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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 Support could be successfully withdrawn in a mean of five days.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).
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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.
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According to the literature, exudative pleurisy and pericarditis are considered rare complications of the new coronavirus infection. This estimation can be explained by the fact that statistical studies cover mainly the hospital treatment of this disease. The true frequency of these complications and their consequences are not fully understood. Aim. The study of late complications of the new coronavirus infection in the form of pleurisy and pericarditis. Conclusion. In our case, a 62-year-old patient with the new coronavirus infection confirmed by polymerase chain reaction, severe bilateral polysegmental viral pneumonia, CT3, 60% on day 43 after the onset of clinical symptoms, was found to have manifestations of pleurisy and pericarditis during outpatient treatment. Cardiac MRI is the most informative method for detecting small pericardial and pleural effusions. The diagnostic capabilities of this method are superior to ultrasounography of the heart and pleural cavities and computed tomography of the lungs. Administration of colchicine 1.0 g per day for 1 month allowed not only to the elimination of pericarditis and pleurisy, but also the reduction of pressure in the right ventricle, probably by reducing the damage to the pulmonary parenchyma.Copyright © Chepurnenko S.A. et al., 2023.
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In this case series, we describe the diagnosis of post-COVID-19 myocarditis in asymptomatic patients with Duchenne Muscular Dystrophy (DMD) and a mild COVID-19 disease course. These patients were referred for CMR due to electrocardiographic and echocardiographic alterations, which did not exist before COVID-19 infection. CMR identified the presence of severe myocardial inflammation in all patients based on abnormally elevated myocardial T2 ratio, late gadolinium enhancement, native T1 mapping, T2 mapping, and extracellular volume fraction. This was paired with concurrent impairment of left ventricular function. Appropriate treatment was initiated in all cases. Two of the four patients developed episodes of ventricular tachycardia during the following 6 months, and a defibrillator was implanted. Despite the mild clinical presentation, this case series demonstrates the diagnostic strength of CMR in the diagnosis and evaluation of post-COVID-19 myocarditis and serves to increase awareness of this potential complication amongst treating physicians.
ABSTRACT
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
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Case Presentation: Term male infant born to SARS-CoV-2 positive mother with infant testing negative. ECG for perinatal bradycardia revealed ventricular pre-excitation. Echocardiogram showed asymmetric LV hypertrophy with prominent trabeculations, subaortic narrowing with no pressure gradient, and normal biventricular systolic function. Rapid increase in RV pressure estimates and NT-proBNP in first week if life concerning for diastolic dysfunction. Anti-arrhythmic therapy initiated for SVT with subsequent resolution. Later, developed progressive LV dilation and systolic dysfunction. Myocardium showed regions resembling non-compaction and others concerning for infiltrative process. Cardiac MRI showed no obvious tumors, but rhabdomyomas could not be ruled out given similar appearance to myocardium. Due to worsening heart failure, everolimus therapy initiated to target potential rhabdomyomas while awaiting genetic testing for tuberous sclerosis. Subaortic narrowing and LV hypertrophy improved within days, and LV appearance became more consistent with non-compaction. Genetic testing revealed a TSC2 gene variant consistent with tuberous sclerosis. Systolic function improved, and patient discharged on afterload reduction. Echocardiogram 6 months post-discharge shows continued LV dilation and mild systolic dysfunction. Discussion(s): Although outflow obstruction and arrhythmias are common with cardiac rhabdomyomas and can cause dysfunction, our patient developed progressive dysfunction in the absence of outflow tract gradient or prolonged arrhythmia. As rhabdomyomas subsided, it became clearer that he had an underlying cardiomyopathy. We suspect that rhabdomyomas in the setting of abnormal myocardium led to abnormalities in myocardial contractility and compliance causing combined systolic and diastolic dysfunction. After complete resolution of rhabdomyomas, cardiac function has improved. However, he continues to have ventricular dilation and mild dysfunction attributable to cardiomyopathy. It is unlikely that mother's SARS-CoV-2 infection played a role as infant tested negative and clinical picture was not consistent with myocarditis.
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Introduction: Acromegaly is an uncommon pituitary disorder with an incidence of six per million persons. While hypertension is often encountered in these patients, heart failure rarely is seen with an incidence rate under 10%. We describe a case of an individual who was diagnosed with acromegaly after an acute exacerbation of heart failure with subsequent management requiring an LVAD to perform Transsphenoidal Surgery (TSS). Case Description: 37-year-old male otherwise healthy initially presented to an emergency room and was found to be in acute heart failure exacerbation. Concerning acromegaly features included macrognathia, enlarged hands and feet, swollen phalanges, widened spacing of teeth, and frontal bossing. IGF-1 level was found 455 ng/mL. MRI showed a 10mm macroadenoma. A right heart catheterization showed elevated filling pressures. Cardiac MRI showed no defects or enhancement. Endomyocardial biopsy showed no inflammatory infiltrates or evidence of infiltrative diseases. Patient had an ejection fraction of 15% corroborated by cardiac MRI along with the presence of aortic root dilatation and mitral regurgitation. The patient started on 0.5mg of Cabergoline twice weekly and 120mg weekly Lanreotide injections. Patient stabilized with plans for further close monitoring and outpatient neurosurgical evaluation. The COVID-19 pandemic and insurance gaps led the patient to spend two years off his medicines and he was unable to be seen by his medical team. Patient was seen by our system after recurrent hospitalizations for heart failure at our sister hospital, AICD was unable to be placed due to the patient's anatomy, he was placed on wearable cardiac defibrillator and required milrinone infusion for progression to end-stage heart failure with cardiac cachexia. At our institution, the patient was evaluated for Orthotopic Heart Transplant (OHT) but due to active GH secreting macroadenoma there was concern for OHT failure without TSS. Decision was made to utilize LVAD as Bridge-to-Transplant for OHT so the patient could be stabilized and safely undergo TSS. The patient tolerated surgeries well and is currently on the active transplant list. Discussion(s): Heart failure is an uncommon presentation of severe acromegaly requiring multidisciplinary management. We describe a case of a patient who initially presented with heart failure too unstable for surgery. Due to the COVID-19 pandemic the patient's disease progressed resulting in end-stage heart failure requiring LVAD placement for further treatment. We would like to draw attention to the use of LVAD placement in acromegalic patients who develop severe cardiovascular disease who are not candidates for OHT.Copyright © 2023
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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.
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Case Presentation: A 23-year-old previously healthy man presented with progressive dyspnea. Physical examination revealed jugular venous distension and lower extremity edema. Laboratory testing demonstrated elevated B-type natriuretic peptide (193 pg/mL) and normal high sensitivity troponin. Echocardiogram revealed small pericardial effusion, respiratory variation in diastolic flow across the mitral valve, diastolic septal bounce, and annulus reversus (Figure). The differential diagnosis for constrictive pericarditis was broadly considered in the context of a recent febrile illness and frequent travel to Hawaii and Vietnam;we included infectious, autoimmune, and malignant etiologies. Cardiac magnetic resonance imaging revealed thickening and diffuse enhancement in the pericardium as well as ventricular interdependence. Chest CT identified hilar and anterior mediastinal lymphadenopathy. Laboratory testing was positive for QuantiFERON gold and negative for COVID-19, HIV, and ANA. Transbronchial biopsy demonstrated non-necrotizing granulomas with negative acid-fast bacilli smear, culture, and polymerase chain reaction for mycobacterial DNA. Reexamination identified a red-brown plaque on the patient's thigh;biopsy showed granulomatous inflammation and rod-shaped organism with positive FITE staining. A presumed unifying diagnosis was made of extrapulmonary tuberculosis (TB) complicated by constrictive pericarditis. Discussion(s): Despite being a primarily pulmonary disease, systemic involvement can occur with TB with the heart being one of the most common extrapulmonary sites. This case highlights 1) the utility of extra-cardiac diagnostic testing (e.g., dermatologic biopsy) in the diagnosis of constrictive pericarditis, and 2) the diagnostic challenge associated with extrapulmonary TB, particularly paucibacillary disease that requires a detailed social history with "out-of-the-box" thinking.
ABSTRACT
According to the literature, exudative pleurisy and pericarditis are considered rare complications of the new coronavirus infection. This estimation can be explained by the fact that statistical studies cover mainly the hospital treatment of this disease. The true frequency of these complications and their consequences are not fully understood. Aim. The study of late complications of the new coronavirus infection in the form of pleurisy and pericarditis. Conclusion. In our case, a 62-year-old patient with the new coronavirus infection confirmed by polymerase chain reaction, severe bilateral polysegmental viral pneumonia, CT3, 60% on day 43 after the onset of clinical symptoms, was found to have manifestations of pleurisy and pericarditis during outpatient treatment. Cardiac MRI is the most informative method for detecting small pericardial and pleural effusions. The diagnostic capabilities of this method are superior to ultrasounography of the heart and pleural cavities and computed tomography of the lungs. Administration of colchicine 1.0 g per day for 1 month allowed not only to the elimination of pericarditis and pleurisy, but also the reduction of pressure in the right ventricle, probably by reducing the damage to the pulmonary parenchyma.Copyright © Chepurnenko S.A. et al., 2023.
ABSTRACT
Purpose of study Since mid-April 2020 in Europe and North America, clusters of pediatric cases with a newly described severe systemic inflammatory response with shock have appeared. Patients had persistent fevers >38.5 C, hypotension, features of myocardial dysfunction, coagulopathy, gastrointestinal symptoms, rash, and elevated inflammatory markers without other causes of infection. The World Health Organization, Centers for Disease Control, and Royal College of Paediatrics associated these symptoms with SARS-CoV-2 as multisystem inflammatory syndrome in children (MIS-C). Cardiac manifestations include coronary artery aneurysms, left ventricular systolic dysfunction evidenced by elevation of troponin-T (TnT) and pro-B-type naturietic peptide (proBNP), and electrocardiogram (ECG) abnormalities. We report the clinical course of three children with MIS-C while focusing on the unique atrioventricular (AV) conduction abnormalities. Case #1:19-year-old previously healthy Hispanic male presented with abdominal pain, fever, and non-bloody diarrhea for three days. He was febrile and hypotensive (80/47 mmHg) requiring fluid resuscitation. Symptoms, lab findings, and a positive COVID-19 antibody test were consistent with MIS-C. Methylprednisolone, intravenous immunoglobulin (IVIG), and enoxaparin were started. He required epinephrine for shock and high flow nasal cannula for respiratory distress. Initial echocardiogram demonstrated a left ventricular ejection fraction (LVEF) of 40% with normal appearing coronaries. Troponin and proBNP were 0.41 ng/mL and proBNP 15,301 pg/mL respectively. ECG showed an incomplete right bundle branch block. He eventually became bradycardic to the 30s-50s and cardiac tracing revealed a complete AV block (figure 1a). Isoproterenol, a B1 receptor agonist, supported the severe bradycardia until the patient progressed to a type 2 second degree AV block (figure 1b). A second dose of IVIG was administered improving the rhythm to a type 1 second degree AV block. An IL-6 inhibitor, tocilizumab was given as the rhythm would not improve, and the patient soon converted to a first-degree AV block. Cardiac magnetic resonance imaging showed septal predominant left ventricular hypertrophy and subepicardial enhancement along the basal inferior/anteroseptal walls typical for myocarditis. Case #2: 9-year-old previously healthy Hispanic male presented after three days of daily fevers, headaches, myalgias, diffuse abdominal pain, and ageusia. He was febrile, tachycardic, and hypotensive (68/39 mmHg). Hypotension of 50s/20s mmHg required 3 normal saline boluses of 20 ml/kg and initiation of an epinephrine drip. Severe hypoxia required endotracheal intubation. After the MIS-C diagnosis was made, he was treated with IVIG, mehtylprednisolone, enoxaparin, aspirin, and ceftriaxone. Due to elevated inflammatory markers by day 4 and patient's illness severity, a 7-day course of anakinra was initiated. Initial echocardiogram showed mild tricuspid and mitral regurgitation with a LVEF of 35-40%. Despite anti-inflammatory therapy, troponin and proBNP were 0.33 ng/mL and BNP of 25,335 pg/mL. A second echocardiogram confirmed poor function so milrinone was started. Only, after two doses of anakinra, LVEF soon normalized. Despite that, he progressively became bradycardic to the 50's. QTc was prolonged to 545 ms and worsened to a max of 592 ms. The aforementioned therapies were continued, and the bradycardia and QTc improved to 405 ms. Patient #3: 9-year-old African American male presented with four days of right sided abdominal pain, constipation, and non-bilious non-bloody emesis. He had a negative COVID test and unremarkable ultrasound of the appendix days prior. His history, elevated inflammatory markers, and positive COVID- 19 antibody were indicative of MIS-C. He was started on the appropriate medication regimen. Initial ECG showed sinus rhythm with normal intervals and echocardiogram was unremarkable. Repeat imaging by day three showed a decreased LVEF of 50%. ECG had since changed to a right bundle branch block. Anakinra as started and steroid dosing was increased. By day 5, he became bradycardic to the 50s and progressed to a junctional cardiac rhythm. Cardiac function normalized by day 7, and anakinra was subsequently stopped. Thereafter, heart rates ranged from 38-48 bpm requiring transfer to the pediatric cardiac intensive care unit for better monitoring and potential isoproterenol infusion. He remained well perfused, with continued medical management, heart rates improved. Methods used Retrospective Chart Review. Summary of results Non-specific T-wave, ST segment changes, and premature atrial or ventricular beats are the most often noted ECG anomalies. All patients initially had normal ECGs but developed bradycardia followed by either PR prolongation or QTc elongation. Two had mild LVEF dysfunction prior to developing third degree heart block and/or a junctional escape rhythm;one had moderate LVEF dysfunction that normalized before developing a prolonged QTc. Inflammatory and cardiac markers along with coagulation factors were the highest early in disease course, peak BNP occurred at approximately hospital day 3-4, and patient's typically had their lowest LVEF at day 5-6. Initial ECGs were benign with PR intervals below 200 milliseconds (ms). Collectively the length of time from initial symptom presentation till when ECG abnormalities began tended to be at day 8-9. Patients similarly developed increased QTc intervals later in the hospitalization. When comparing with the CRP and BNP trends, it appeared that the ECG changes (including PR and QTc elongation) occurred after the initial hyperinflammatory response. Conclusions Although the mechanism for COVID-19 induced heart block continues to be studied, it is suspected to be secondary to inflammation and edema of the conduction tissue. Insufficiency of the coronary arterial supply to the AV node and rest of the conduction system also seems to play a role. Although our patients had normal ECG findings, two developed bundle branch blocks prior to more complex rhythms near the peak of inflammatory marker values. Based on the premise that MIS-C is a hyperinflammatory response likely affecting conduction tissue, our group was treated with different regimens of IVIG, steroids, anakinra, and/or tocilizumab. Anakinra, being an IL-1 inhibitor, has been reported to dampen inflammation in viral myocarditis and tocilizumab has improved LVEF in rheumatoid arthritis patients. Based on our small case series, patient's with MISC can have AV nodal conduction abnormalities. The usual cocktail of IVIG and steroids helps;however, when there are more serious cases of cardiac inflammation, adjuvant immunosuppresants like anakinra and toculizumab can be beneficial. (Figure Presented).
ABSTRACT
Background: Previous studies have reported ongoing cardiac inflammation as assessed by cardiac magnetic resonance imaging (CMR) in a significant proportion of patients several months after recovery from SARSCoV- 2 infection, many of whom had no or minimal symptoms at the time of infection. Purpose(s): The aim of SETANTA was to investigate the prevalence of cardiac abnormalities by CMR in unselected patients in Ireland after acute SARS-CoV-2 infection and the correlation with immunological response and biomarkers of coagulation. Method(s): This was a prospective, observational, community-based study (clinicaltrials.gov identifier NCT04823182). Consecutive patients recovered from recent SARS-CoV-2 infection at 3 primary care sites were invited to participate. Key inclusion/exclusion criteria and outcomes of interest are shown in Figure 1. Result(s): 100 participants were enrolled (Feb-Sept 2021) at a median of 188 (IQR, 125, 246) days after positive SARS-CoV-2 swab. At index infection, 18% and 35% reported severe and moderate symptoms, respectively;14% were hospitalized;3% were admitted to intensive care for ventilatory support. At enrolment, 83% had ongoing symptoms. 85% had detectable SARS-CoV-2 antigens. CMR and laboratory findings are shown in Figure 1. Conclusion(s): Among an unselected cohort of patients recovered from acute SARS-CoV2 infection, we report a low prevalence of cardiac abnormalities by CMR, despite a high prevalence of moderate/severe symptoms at presentation and a high prevalence of persistent symptoms. Correlation with biomarkers of immunity and coagulation will be available at ESC 2022.
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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.
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Background. Environmental factors such as infections and vaccines are known to trigger dermatomyositis (DM), and during the recent SARS-CoV-2 pandemic this has become even clearer. SARS-CoV-2 infection may share features with anti-MDA5 DM, such as rapidly progressive lung involvement, cutaneous lesions and cytokine release syndrome. A few case reports of DM following SARSCoV-2 vaccination have been published, suggesting the onset of an aberrant immune response leading to DM with specific autoantibody signatures and severe organ impairment. Methods. Clinical and laboratory data of the 2 case reports were obtained from electronic clinical charts in Humanitas Research Hospital (Rozzano, Milan, Italy). Autoantibody analysis was performed by protein-immunoprecipitation for anti-MDA5 and immunoblot for anti-Ro52 and TIF1gamma antibodies as per protocol. Results. Case report 1 is a 71-year-old woman who developed fever, cough, and anosmia, which resolved spontaneously in two weeks, but did not undergo a nasopharyngeal swab, while her relatives were diagnosed with SARS-CoV-2 infection. When symptoms improved, she developed arthralgia and skin lesions on her face, chest, and hands for which she started topical treatment, with negative SARSCoV-2 nasopharyngeal swab and positive serum test for IgG against SARS-CoV-2 spike protein. For the persistence of the skin rash and arthralgia, she was admitted to our Department in March 2021. Blood tests showed mild elevation of C reactive protein (2.1 mg/L -normal value NV<5), aspartate (84 UI/L) and alanine aminotransferase (133 UI/L -NV<35), ferritin (595 ng/ml -NV<306), troponin I (19 ng/L -NV<14), and BNP (251 pg/ml -NV<100) with normal complete blood cell count, creatine kinase, C3 and C4. IgG antibodies for SARS-CoV-2 spike protein were confirmed to be elevated (96 AU/ml -NV<15). Autoantibodies associated with connective tissue diseases were tested and only anti-MDA5 antibodies were positive at immunoprecipitation. A punch biopsy of a Gottron-like lesion on the left hand showed leukocytoclastic vasculitis. We observed reduced capillary density with neoangiogenesis and ectasic capillaries at the nailfold capillaroscopy. EKG and ecocardiography were normal, while cardiac magnetic resonance detected abnormalities in the parametric sequences, consistent with signs of previous myocarditis. A lung CT scan revealed pulmonary emphysema while respiratory function tests demonstrated reduced volumes (FVC 82%, FEV1 64%, inadequate compliance CO diffusion test). Based on the biochemical and clinical findings, a diagnosis of anti-MDA5-associated DM with skin and heart involvement was made and treatment with low-dose methylprednisolone (0.25 mg/kg daily) and azathioprine 100 mg was started, then switched to mycophenolate because not effective on skin lesions. Case report 2 is an 84-year-old woman with history of colon cancer (surgical treatment) and oral lichen treated with low doses steroids in the last 2 years. After the 2nd dose of SARS-CoV-2 mRNA vaccination, in March 2021 she developed skin rash with V-sign, Gottron's papules, periungueal ulcers, muscle weakness and fatigue, thus she performed a rheumatologic evaluation. Blood tests showed mild elevation of creatine kinase (484 UI/L, NV <167), CK-MB (9.6ng/ml, NV <3.4), BNP (215 pg/ml -NV<100) with normal values of complete blood cell count, C3 and C4. Anti-Ro52kDa and TIF1gamma were positive at immunoblot, thus we confirmed a diagnosis of DM. The clinical evaluation also showed active scleroderma pattern at nailfold capillaroscopy, normal echocardiography, bronchiectasia but not interstitial lung disease at lung CT, and normal respiratory function tests (FVC 99%, FEV1 99%, DLCO 63%, DLCO/VA 81%). A PET-CT scan was performed to exclude paraneoplastic DM, and treatment with steroids and mycophenolate was started. Conclusions. SARS-CoV-2 may induce mechanisms for escaping the innate immunity surveillance and causing autoimmune diseases, but more clinical and functional studies are needed to demonstrate this possible association.
ABSTRACT
Background: Identification of athletes with cardiac inflammation following COVID-19 can prevent exercise fatalities. The efficacy of pre and post COVID-19 infection electrocardiograms (ECGs) for detecting athletes with myopericarditis has never been reported. We aimed to assess the prevalence and diagnostic significance of novel 12-lead ECG patterns following COVID-19 infection in elite soccer players. Method(s): We conducted a multicentre study over a 2-year period involving 5 centres and 34 clubs and compared pre COVID and post COVID ECG changes in 455 consecutive athletes. ECGs were reported in accordance with the International recommendations for ECG interpretation in athletes. The following patterns were considered abnormal if they were not detected on the pre COVID-19 infection ECG: (a) biphasic T-waves;(b) reduction in T-wave amplitude by 50% in contiguous leads;(c) ST-segment depression;(d) J-point and ST-segment elevation >0.2 mV in the precordial leads and >0.1 mV in the limb leads;(e) tall T-waves >=1.0 mV (f) low QRS-amplitude in >3 limb leads and (g) complete right bundle branch block. Athletes exhibiting novel ECG changes underwent cardiovascular magnetic resonance (CMR) scans. One club mandated CMR scans for all 28 (6%) athletes, despite the absence of cardiac symptoms or ECG changes. Result(s): Athletes were aged 22+/-5 years (89% male and 57% white). 65 (14%) athletes reported cardiac symptoms. The mean duration of illness was 3+/-4 days. The post COVID ECG was performed 14+/-16 days following a positive PCR. 440 (97%) athletes had an unchanged post COVID- 19 ECG. Of these, 3 (0.6%) had cardiac symptoms and CMRs resulted in a diagnosis of pericarditis. 15 (3%) athletes demonstrated novel ECG changes following COVID-19 infection. Among athletes who demonstrated novel ECG changes, 10 (67%) reported cardiac symptoms. 13 (87%) athletes with novel ECG changes were diagnosed with inflammatory cardiac sequelae;pericarditis (n=6), healed myocarditis (n=3), definitive myocarditis (n=2), and possible/probable myocarditis (n=2). The overall prevalence of inflammatory cardiac sequelae based on novel ECG changes was 2.8%. None of the 28 (6%) athletes, who underwent a CMR, in the absence of cardiac symptoms or novel ECG changes revealed any abnormalities. Athletes revealing novel ECG changes, had a higher prevalence of cardiac symptoms (67% v 12% p<0.0001) and longer symptom duration (8+/-8 days v 2+/-4 days;p<0.0001) compared with athletes without novel ECG changes. Among athletes without cardiac symptoms, the additional yield of novel ECG changes to detect cardiac inflammation was 20% (n=3). Conclusion(s): 3% of elite soccer players demonstrated novel ECG changes post COVID-19 infection, of which almost 90% were diagnosed with cardiac inflammation during subsequent investigation. Most athletes with novel ECG changes exhibited cardiac symptoms. Novel ECGs changes contributed to a diagnosis of cardiac inflammation in 20% of athletes without cardiac symptoms.
ABSTRACT
Introduction: Although cardiac allograft vasculopathy (CAV) remains one of the leading causes of graft failure after heart transplantation (HTx), simultaneous thrombosis of multiple epicardial coronary arteries (CA) is an uncommon finding. Case Report: A 43-year-old male patient with non-ischemic dilated cardiomyopathy underwent successful HTx in 2019. The first two years after HTx were uneventful, surveillance endomyocardial biopsies (EMB) did not reveal any rejection episodes, coronary CTA revealed only minimal non-calcified CA plaques. The patient was admitted to hospital due to fever and chest pain in 2021. Immunosuppressive therapy consisted of tacrolimus, mycophenolate-mofetil and methylprednisolone. ECG verified sinus rhythm. Laboratory test revealed elevated hsTroponin T, NT-proBNP and CRP levels. Cytomegalovirus, SARS-CoV-2-virus and hemoculture testing was negative. Several high-titre donor-specific HLA class I and II antibodies (DSAs;including complement-binding DQ7) could have been detected since 2020. Echocardiography confirmed mildly decreased left ventricular systolic function and apical hypokinesis. EMB verified mild cellular and antibody-mediated rejection (ABMR) according to ISHLT grading criteria. Cardiac MRI revealed inferobasal and apical myocardial infarction (MI);thus, an urgent coronary angiography was performed. This confirmed thrombotic occlusions in all three main epicardial CAs and in first diagonal CA. As revascularization was not feasible, antithrombotic therapy with acetylsalicylic acid, clopidogrel and enoxaparin was started for secondary prevention. Tests for immune system disorders, thrombophilia and cancer were negative. Patient suddenly died ten days after admission. Necropsy revealed intimal proliferation in all three main epicardial CAs, endothelitis, thrombosis, chronic pericoronary fat inflammation, fat necrosis, and subacute MI. CA vasculitis owing to persistent high-titre DSAs, chronic ABMR and acute cellular and antibody-mediated rejection led to multivessel CA thrombosis and acute multiple MI. ABMR after HTx may be underdiagnosed with traditional pathological methods. Pathologies affecting coronary vasculature of HTx patients with DSAs, unique manifestations of CAV lesions and occlusive thrombosis of non-stenotic, non-atherosclerotic lesions should be emphasized.Copyright © 2023
ABSTRACT
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.
ABSTRACT
Background: Several studies described occurrence of myocarditis after SARS-CoV-2 vaccination in pediatric patients. Weaimed to characterize the clinical course of myocarditis following SARS-CoV2 vaccination including follow-up data within the prospective German registry for suspected myocarditis in children and adolescents "MYKKE." Method: Patients younger than 18 years with suspected myocarditis and onset of symptoms within 21 days followingSARS-CoV2 vaccination were enrolled within the MYKKE registry. The suspect of myocarditis is valid in patients with clinical symptoms and diagnostic findings typically seen in myocarditis. Clinical data are monitored at initial admission and duringshort-term and long-term follow-up. Result(s): Between July 2021 and August 2022, a total of 48 patients with a median age of 16.2 years (IQR: 15.2-16.8)were enrolled by 13 centers, 88% male. Onset of symptoms occurred at a median of 3 days (IQR: 2-7) after vaccine administration, most frequently after the second dose (52%). Most common symptoms at initial admission were anginapectoris (81%), fatigue (56%), dyspnea (24%) and documented arrhythmias (17%). Initial ECG abnormalities included ST-elevation (48%) and T-wave inversion (23%). Elevated Tropon in was observed in 32 patients (67%) and in 19 cases (40%)NT-proBNP was above the normal range with a median level of 171 pg/mL (IQR: 32-501). 11 (23%) patients presentedwith mildly reduced systolic function at initial echocardiography or cardiac MRI. In 40 patients cardiac MRI and/orendomyocardial biopsy was performed (83%) and diagnosis of myocarditis could be verified in 27 cases (68%). Thirty-nine patients underwent short-term follow-up with a median of 2.8 months (IQR: 1.9-3.9) after discharge. 19 patients (49%)presented with either clinical symptoms (n = 9) and/or diagnostic abnormalities (n = 16) at follow-up. 12 patients (38%)still had medical treatment. Except for one patient with malign arrhythmias (ventricular tachycardia), no major cardiac adverse events were observed during initial admission and follow-up. Conclusion(s): Our data confirm that SARS-CoV-2 vaccine-related myocarditis is characterized by a mild disease course. However, after short-term follow-up a considerable number of patients still presented with symptoms and/or diagnostic abnormalities. Data on long-term follow-up are awaited.
ABSTRACT
A 49-year-old man presented with shortness of breath and fever. He was in diabetic ketoacidosis on admission and tested positive for COVID-19 on PCR. He became bacteraemic with streptococcus pneu- moniae secondary to a super-added left lower lobe pneumonia. He developed new heart failure felt to be secondary to myocarditis, evidenced by a resolving ejection fraction throughout his admission and an unremarkable cardiac MRI. After developing confusion on the ward, a CT head and MRI brain identified a spontaneous frontal haematoma and multiple micro-haemorrhages throughout the cerebral hemi- spheres, cerebellum and the pons. Repeat MRI brain with diffusion weighted imaging identified multiple silent infarcts in the small vessel territories. Bacterial endocarditis was excluded with Cardiology input and hypoperfusion also excluded based on normotension throughout admission. The case was discussed at the Encephalitis and Neurovascular MDT meetings where MRI vessel wall imaging was reviewed and felt to represent a post-infectious endotheliitis. He was treated with intravenous methylprednisolone for 3 days and a further 5 days, due to new silent infarcts on a subsequent MRI brain, before a 10 week oral steroid taper. Multi-system complications from COVID-19 are not limited to those in the intensive care unit or with severe respiratory illness.
ABSTRACT
Widely considered safe, effective, and essential for pathogenic immunity, vaccines have proven to be one of the most important discoveries to date in medicine. Adverse reactions to vaccines are typically trivial but there have been extremely rare reports of vaccine induced myocarditis, particularly with the Tdap vaccine. This is thought to be due to a hypersensitivity reaction. In efforts to combat the SARS-CoV-2, prompt response from Pfizer-BioNTech and Moderna lead to vaccine development with a novel method, synthesized from modified messenger RNA. Despite minimal side effects on initial trials, reports of vaccine induced myocarditis have resulted. A majority of these cases occurred following subsequent doses for those previously inoculated. A descriptive study published in JAMA in January 2022 reviewed the Vaccine Adverse Event Reporting System (VAERS) in collaboration with the CDC described only 1626 cases of myocarditis, of which the majority occurred within days of the second dose. This review was limited by reviewing a passive reporting syndrome with variable quality data and without follow up data post diagnosis of myocarditis. Here we present a case of myocarditis occurring less than 24 hours after the second dose of Pfizer-BioNTech vaccine with 3 month follow up. A 23 year old man received his second dose of the COVID-19 vaccine in the morning. Within a few hours he experienced chest pain, chills, weakness, and fatigue. These dissipated by 7pm. He is a member of the National Guard and during drills the next day experienced stabbing substernal chest pain for which he sought evaluation. The pain radiated into his left jaw, worse with deep inspiration and worse in the left lateral decubitus position. He is a 1 PPD smoker with no personal or family history or cardiac disease. A friction rub was heard on physical exam. His troponin I peaked at 2.6ng/mL. His EKG showed normal sinus rhythm, a TTE showed a normal EF with no pericardial effusion. He was given aspirin 81 mg and started on a heparin drip for possible NSTEMI. The next day his pain decreased and a cardiac MRI demonstrated no inflammation. His serum coxsackie and parvovirus titers were negative. He was instructed to continue the aspirin, limit exercise for 8 weeks, and stop smoking. Upon follow up 3 months later the patient denied any recurrent chest pain and was advised to continue the aspirin. But the original bout of myocarditis limited his participation in the National Guard. Our case illustrates that exposure to an immunological trigger, the COVID-19 vaccine, leading to myocarditis was extremely short compared to typical cases of viral induced or vaccine hypersensitivity reaction. A proposed mechanism is molecular mimicry between the spike protein and myocardial contraction proteins. It also demonstrates that the vaccine can cause morbidity in patients, especially younger males. It also exemplifies that this may be a short lived phenomenon, long term follow up is still needed. With the rate of vaccination increasing, there needs to be a low threshold to consider myocarditis in young adults who have new chest pain after receiving an mRNA based vaccine.Copyright © 2022