estimated elevated when mapping values measured above 1030ms, T2 mapping values were estimated elevated when greater than 55 ms. Mid wall or subepicardial late gadolinium enhancement, pericardial effusions and extracardiac findings were evaluated. Chi-square test was used. Result(s): Out of 141 patients, 78 patients (55%) had at least one cardiac magnetic resonance finding: Either increased T1 (22%), T2 mapping (7%), T2 STIR (1.4%), left gadolinium enhancement (30%), small pericardial effusion (26%) or lung parenchymal changes (12%) after COVID-19. Twenty out of 141 patients (14%) fulfilled the criteria for myocarditis. Out of these 20 patients, 14 patients (70%) received treatment at an outpatient clinic, while 6 patients (30%) were treated from COVID-19 in a hospital (p<0.053). The most prevalent symptoms were effort intolerance and palpitations (50% and 26% respectively). There was no statistical difference in myocarditis prevalence, between hospitalized patients treated with or without corticosteroids (p=0.65), as well as between patients treated with hemodiafiltration (Oxiris filter) and patients without hemodiafiltration (p=0.95). Also, there was no statistical difference between T1 mapping among the inpatients and outpatients (p=0.58), as well as the severity of the clinical picture (p=0.72). There was no statistical difference between the in-and outpatient groups according to age (p=0.46). None of these patients had signs of fulminant myocarditis. Conclusion(s): The prevalence of myopericardial and/or lung involvement after SARS-CoV-2 infection is present in every other cardiac magnetic resonance examination performed for persistent symptoms after a survived COVID-19. Myocarditis after SARS-CoV-2 infection develops regardless of the severity of the symptoms or the treatment method. We can conclude that we have to look for the reasons for myocarditis, beyond the clinical picture and the treatment strategies.

Fulminant myocarditis following SARS-CoV-2 mRNA vaccination rescued with venoarterial ECMO: A report of two cases.

INTRODUCTION: Cases of myocarditis after COVID-19 messenger RNA (mRNA) vaccines administration have been reported. Although the majority follow a mild course, fulminant presentations may occur. In these cases, cardiopulmonary support with venoarterial extracorporeal membrane oxygenation (V-A ECMO) may be needed. RESULTS: We present two cases supported with V-A ECMO for refractory cardiogenic shock due to myocarditis secondary to a mRNA SARS-CoV2 vaccine. One of the cases was admitted for out-of-hospital cardiac arrest. In both, a peripheral V-A ECMO was implanted in the cath lab using the Seldinger technique. An intra-aortic balloon pump was needed in one case for left ventricle unloading. Support could be successfully withdrawn in a mean of five days. No major bleeding or thrombosis complications occurred. Whereas an endomyocardial biopsy was performed in both, a definite microscopic diagnosis just could be reached in one of them. Treatment was the same, using 1000mg of methylprednisolone/day for three days. A cardiac magnetic resonance was performed ten days after admission, showing a significant improvement of the left ventricular ejection fraction and diffuse oedema and subepicardial contrast intake in different segments. Both cases were discharged fully recovered, with CPC 1. CONCLUSIONS: COVID-19 vaccine-associated fulminant myocarditis has a high morbidity and mortality but presents a high potential for recovery. V-A ECMO should be established in cases with refractory cardiogenic shock during the acute phase.

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

Fulminant Myocarditis (Fm) Requiring Heart Transplantation: A Rare Sequela of Sars-Cov-2 Infection

Background SARS-CoV-2 infection, the cause of COVID-19, has been associated with myocarditis. Fulminant myocarditis (FM) is rare. Case A 30-year-old male with a past medical history of SARS-CoV-2 infection 7 months prior, presented with a 2-week history of malaise, cough, dyspnea, and signs of cardiogenic shock. He was fully vaccinated 9 months prior. Respiratory viral PCR testing, including SARSCoV-2, was negative. HS-troponin was >20,000 ng/L (NR: 0-53 ng/L). An echocardiogram revealed a dilated cardiomyopathy with an EF of 15-20%. Cardiac catheterization revealed no CAD. Workup for an autoimmune etiology was unrevealing. His condition worsened and he required inotropic support, eventual placement of an LVAD, and initiation of ECMO. He was not able to tolerate cardiac MRI or endomyocardial biopsy. Ultimately, he underwent orthotopic heart transplantation. Pathologic examination of the explanted heart confirmed lymphocytic myocarditis. Decision-making Myocardial injury due to the cardiotropic nature of SARS CoV-2 has been increasingly reported. There has been a 42% increase in viral myocarditis, and the risk is 16 times greater with a history of COVID-19. Symptomatic myocarditis typically manifests within weeks of infection. Such a delayed presentation has not been described. Data from autopsies of deceased COVID-19 patients revealed a 25% to 50% detection rate of SARS-CoV-2 mRNA in the myocardium. One case report described a deceased FM patient with multiple negative SARS-CoV-2 PCR tests, including bronchial lavage samples, having confirmed SARS-CoV-2 within the myocardium postmortem. Hence SARS-Cov-2 can persist in the heart after the resolution of respiratory infection, possibly leading to ongoing inflammation and myocardial damage. This may explain why our patient presented 7 months after a resolved infection. Conclusion SARS-CoV-2 is cardiotropic and can cause fulminant myocarditis even in the absence of a detectable respiratory infection. Hence closer monitoring of post-COVID-19 patients, including screening for subclinical myocarditis, may be prudent. Further research on monitoring and an evaluation of the clinical utility of medical therapy, is also warranted.Copyright © 2023 American College of Cardiology Foundation

A case of COVID-19-associated fulminant myocarditis due to SARS-CoV-2 omicron BA.2 sub-lineage in an unvaccinated female.

COVID-19-associated myocarditis can be a lethal complication in previous variants, but it is not well understood in the Omicron variant. We present an unvaccinated case of COVID-19-associated fulminant myocarditis due to the Omicron BA.2 sub-lineage requiring mechanical circulatory support (MCS). A 66-year-old female without vaccination against SARS-CoV-2 was hospitalized due to COVID-19. On the next day, she was transferred to our hospital due to the development of fulminant myocarditis. After arrival, she was treated with Impella CP and venoarterial extracorporeal membrane oxygenation due to unstable hemodynamics. In addition to MCS, we treated her with inotropes, methylprednisolone, tocilizumab, and remdesivir. Left ventricular contraction gradually improved, and MCS was removed on day 8. Endomyocardial biopsy showed mild interstitial infiltration of CD3+-T lymphocytes and CD68+-macrophages with no remarkable necrosis or fibrosis. This case showed similar histological characteristics to COVID-19-associated myocarditis before the Omicron variant. The vaccination against the Omicron variant should be considered to prevent the development of severe illness, including fulminant myocarditis. Learning objective: Although the Omicron variant is thought to be generally less severe, COVID-19-associated fulminant myocarditis, as in this case, can occur. The vaccination against the Omicron variant should be considered to prevent from developing severe illness.

Fulminant Myocarditis and Cardiogenic Shock Following COVID-19 Infection Versus COVID-19 Vaccination: A Systematic Literature Review.

BACKGROUND: Myocarditis, diagnosed by symptoms and troponin elevation, has been well-described with COVID-19 infection, as well as shortly after COVID-19 vaccination. The literature has characterized the outcomes of myocarditis following COVID-19 infection and vaccination, but clinicopathologic, hemodynamic, and pathologic features following fulminant myocarditis have not been well-characterized. We aimed to compare clinical and pathological features of fulminant myocarditis requiring hemodynamic support with vasopressors/inotropes and mechanical circulatory support (MCS), in these two conditions. METHODS: We analyzed the literature on fulminant myocarditis and cardiogenic shock associated with COVID-19 and COVID-19 vaccination and systematically reviewed all cases and case series where individual patient data were presented. We searched PubMed, EMBASE, and Google Scholar for "COVID", "COVID-19", and "coronavirus" in combination with "vaccine", "fulminant myocarditis", "acute heart failure", and "cardiogenic shock". The Student's t-test was used for continuous variables and the χ2 statistic was used for categorical variables. For non-normal data distributions, the Wilcoxon Rank Sum Test was used for statistical comparisons. RESULTS: We identified 73 cases and 27 cases of fulminant myocarditis associated with COVID-19 infection (COVID-19 FM) and COVID-19 vaccination (COVID-19 vaccine FM), respectively. Fever, shortness of breath, and chest pain were common presentations, but shortness of breath and pulmonary infiltrates were more often present in COVID-19 FM. Tachycardia, hypotension, leukocytosis, and lactic acidosis were seen in both cohorts, but patients with COVID-19 FM were more tachycardic and hypotensive. Histologically, lymphocytic myocarditis dominated both subsets, with some cases of eosinophilic myocarditis in both cohorts. Cellular necrosis was seen in 44.0% and 47.8% of COVID-19 FM and COVID-19 vaccine FM, respectively. Vasopressors and inotropes were used in 69.9% of COVID-19 FM and in 63.0% of the COVID-19 vaccine FM. Cardiac arrest was observed more in COVID-19 FM (p = 0.008). Venoarterial extracorporeal membrane oxygenation (VA-ECMO) support for cardiogenic shock was also used more commonly in the COVID-19 fulminant myocarditis group (p = 0.0293). Reported mortality was similar (27.7%) and 27.8%, respectively) but was likely worse for COVID-19 FM as the outcome was still unknown in 11% of cases. CONCLUSIONS: In the first series to retrospectively assess fulminant myocarditis associated with COVID-19 infection versus COVID-19 vaccination, we found that both conditions had a similarly high mortality rate, while COVID-19 FM had a more malignant course with more symptoms on presentation, more profound hemodynamic decompensation (higher heart rate, lower blood pressure), more cardiac arrests, and higher temporary MCS requirements including VA-ECMO. In terms of pathology, there was no difference in most biopsies/autopsies that demonstrated lymphocytic infiltrates and some eosinophilic or mixed infiltrates. There was no predominance of young males in COVID-19 vaccine FM cases, with male patients representing only 40.9% of the cohort.

Cardiac recovery from COVID-19-associated fulminant myocarditis by extracorporeal biventricular assist.

We report a case of cardiac recovery from coronavirus disease 2019 (COVID-19)-associated fulminant myocarditis in a 48-year-old woman diagnosed with COVID-19 infection 4 days before, whose hemodynamic collapse were resuscitated first with venoarterial extracorporeal membranous oxygenation, followed by escalation to extracorporeal biventricular assist devices (ex-BiVAD) using two centrifugal pumps and an oxygenator. She was likely to be multisystem inflammatory syndrome in adults (MIS-A) negative. Cardiac contractility gradually recovered after the 9th day of ex-BiVAD support, and the patient was successfully weaned from ex-BiVAD on the 12th day of support. Due to postresuscitation encephalopathy, she was transferred to the referral hospital for rehabilitation with recovered cardiac function. The histopathology of the myocardial tissue showed smaller amounts of lymphocytes and more infiltration of macrophages. It is important to recognize two phenotypes of MIS-A+ or MIS-A-, with distinct manifestations and outcomes. It is also important to refer urgently such patients with COVID-19-associated fulminant myocarditis, showing different histopathology from usual viral myocarditis, with evolution toward refractory cardiogenic shock to a center with capability for advanced mechanical support to avoid a too-late cannulation. Learning objective: We should recognize the clinical course and histopathology of the multisystem inflammatory syndrome in adults phenotype of coronavirus disease 2019-associated fulminant myocarditis. We should urgently refer such patients with evolution toward refractory cardiogenic shock to a center with capability for advanced mechanical support, such as venoarterial extracorporeal membrane oxygenation, Impella (Abiomed, Danvers, MA, USA), and extracorporeal biventricular assist devices.

Fulminant myocarditis with COVID-19 infection having normal C-reactive protein and serial magnetic resonance follow-up.

A 44-year-old woman who was quarantined for 5 days after the diagnosis of coronavirus disease of 2019 (COVID-19) was transferred to our hospital with the complaint of chest pain. The patient was unvaccinated. Electrocardiography revealed ST elevation in the lateral leads. Echocardiographic biventricular dysfunction with oedematous wall thickening was identified. Cardiac enzyme levels were elevated; however, C-reactive protein (CRP) levels, and the coronary angiogram were normal. The patient required mechanical circulatory support to stabilize haemodynamics and was treated with remdesivir, baricitinib, and intravenous methylprednisolone. She recovered after 13 days of mechanical support. Serial cardiac magnetic resonance imaging revealed acute myocardial oedema and subsequent fibrosis. An endomyocardial biopsy on admission showed mild interstitial inflammatory infiltrates with endomyocardial fibrous thickening and mild interstitial fibrosis of the myocardium. Normal CRP levels suggested minor involvement of interleukin (IL)-6, supporting the efficacy of baricitinib.

Research focus and theme trend on fulminant myocarditis: A bibliometric analysis.

Aims: This study intends to explore the research focus and trends of fulminant myocarditis (FM) to have a better understanding of the topic. Materials and methods: The data were downloaded from the Web of Science (WoS) database using the topic (TS) advanced search strategy. Many instruments were used to extract, analyze, and visualize the data, such as Microsoft Excel, HistCite Pro, GunnMap, BibExcel, and VOSviewer. Results: From 1985 to 2022, 726 documents were indexed in the WoS. The United States and Columbia University were the most productive country and institutions. Keywords co-occurrence was carried out and four research themes were identified. In addition, the top three prolific authors, the first three highly cited authors, and the core authors of the author co-citation network were identified. The topics that they kept an eye on were analyzed, and the research areas of key authors were similar to the results of keyword co-occurrence. The hot topics of FM were related to the mechanical circulatory support, etiology, diagnosis, and the disease or therapy associated with FM. Conclusion: This study carried out a systematic analysis of the documents related to FM from 1985 to 2022, which can provide a guideline for researchers to understand the theme trend to promote future research to be carried out.

Full myocardial recovery following COVID-19 fulminant myocarditis after biventricular mechanical support with BiPella: a case report.

Background: Fulminant myocarditis is a rare yet dreadful condition, which requires evaluation for mechanical support. The concomitant use of an Impella pump in the left and of one in the right ventricle-the so-called 'BiPella approach'-might allow recovery of the failing heart in selected cases. We report a peculiar case, in which mechanical circulatory support was used as the sole strategy to promote myocardial recovery, without the administration of any immunosuppressants in coronavirus disease (COVID)-19 fulminant myocarditis. Case summary: A previously healthy 49-year-black man presented to the emergency department with dyspnoea and severe metabolic acidosis. His nasopharyngeal swab resulted positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Echocardiography documented severe biventricular dysfunction which required support with two Impella pumps-the so-called 'BiPella approach'. Myocarditis was suspected on clinical basis. Endomyocardial biopsy showed SARS-CoV-2 localization within the endothelial cells. No antiviral or immunosuppressive therapy was administered. After 10 days of support, the patient was weaned from both right- and left-ventricular supports as complete recovery of cardiac function and end-organ damage was observed. The patient was discharged from the intensive care unit after 15 days and discharged home 1 month after presentation. The patient had no further episodes of heart failure at 6 months follow up. Discussion: Prolonged mechanical unloading with two Impella pumps in fulminant COVID-19 myocarditis is a viable and reliable strategy, as it provides the benefits of mechanical circulatory support plus additional disease-modifying effects, reducing wall stress and inflammatory response.

A case of COVID-19-associated fulminant myocarditis successfully treated with mechanical circulatory support.

A 49-year-old man, who had not been vaccinated against COVID-19 visited the hospital for fever and cough, and a PCR test for COVID-19 was positive on the Day X. Initially, there was no decrease in oxygen saturation and the patient was under observation as a mild case without medication. Five days after the onset (Day X + 5), chest pain appeared. Electrocardiogram showed widespread ST-segment elevation, and blood tests showed high levels of troponin I. However, given that there was no stenotic lesion on coronary computed tomography, myocarditis was suspected, and he was transferred to our hospital on the Day X + 6. We started treatment with lemdesivir and dexamethasone. On the Day X + 7, the patient developed decreased left ventricular ejection fraction, hypotension, and hyperlactatemia. We decided that mechanical circulatory support was necessary and an Impella 5.0 was inserted under ventilator management. The patient was successfully weaned from the Impella 5.0 on the Day X + 17, was transferred to the general ward on the Day X + 24, continued rehabilitation, and was discharged home on the Day X + 39 with no heart failure symptoms. In this case, we performed daily bedside echocardiography and chose the Impella 5.0 instead of extra corporeal membrane oxygenation (ECMO) because there were no findings of severe pneumonia or right heart failure. The Impella 5.0 device was inserted via an axillary artery approach, given that it provides more assisted flow than the Impella CP inserted through the inguinal route. Furthermore, early rehabilitation was possible due to the lack of restriction of the lower body.

Case Report: Successful Treatment of a Child With COVID-19 Reinfection-Induced Fulminant Myocarditis by Cytokine-Adsorbing oXiris® Hemofilter Continuous Veno-Venous Hemofiltration and Extracorporeal Membrane Oxygenation.

Background: Indirect cardiomyocyte damage-related hyperinflammatory response is one of the key mechanisms in COVID-19-induced fulminant myocarditis. In addition to the clinical benefit of using cytokines absorption hemofiltration, the effectiveness of instituting veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support for cardiac compromise has been reported. However, current literature enunciates a paucity of available data on the effectiveness of these novel modalities. Case Presentation: We reported a 9-year-old boy with recurrent COVID-19 infection-causing fulminant myocarditis, who was treated successfully by using novel modalities of oXiris ® hemofilter continuous venovenous hemofiltration (CVVH) and VA-ECMO. The patient made a full recovery without any sequelae. Conclusion: We conclude that the novel highly-absorptive hemofilter CVVH and VA-ECMO may be effective treatment modalities in managing SARS-CoV-2-induced fulminant myocarditis. Our report highlights the need for further well-designed investigations to confirm this extrapolation.

Phenotypic Heterogeneity of Fulminant COVID-19--Related Myocarditis in Adults.

BACKGROUND: Adults who have been infected with SARS-CoV-2 can develop a multisystem inflammatory syndrome (MIS-A), including fulminant myocarditis. Yet, several patients fail to meet MIS-A criteria, suggesting the existence of distinct phenotypes in fulminant COVID-19-related myocarditis. OBJECTIVES: This study sought to compare the characteristics and clinical outcome between patients with fulminant COVID-19-related myocarditis fulfilling MIS-A criteria (MIS-A+) or not (MIS-A-). METHODS: A monocentric retrospective analysis of consecutive fulminant COVID-19-related myocarditis in a 26-bed intensive care unit (ICU). RESULTS: Between March 2020 and June 2021, 38 patients required ICU admission (male 66%; mean age 32 ± 15 years) for suspected fulminant COVID-19-related myocarditis. In-ICU treatment for organ failure included dobutamine 79%, norepinephrine 60%, mechanical ventilation 50%, venoarterial extracorporeal membrane oxygenation 42%, and renal replacement therapy 29%. In-hospital mortality was 13%. Twenty-five patients (66%) met the MIS-A criteria. MIS-A- patients compared with MIS-A+ patients were characterized by a shorter delay between COVID-19 symptoms onset and myocarditis, a lower left ventricular ejection fraction, and a higher rate of in-ICU organ failure, and were more likely to require mechanical circulatory support with venoarterial extracorporeal membrane oxygenation (92% vs 16%; P < 0.0001). In-hospital mortality was higher in MIS-A- patients (31% vs 4%). MIS-A+ had higher circulating levels of interleukin (IL)-22, IL-17, and tumor necrosis factor-α (TNF-α), whereas MIS-A- had higher interferon-α2 (IFN-α2) and IL-8 levels. RNA polymerase III autoantibodies were present in 7 of 13 MIS-A- patients (54%) but in none of the MIS-A+ patients. CONCLUSION: MIS-A+ and MIS-A- fulminant COVID-19-related myocarditis patients have 2 distinct phenotypes with different clinical presentations, prognosis, and immunological profiles. Differentiating these 2 phenotypes is relevant for patients' management and further understanding of their pathophysiology.

Fulminant Myocarditis Following SARS-CoV-2 Infection: JACC Patient Care Pathways.

A 60-year-old woman with a past medical history of asthma presented with fulminant myocarditis 9 days after testing positive for SARS-CoV-2 and 16 days after developing symptoms consistent with COVID-19. Her hospital course was complicated by the need for veno-arterial extracorporeal membrane oxygenation, ventricular arrhythmias, and pseudomonas bacteremia. She ultimately recovered and was discharged to home with normal left ventricular systolic function. Thereafter, she developed symptomatic ventricular tachycardia, for which she received an implantable cardioverter-defibrillator and antiarrhythmic drug therapy.

ACUTE PEDIATRIC MYOCARDITIS BEFORE AND DURING SARS-CoV-2 PANDEMIC

Introduction: Acute myocarditis (AM) is an inflammatory disease of the myocardium. Myocardial injury in COVID-19 could appear as a result of the directvirus attacking, or viral-inducedmyocardial inflammationas a consequence of the aggressiveimmuneresponse.The aim of our study is a comparative analysis of the difference between children with AM before and during the SARS-CoV-2 pandemic. Methods: The retrospective analysis included all patients treated in our Institute with a diagnosisofAMfromJanuary2018toNovember 2020. Results: 24 patients were included in the study;in all patients (7/24) treated from April to November 2020, the infection was caused by SARS-CoV-2 (2 PCR, 5 serological tests of IgM antibodies). All patients with AM during the pandemic were older than 7 years. They were more likely to have abdominal pain (p=0.014), headache (p=0.003), cutaneous rash (p=0.003), conjunctivitis (p=0.003), while fulminant myocarditis was more commonly registered before the pandemic (p=0.04). A multisystem inflammatory syndrome in children associated with COVID-19 was present in 6 patients. Patients with AM in the pandemic had significantly lower values of troponin I (cTnI) (p=0.012), and platelets (p<0.001), but higher values of serum creatinine (p=0.013) and CRP (p=0.04) compared with patients before the pandemic. In the group of patients during the pandemic, a significant CRP reduction (p=0.007) was observed on the day of discharge compared to admission value. In the group of patients before the pandemic, cTnI values were significantly reduced (p=0.002). A significant recovery of systolic function was registered on the third in-hospital day in the group of patients presented during the pandemic (EF p=0.001;FS p=0.019);improvement was not observed in the group before COVID-19 pandemic. Adverse events were observed frequently in patients before the pandemic (p=0.04;3 died, and 4 dilated cardiomyopathy). Conclusions: In contrast to patients before the pandemic, in patients with AM during the COVID-19 pandemic, significantly higher values of inflammatory parameters, polymorphic clinical presentation as well as prompt recovery of LV function after applied therapy noticed in patients during SARS-CoV-2 pandemic underlie a possible new spectrum inflammatory disease with consequence viral-related myocardial inflammation with favorable prognosis.