Late gadolinium enhancement following covid-19 infection does not predict outcome: a single-centre study

182 Figure 1Cardiovascular events in COVID-19 Survivors by LGE Status[Figure omitted. See PDF] 182 Figure 2All-cause mortality in COVID-19 Survivors by LGE Status[Figure omitted. See PDF]Conflict of InterestNone

PPP1R13L-Related Cardiomyopathy Stability Following IL1 Inhibition

Introduction: Variants in PPP1R13L are associated with severe childhood-onset cardiomyopathy resulting in rapid progression to death or cardiac transplantation. PPP1R13L is proposed to encode a protein that limits the transcriptional activity of the NFkappaB pathway leading to elevated IL-1, IL-6, and TNF-alpha production in murine models. Optimal medical management for PPP1R13L-related cardiomyopathy is unknown. Here we report usage of a targeted anti-IL-1 immuno-modulatory therapy resulting in cardiac stabilization in a pediatric patient with congenital cardiomyopathy secondary to PPP1R13L variants. Case Report: A 4-year-old boy presented acutely with fever in the setting of persistent abdominal pain, vomiting, fatigue, and decreased appetite for two months following a mild COVID-19 related illness. Echocardiogram revealed severely depressed biventricular systolic function with an ejection fraction of 30%. Due to acute decompensated heart failure symptoms with hemodynamic instability, he was intubated and placed on continuous inotropic infusions with aggressive diuresis. Cardiac MRI demonstrated extensive subepicardial to near transmural fibrosis by late gadolinium enhancement in right and left ventricles. An implantable cardioverter-defibrillator (ICD) was placed due to frequent runs of polymorphic non-sustained ventricular tachycardia. Testing for viral pathogens was positive for rhino/enterovirus. Initial genetic testing was non-diagnostic (82-gene cardiomyopathy panel) but given the patient's significant presentation whole genome sequencing was pursued that showed two separate PPP1R13L variants in trans (c.2167A>C,p.T723P and c.2179_2183del,p. G727Hfs*25, NM_006663.4). Patient serum cytokine testing revealed elevations in IL-10 (4.7 pg/mL) and IL-1beta (20.9 pg/mL). Given the patient's tenuous circumstances and concern for continued progression of his cardiac disease, a trial of IL-1 inhibition via anakinra dosed at 3 mg/kg or 45 mg daily was initiated following hospital discharge. With approximately 6 months of therapy, the patient's cardiac function is stable with normalization of IL-10 and IL-1beta serum levels. Notably, the ventricular arrhythmia decreased after initiation of anakinra with no ICD shocks given. Therapy overall has been well tolerated without infectious concerns. Conclusion(s): In patients with PPP1R13L-related cardiomyopathy, immuno-modulatory therapies should be considered in an attempt to slow cardiac disease progression.Copyright © 2023 Elsevier Inc.

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

Covid-19 Vaccine Associated Acute Myocarditis

Case Presentation: A 19 year old male presented with sudden onset chest pain radiating to back. He was a smoker and denied using cocaine since his last hospitalization for cocaine-induced myocardial infarction 2 years ago. UDS was negative. EKG showed normal sinus rhythm with no ST-T wave changes. Initial troponin was 0.850. Potassium levels were low at 2.9 mmol/L but other labs were normal. Chest CT angiography ruled out aortic dissection. He was started on heparin drip. Stat Echocardiogram showed LVEF of 55-60% with no wall motion abnormalities. Repeat potassium levels normalized after replacement, however, his troponins were trending up from 3.9 and 11.5. He continued to complain of severe chest pain, so underwent cardiac catheterization which showed normal coronary arteries and LVEF 55-60%. Heparin drip was discontinued and NSAIDs and colchicine were started. Cardiac MRI (see Figure) was done that showed patchy mid-wall and epicardial delayed gadolinium enhancement involving the basal inferolateral wall, with mild hyperintense signal on the triple IR sequence, suggestive of myocarditis. On further probing, he reported receiving a second dose of Moderna COVID vaccine 3 days prior to presentation. Discussion(s): In December 2019, a novel RNA virus causing COVID-19 infection was reported, which quickly reached a pandemic level. COVID-19 vaccines were granted emergency use authorization by FDA. With millions of people receiving COVID-19 vaccinations worldwide, rare adverse effects are now being reported. The benefits of vaccination undoubtedly outweigh any minor side effects. However major adverse effects like this are potentially fatal. This case report warrants further investigation into the association of myocarditis with COVID-19 vaccinations and further recommendations regarding vaccination in younger adults.

Delayed type hypersensitivity reaction to oral intake of trometamol

Case report Trometamol (tromethamine, tris(hydroxymethyl)aminomethane (TRIS)) is an excipient frequently used as buffer in fluids and semisolid agents, including many drugs such as antibiotics, iodinated contrast agents and the COVID-19 vaccine mRNA-1273. Here, we report the first case of a delayed-type hypersensitivity after oral intake of trometamol. A 64-year- old female patient presented to our emergency department with generalized erythematous rash, pruritus and swelling of the face five hours after the intake of one tablet of fosfomycin trometamol for a urinary tract infection. Further medical history revealed a previous erythematous rash five to six hours after administration of the iodinated contrast agent iopromide. We performed skin prick and intradermal tests with trometamol, fosfomycin trometamol and various iodinated contrast agents, including iopromide, iomeprol, iobitridol, iopamidol and iodixanol. These tests showed no reactions initially. However, 48 hours after intradermal testing, macular erythematous lesions developed at the sites tested with trometamol 0.1%, trometamol 0.01% and all sites tested with iodinated contrast agents. Furthermore, when we performed a lymphocyte transformation test with trometamol, fosfomycin trometamol and iopromide, we recorded a positive reaction with cytokine release after stimulating T cells with trometamol and iopromide. In contrast, basophil activation testing showed a negative result for these agents. Based on these results and our patient's history, we diagnosed a clinically relevant type IV sensitization to trometamol. There are only a few case reports about immediate-type allergic reactions to gadolinium contrast agents caused by the excipient trometamol. There are some published cases which report contact dermatitis after topical administration of trometamol-containing agents. To our knowledge, ours is the first case to report a delayed hypersensitivity reaction to oral administration of trometamol. Excipients are indispensable for drugs, vaccines and other products since they stabilize and preserve the active agents. Nevertheless, excipients should always be considered during an allergy workup, especially if the patient reports prior drug reactions that cannot be explained by a chemical cross-reaction. In our case, we diagnosed delayed-type hypersensitivity to the excipient trometamol. This is a consequential diagnosis for the patient, because trometamol is contained in many drugs and in the COVID-19 vaccine mRNA-1273.

Predictors and clinical consequences of heart damage in CMR in patients after COVID-19

Methods: Out-hospital clinic patients (pts) recovered from COVID-19 were prospectively recruited and underwent cardiac magnetic resonance (CMR) examination with a protocol including: Edema, hyperemia, and necrosis or scar-derived from signal intensity assessment in T2-weighted, early gadolinium enhancement (EGE) and late gadolinium enhancement (LGE) CMR images. Result(s): A total of 702 patients (mean age 50+/-12 years, 62% female) were included. The median (IQR) time interval between COVID-19 diagnosis and CMR was 13 (8-22) weeks. In none pts signs of edema, hyperemia and necrosis derived from signal intensity assessment in T2-weighted and early gadolinium enhancement was found. LGE was found in 152 (22%). LGE+ patients had significantly lower left ventricular (LV) ejection fraction (58.5+/-7.7 vs 61.1+/-7.9%, p<0.001) and greater LV end-diastolic (117.0+/-52.2 vs 103,0+/-36.3 ml, p=0.023) and end-systolic (50.3+/-28.0 vs 41.0+/-17.5 ml, p=0.010) volumes when compared with LGE- patients. In the resting electrocardiogram (ECG) fragmented QRS was observed significantly more frequently (46% vs 25%, p<0.001) in LGE+ group, whereas in 24h Holter ECG neither single premature, nor complex ventricular extrasystole burden did not differ between groups (p>0.05). There were observed no differences between symptoms of COVD-19 and comorbidities between LGE+ and LGE- pts. In the multivariable logistic regression analysis: Fragmented QRS [OR and 95% CI: 2.85 (1.93-4.21)] and any ST-T segment deviation in resting ECG [OR: 1.93 (1.15-3.25)] were identified as independent predictors of LGE, even after adjustment for comorbidities and COVID-19 symptoms. Conclusion(s): 1. In patients with fibrosis after COVID-19 reduced left ventricular ejection fraction and greater volume of the heart was found. 2. Fragmented QRS and ST-T abnormalities were independent predictors for LGE in patients after COVID-19.

Frequency of Pathological MRI Findings in Suspected Myocarditis during the COVID-19Pandemic

Background: COVID-associated and vaccine-triggered myocarditis in young people have received much attention over the course of the pandemic due to early results of vaccination associated myocarditis. This may have led to an increase in myocarditis suspicions. In this study we wanted to examine the actual amount of COVID-associated myocarditis in ourtertiary center. Method(s): We included all cardiac MRIs performed in our institution for the indication of suspected myocarditis between 2020and 2022. We excluded patients with primary cardiomyopathy. We divided the patients into three groups: Group 1 had noCOVID infection or COVID-vaccine associated with their suspected myocarditis, group 2 had received a COVID vaccination prior to developing symptoms, group 3 had had an acute COVID infection and group 4 had a clinical diagnosis of Pediatric inflammatory multisystem syndrome (PIMS). Result(s): Overall, 28 patients had MRIs for suspected myocarditis performed at our center in the investigated time frame. They were 10 to 18 years of age (mean: 15.1 years). Symptoms included chest pain, fatigue, palpitations and reduction in exercise tolerance. Nineteen patients were in group one, 4 patients had symptoms associated with COVID vaccination, three had acute infection and two had a clinical diagnosis of PIMS. Late gadolinium enhancement (LGE) was found in 7 patients. None of these were in groups 2 or 3. Both patients with PIMS(n = 2) had myocarditis on biopsy but only one on MRI. Myocardial biopsy was performed in 8 patients. They showed myocarditis in 6 patients. Apart from the PIMS cases, none of them were associated with Corona infection or COVID vaccine. Three patients had parvovirus B19 on biopsy and one also had EBV. One of the PIMS patients also had HHV6. Theother four biopsies did not yield any viral DNA on PCR. Conclusion(s): Myocarditis associated with acute COVID infection or vaccination was not found in our cohort. Exercise intolerance or chest pain was not reliable indicators of cardiac causes. Even in the pandemic, coronavirus and COVID-19vaccines are unlikely causes of myocarditis. Most cases were associated with classic cardiotropic viruses. However, in cases of PIMS, cardiac involvement is likely and should be investigated accordingly.

Unusual Myositis of the Temporalis Muscle Occurring with Acute Covid-19

Background. SARS-CoV-2 infection can be accompanied by neuromuscular disorders. Rhabdomyolysis and Guillain-Barre syndrome have been described repeatedly. There are case reports of inflammatory myopathies manifesting during COVID-19, presenting as dermatomyositis, polymyositis or immune-mediated necrotizing myopathy, with dermatomyositis-like presentations most commonly reported. Larger cases series are from postmortem examinations of COVID-19 patients, where variable inflammatory pathology of the skeletal muscle has been found frequently but without local detection of the actual virus. Thus, autoimmune mechanisms or the systemic interferon response are discussed as causes. We report a case of focal inflammatory myopathy with perimysial pathology of the temporalis muscle occurring with acute, but mild COVID-19. Methods. Case report of clinical observations, cranial MRI, histopathological, and laboratory findings. 3T cranial MRI was performed with gadolinium contrast. Open temporalis muscle biopsy was performed. The sample underwent standard cryohistological studies as well as immunohistochemistry with antibodies against MHC-I and II, CD3, CD4, CD19, CD68, anti-MAC, p62 and MxA. Testing for auto-antibodies was based on immunoblots or ELISA. RT-PCR for SARS-CoV-2 was run with RNA extracted from cryopreserved muscle. Results. A Caucasian woman in her 60s with no history of autoimmune or muscle complaints developed swelling and pain of the right jaw musculature five days after testing positive for SARS-CoV-2 due to respiratory tract symptoms. In addition, she experienced trismus, but no further neuromuscular complaints. The course of respiratory tract symptoms stayed mild. She had been vaccinated previously with single shot SARS-CoV-2 vector vaccine. Due to persistent swelling and complaints, giant cells arteritis was excluded by unresponsiveness to five days oral steroids and sonography of the temporal artery. Cranial MRI was performed nearly four weeks after the SARS-CoV-2 infection and showed marked swelling and oedema of the temporalis muscle. Its biopsy showed numerous CD68 and acid phosphatase positive cells infiltrating from perimysial perivascular foci towards the endomysium with perimysial damage but little damage of adjacent, perifascicular muscle fibres. Muscle fibres did not react with anti-MHC-II, anti-MAC or -MxA. Capillaries did not react with anti-MAC or -MxA. SARS-CoV-2 RNA was not detected in muscle tissue. Serum creatine kinase was not elevated in the subacute phase. Slightly elevated ANA titre led to detection of autoantibodies against proliferating cell nuclear antigen (PCNA). No pathological results for other autoantibodies, including myositis-specific antibodies and anti-ds-DNA, were found in blood. Neither were antibodies against hepatitis C and B viruses. Retesting 15 weeks after infection, anti-PCNA immunoblot was still positive, but ELISA did not indicate a pathologic titre. The swelling, myalgia and trismus regressed spontaneously a month after onset, yet the latter still persists at the time of reporting. Conclusion. Our case diverges from the majority of COVID-19 associated my-ositis reports in the unusual location of the focal myositis and the histopathological pattern of predominantly perimysial damage and histiocytic infiltration. It concurs with the literature as no SARS-CoV2 RNA could be detected in the muscle. Anti-PCNA is associated very rarely with myositis. Other associated disorder (systemic lupus erythematosus, chronic viral hepatitis B or C) were not found. Increased levels of autoantibodies are reported in COVID-19 and mostly attributed to loss of self-tolerance during the acute disease phase. Interestingly, the structural protein M of SARS-CoV-2 appears to interact notably with PCNA in infected cells. Still, the causal connection between the myositis and COVID-19 in this case is based on the close temporal association in the absence of alternative, competing explanations from the medical history and findings.

Relationships between plasma cytokine balance and cardiac magnetic resonance imaging in long-term post-COVID follow-up: A cross-sectional preliminary study

Background: COVID-19 infection can lead to a constellation of longlasting post-infectious sequelae, including myocardial dysfunction, whose outcome is strongly affected by a fine-tuned balance between pro-and anti-inflammatory systemic immune responses. Plasma cytokines are key mediators of this immunological balance. In this preliminary study we evaluated the cross-sectional association between the circulating levels of the main pro-and anti-inflammatory cytokines and cardiac magnetic resonance (CMR) abnormalities. Method(s): 71 subjects (59% female, mean age 52+/-14) with previous diagnosis of COVID-19 infection were enrolled at our institution for MULTICOVID protocol, comprehensive of CMR and biomarkers assessment performed >3 months and <1 year following the first negative swab test. CMR protocols consisted of conventional sequences (cine, T2-weighted imaging, and late gadolinium enhancement [LGE]) and quantitative mapping sequences (T1, T2, and extracellular volume [ECV] mapping). Plasma levels of cytokines TNF-alpha, IL-1beta, IL-1alpha, IFN-alpha2, IL-6, IL-8, IL-13, IL-10, IL-17A, IL-18, IP-10, MIG and MCP-1 were quantified by Multiplex Immunoassays on the Luminex technology platform. Soluble cardiologic and biochemical biomarkers were measured by routine laboratory analysis. Result(s): After a median of 9 (IQR 6-11) months following negative swab, CMR was normal in 48 subjects, while in 23 (32%) it revealed tissue characterization abnormalities (myocardial late enhancement and/or edema). By multivariate regression analysis (adjusted for age, sex, vaccination, severity degrees of the initial COVID disease, presence of comorbidities, smoke, time interval between COVID diagnosis and CMR assessment) the cytokine ratio TNF-alpha/(IL-10+IL-13) was independently associated (OR=2.89, 95% CI 1.19-7.04, p=0.02) with CMR abnormalities. Interestingly, the cumulative pro-/anti-inflammatory cytokine ratio (IL-1beta+TNF-alpha+IFN-alpha2+IL-6+IL-17A+IL-8)/(IL-10+IL-13) showed a positive (OR=1.70, 95% CI: 1.04-2.75) and significant (p=0.03) association with CMR imaging aspects. Also, the ratio IFN-alpha2/(IL-10+IL-13), although without achieving a complete statistical significance (p=0.09), was associated positively with CMR findings. Conclusion(s): The preliminary results of this cross-sectional study suggest that the systemic inflammatory environment, long-lasting unbalanced towards a prevalent cytokine-driven pro-inflammatory condition following COVID infection, could affect the development of CMR-detectable myocardial edema and fibrosis in long-term post-COVID subjects.

CMR Tissue Characterization and Course of Acute SARS-CoV-2 type B.1.1.529-Associated Myocarditis in a Professional Soccer Player

› We report the case of a young professional soccer player who underwent cardiac MRI (CMR) for work-up of discrete intermit-tent chest pain and subtle ST segment elevations in the ECG after having been tested positive for SARS-CoV-2 type B.1.1.529 despite full vaccination including recent mRNA booster. › Troponin levels were significantly increased and myocarditis was suspected. Comprehensive CMR including CINE and late gadolinium enhancement as well as multi-parametric T1/T2 mapping techniques revealed local hypokinesia and swelling of the posterolateral wall with non-ischemic late gadolinium enhancement and increased T2 relaxation time compatible with acute viral myocarditis. The patient was admitted to a cardiology ward for rhythm and troponin monitoring and was discharged after two days of uneventful rhythm monitoring and with decreased troponin levels. › Adhering to current recommendations the patient was advised to abstain from moderate-to high-intensity sports and exercise for 3-6 months. After 6 months of exercise avoidance, follow-up ECG showed regression of prior ST segment elevations, and Holter ECG as well as a treadmill exercise stress test did not reveal any abnormalities. Follow-up CMR was performed before return-to-sports which revealed persisting myocardial fibrosis but complete regression of myocardial edemam and excluded ongoing inflammation. › This example underscores the value of multi-parametric CMR tissue characterization for the work-up of suspected SARS-CoV-2 associated myocarditis, as well as for follow-up before return-to-sports. © 2023, Dynamic Media Sales Verlag. All rights reserved.

Superior Cerebellar Artery Dissection in a Patient Diagnosed with Reversible Cerebral Vasoconstriction Syndrome: A Case Report

Arterial dissection is an uncommon complication of reversible cerebral vasocon-striction syndrome (RCVS). We describe the case of a 35-year-old woman with a migraine history who presented with recurrent thunderclap headache and focal neurological signs, including right hemiataxia. She had been diagnosed with COVID-19 disease two weeks earlier. Neuroimaging revealed multifocal stenosis of the posterior circulation arteries and dissection of the right superior cerebellar artery. She improved significantly throughout her one-week hospitalization and maintained only mild ataxia. The interplay between COVID-19 disease, RCVS, and arterial dissection requires further investigation.Copyright © Author(s) (or their employer(s)) and Sinapse 2022.

Early switch from cladribine to alemtuzumab in highly-active relapsing-remitting multiple sclerosis: A case report

Background Management of patients with multiple sclerosis (MS) and evidence of disease activity during treatment with cladribine tablets represents a challenging point. Objectives To report a patient with highly active multiple sclerosis (HAMS) who has been early switched from cladribine to alemtuzumab owing to tumultuous clinical and radiological activity Methods A single retrospective case report. Results. Treatment with alemtuzumab has led to a complete suppression of disease activity without any evidence of infections or acquired autoimmune diseases. Conclusion Our report suggests that an early switch from cladribine to alemtuzumab, may be safe and efficacious in selected HAMS cases.Copyright © 2022 The Authors

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.

Myocarditis Following Covid-19 Vaccination In Adolescents And Adults In 2021

Background: Clinical course and outcomes of myocarditis after COVID-19 vaccination remain variable. Method(s): We retrospectively collected data on patients >12 years old from 01/01/2021 to 12/30/2021 who received COVID-19 vaccination and were diagnosed with myocarditis within 60 days of vaccination. Myocarditis cases were based on case definitions by authors. Result(s): We report on 238 patients of whom most were male (n=208;87.1%). The mean age was 27.4 +/- 16 (Range 12-80) years. Females presented at older ages (41.3 +/- 21.5 years) than men 25.7 +/- 14 years (p=0.001). In patients >20 years of age, the mean duration from vaccination to symptoms was 4.8 days +/-5.5 days but in <20, it was 3.0 +/- 3.3 days (p=0.04). Myocarditis occurred most commonly after the Pfizer-BioNTech vaccine;(n=183;76.45) and after the second dose (n=182;80%). Symptoms started 3.95 +/-4.5 days after vaccination. The commonest symptom was chest pain (n=221;93%). Patients were treated with non-steroidal anti-inflammatory drugs (n=105;58.3%), colchicine (n=38;21.1%), or glucocorticoids (n=23;12.7%). About 30% of the patients had left ventricular ejection fraction but more than half recovered on repeat imaging. Abnormal cardiac MRI was common;168 patients (96% of 175 patients that had MRI) had late gadolinium enhancement, while 120 patients (68.5%) had myocardial edema. Heart failure guideline-directed medical therapy use was common (n=27;15%). Eleven patients had a cardiogenic shock, and 4 patients required mechanical circulatory support. Five patients (1.7%) died, of these, 3 patients had endomyocardial biopsy/autopsy-confirmed myocarditis. Conclusion(s): Most cases of COVID-19 vaccine myocarditis are mild. Females presented at older ages than men and the duration from vaccination to symptoms was longer in patients >20 years. Cardiogenic shock requiring mechanical circulatory support was seen and mortality was low. Future studies are needed to better evaluate risk factors and long-term outcomes of COVID-19 vaccine myocarditis.Copyright © 2022

Evaluation of cardiac involvement in patients with clinical post-COVID-19 syndrome

Introduction: The underlying pathophysiology of Post-COVID-19 syndrome remains unknown, but increased cardiometabolic demand and state of mitochondrial dysfunction have emerged as candidate mechanisms. Cardiovascular magnetic resonance (CMR) provides insight into pathophysiological mechanisms underlying cardiovascular disease and 31-phosphorus magnetic resonance spectroscopy (31P-MRS) allows noninvasive assessment of the myocardial energetic state. Purpose(s): We sought to assess whether Post-COVID-19 syndrome is associated with abnormalities of myocardial structure, function, perfusion and tissue characteristics or energetic derangement. Method(s): Prospective case-control study. A total of 20 patients with a clinical diagnosis of Post-COVID-19 syndrome (seropositive) and no prior underlying cardiovascular disease (CVD) and ten matching controls underwent 31P-MRS and CMR at 3T at a single time point. (Figure 1) All patients had been symptomatic with acute COVID-19, but none required hospital admission. Result(s): Between the Post-COVID-19 syndrome patients and matched contemporary controls there were no differences in myocardial energetics (phosphocreatine to ATP ratio), in cardiac structure (biventricular volumes, left ventricular mass), function (biventricular ejection fractions, global longitudinal strain), tissue characterization (T1 and extracellular volume [ECV] fraction mapping, late gadolinium enhancement) or perfusion (myocardial rest and stress blood flow, myocardial perfusion reserve). One patient with Post-COVID-19 syndrome showed subepicardial hyperenhancement on the late gadolinium enhancement imaging compatible with prior myocarditis, but no accompanying abnormality in cardiac size, function, perfusion, ECV, T1, T2 mapping or energetics. This patient was excluded from statistical analyses. (Table 1) Conclusion(s): In this study, the overwhelming majority of patients with a clinical Post-COVID-19 syndrome with no prior CVD did not exhibit any abnormalities in myocardial energetics, structure, function, blood flow or tissue characteristics.

Structural Valve Dysfunction As An Atypical Presentation Of Cardiac Sarcoidosis

Introduction: Cardiac sarcoidosis (CS) classically manifests as a restrictive cardiomyopathy or conduction abnormalities, though the full scope of phenotypes may be underrecognized. We present an atypical case of mitral regurgitation (MR) and aortic regurgitation (AR) attributed to CS. Case Presentation: A 33-year-old woman with a history of hypertension, tobacco use, and COVID-19 infection two months prior presented with worsening dyspnea on exertion, orthopnea and lower extremity edema. Initial work up revealed elevated pro-BNP and troponin, and a CXR with pulmonary edema. A prior CTA showed mediastinal and hilar lymphadenopathy. Echocardiogram was notable for mildly dilated LV, severe hypokinesis of the basal inferior myocardium, LVEF 50-55%, moderate MR and moderate AR. cMR revealed multiple foci of predominantly mid-wall late gadolinium enhancement (LGE) in the LV, including a focus adjacent to the posteromedial papillary muscle (Fig. 1). Cardiac PET showed extensive patchy, focal hypermetabolic activity in the LV inferobasal, anterobasal and anterolateral walls. With high suspicion for CS, the patient opted for treatment with steroids and follow-up PET over extracardiac lymph node biopsy due to procedural risk. Discussion(s): Isolated CS is underdiagnosed and can present with a wide range of symptoms. Detection is limited by current diagnostic criteria, namely difficulty ascertaining affected tissue, which may limit recognition of the full range of presentations. Diagnosis and treatment vary widely among institutions but there is consensus on starting immunosuppression and pursuing follow-up cardiac PET for suppression of inflammatory activity in cases of high clinical suspicion. Our patient plans to undergo repeat PET and have ongoing discussion about lymph node biopsy. COVID-19 myocarditis remains on our differential, however given the patchy nature of LGE on cMR which correlated with the FDG uptake on PET, CS is considered the most probable diagnosis. Conclusion(s): CS should be considered in the differential diagnosis for young patients with structural valve abnormalities, even in the absence of arrhythmias or cardiomyopathy. High clinical suspicion may justify early immunosuppressive treatment to prevent irreversible myocardial injury and/or fatal arrhythmias. Whether this treatment will result in resolution of the structural defects remains to be seen and further investigated.Copyright © 2022

Recurrent Angina in a Patient With Myocardial Infarction With Non-obstructive Coronary Arteries.

The ubiquity of coronary angiography has increased the identification of myocardial infarction with non-obstructive coronary arteries. Currently among cardiologists, there is neither a consensus nor comprehensive diagnostic blueprint for accurate evaluation of patients with myocardial infarction with non-obstructive coronary arteries. We present a case of a patient with recurrent chest pain. A diagnosis of myocardial infarction with non-obstructive coronary arteries secondary to coronary artery vasospasm was determined with the use of multimodality imaging cardiac imaging.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) complicating myocarditis

Myocarditis can lead to myocardial infarction in the absence of coronary artery obstruction. We report a case of probable myocarditis, complicated by myocardial infarction with non-obstructive coronary arteries. A 19-year-old man presented with chest pain typical of myocarditis. He was a smoker but was otherwise well. Electrocardiogram revealed diffuse ST-elevation and echocardiography revealed a thin, akinetic apex. Troponin-T levels on admission were raised leading to an initial diagnosis of myocarditis being made. However, late gadolinium enhancement study on cardiac magnetic resonance imaging demonstrated transmural enhancement typical of ischaemia. Coronary angiogram was normal, leading to a likely diagnosis of myocardial infarction with non-obstructive coronary arteries. It is important to highlight that coronary assessment remains important when working up for myocarditis, as myocardial infarction with non-obstructive coronary arteries can often complicate myocarditis in cases of normal angiography. Another important lesson was on how cardiac magnetic resonance imaging provided vital evidence to support underlying ischaemia despite normal coronary angiogram, leading to a diagnosis of myocardial infarction with non-obstructive coronary arteries. Myocardial infarction with non-obstructive coronary arteries remains a broad 'umbrella' term and cardiac magnetic resonance imaging, as well as more invasive coronary imaging techniques during angiography, can further assist in its diagnosis. Our case provides a reminder that myocardial infarction with non-obstructive coronary arteries, although increasingly recognised, remains under-diagnosed and can often overlap with peri-myocarditis, highlighting the need to employ multi-modality imaging in guiding management.Copyright © The Author(s) 2021.

Cardiac and vegetative manifestations of long-COVID in children.

Approximately 5-15% of children develop post-COVID-19 syndrome after SARS-CoV-2 infection, which manifests itself with various pathological symptoms for more than 12 weeks. Cardiovascular symptoms range from serious myocardial inflammation, manifestations of essential hypertension to signs of autonomic dysfunction with a tendency to hypersympathicotonia, which negatively affects the quality of life of children. We report a case of subacute myocarditis in a patient with long-COVID after a low-symptomatic acute disease. This case illustrates high clinical significance of timely diagnosis of long-COVID using gadolinium-enhanced magnetic resonance imaging, which was performed in our country for the first time in pediatric practice. We developed criteria for early diagnosis of autonomic dysfunction specific for children and adolescents. We also developed treatment recommendations, including behavioral therapy, drug, and non-drug treatments.Copyright © 2022, Dynasty Publishing House. All rights reserved.

Facial herpes zoster associated with disease reactivation in a patient with multiple sclerosis under dimethyl fumarate treatment

Background: Dimethyl fumarate (DMF) is an approved treatment for multiple sclerosis (MS). Due to its efficacy and safety profile, DMF is the most prescribed oral medication for relapsing remitting (RR) MS. Given the long-term course of treatment with DMF in MS, continuous surveillance of opportunistic infections is fundamental. Case presentation: We report the occurrence of facial herpes zoster (HZ) associated with MS disease reactivation in a person with RRMS after 6 years of DMF therapy. Case report: A 44-year-old woman with RRMS developed right temple pain and blisters over the right cheek, suggestive of facial HZ. A normal lymphocyte count with however relatively lower proportions of CD8+ T cells and higher percentages of natural killer cells were detected in blood. The patient failed oral treatment and required hospitalization for intravenous acyclovir. She eventually developed symptoms of an MS exacerbation featured by lower extremities weakness and urinary retention. Conclusion(s): Our case highlights the importance of counseling patients on the possibility of HZ reactivation even in the setting of a normal lymphocyte count, the risk of MS exacerbation possibly associated with HZ occurrence and the importance of timely vaccination.Copyright © 2022