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Myocarditis is a heart condition characterized by inflammation of cardiac myocytes. This inflammation is instigated by the activation of both the innate and acquired immune responses and is most often caused by viruses (flu, hand foot and mouth and COVID-19). Myocarditis may progress to dilated cardiomyopathy (DCM), a chronic heart condition in which fibrosis and remodeling weakens the ability of the heart to effectively pump. Myocarditis is a leading cause of sudden death in children and young adults. In this study, we investigated the progression and severity of myocarditis within the pediatric population as compared to an adult population. Prior to this study there were no mouse models for pediatric myocarditis but a large percent of patients with myocarditis are children. We utilized our knowledge from our adult mouse model of coxsackievirus B3 (CVB3) myocarditis to create a pediatric CVB3 myocarditis model in order to better understand the development of myocarditis in children. We hypothesized that myocarditis would have sex-specific differences in the manifestation and severity similar to the adult model but the mechanisms of disease would very between ages. We utilized 4-week-old male and female BALB/c mice to model pediatric myocarditis as compared to 8-week-old mice. Mice were be infected with heart-passaged CVB3 intraperitoneally (ip) on day (d) 0. Disease severity and progression was evaluated during acute myocarditis (d8-12 pi) and during DCM (d35pi). After anesthesia, body weight, heart weight and tibia length, blood, hearts, pancreas and spleens were harvested. Echocardiography was conducted on mice at the chronic DCM timepoint. We found that adult male and female mice develop myocarditis with male mice have more severe disease and progress to DCM as compared to female mice. The main immune cells and pathways involved in myocarditis severity were macrophages, complement and the inflammasome in male adult mice. This increase in disease was driven by testosterone and reduced by estrogen as seen utilizing gonadectomies. In the pediatric population we did not see as drastic of differences in sex hormone levels as the mice are pre-pubescent, this led to less dramatic sex differences in disease and altered immune mechanisms leading to disease in the pediatric population compared to the adults. We do see induction of myocarditis in both male and female pediatric mice compared to uninfected controls but severity in the pediatric population is less than adult population. Successful development of a pediatric translational mouse model of viral myocarditis will significantly impact the myocarditis field by allowing the ability to assess differences between pediatric and adult populations and develop targeted diagnostics and treatments.Copyright © 2022
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Calcium levels in the Coronary Artery are an indicative marker of the presence and extent of atherosclerosis. This serves as an additional prognostic indicator in addition to traditional risk factors. Moreover, the coronary calcium test is associated with a descriptor known as the calcium score or calcium score (Cs), which is primarily useful for stratifying the risk of asymptomatic patients, while for patients with acute or chronic chest pain, coronary axial computed tomography is generally required. A retrospective analysis of data was conducted in the radiology department of King Salman Specialist Hospital in Hail City, the kingdom of Saudi Arabia, between January and May 2022. A total of 40 patients were randomly selected, 25 males and 15 females. The study included all patients with or suspected of having a calcium deposit who underwent a CT scan using the Siemens SOMATOM definition MDC scan. Patients underwent a scan with the preparations and laboratory tests required for their coronary artery calcium scores. In this study, males were more likely to be affected by calcium deposits (64%), whereas females were 36%. Approximately 50 percent of the study populations were found to be normal (no identifiable calcium deposits) and 37.5% to have moderate calcium deposits. There is a significant association between CACS and moderate CVD risks based on age and gender in this study. Better control of cardiovascular system (CVS) risks is recommended in all primary care centers in the Kingdom of Saudi Arabia (KSA).Copyright © 2022 International Journal of Pharmaceutical Research and Allied Sciences. All rights reserved.
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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
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Background: The role of genetic conditions in the development of cardiomyopathy is well established;however, recognition and referral for genetic testing remains underutilized. Systematic review of complex cases can increase general awareness in this area of practice. Here we describe the case of a patient with resolved severe stress induced cardiomyopathy (SIC), who was ultimately found to have heterozygous transthyretin-mediated amyloidosis (TTRA). Case: A 27-year-old man (family history positive for a brother status post heart transplant) presented with ataxia and cough due to legionella pneumonia. TTE showed left ventricular (LV) diastolic diameter of 6.2cm, LV ejection fraction 20-25%. He suffered rapid decompensation with mixed cardiogenic/septic shock requiring peripheral VA ECMO and Impella-CP placement. Course notable for brief cardiac arrest on hospital day (HD) 2, incidental diagnosis of COVID 19 on HD 14, conversion to VV ECMO on HD 15, and ECMO decannulation on HD 23. Repeat TTE prior to discharge showed normalization of biventricular function. Discussion(s): Despite resolution of refractory shock and normalization of biventricular function prior to discharge, the TTE finding of mild LV dilation and strong family history prompted outpatient pursuit of genetic testing which revealed a heterozygous TTRA mutation (val142ile). Work-up to assess cardiac involvement included: a 99m-technetium pyrophosphate scintigraphy found to be indeterminate, an aborted endomyocardial biopsy due to inability to smoothly advance a bioptome (presumably related to ECMO cannulation), and a cardiac MRI (pending at the time of this submission). If a cardiac phenotype is discovered, the patient will be started on targeted treatment of cardiac amyloid. Screening of first-degree family members has been initiated. Conclusion(s): Given the current state of under-diagnosis of genetic cardiomyopathies and its association with significant morbidity and mortality, it is prudent to consider genetic testing in young patients based on clinical history. Examples of clinical scenarios to prompt further testing include: anatomical findings (i.e. cardiac chamber enlargement, left ventricular hypertrophy), family history of cardiomyopathy, or clinical markers suggestive of alternative diagnoses (i.e. neuropathy, renal insufficiency, mediastinal lymphadenopathy). This thoughtful and algorithmic use of genetic testing may help improve long-term patient outcomes given improvements in both detection, family screening, and treatment for disease-specific cardiomyopathies.Copyright © 2022
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Clinical data and follow-up of a case of congenital disorder of glycosylation type Ia (CDG-Ia) combined with dilated cardiomyopathy admitted to the Department of Cardiology, Children's Hospital of Nanjing Medical University were analyzed retrospectively.The 5-year-old female patient was admitted in December 2016 due to recu-rrent shortness of breath for 2 months.Clinical symptoms and signs included repeated attacks of shortness of breath, physical retardation, malnutrition, binocular esotropia, multiple episodes of hypoglycemia, hepatosplenomegaly, hypotonia and other multi-system damages.Cardiac echocardiography suggested the feature of dilated cardiomyopathy, including the significant enlargement of the left ventricle, and decreased systolic function.Genetic testing revealed a compound heterozygous mutation in the PMM2 gene, and as a result, the patient was diagnosed as CDG-Ia.The patient's condition improved after symptomatic treatments such as Cedilanid, Dopamine, Dobutamine, Furosemide, as well as support treatments like myocardium nutrition, blood sugar maintenance, liver protection, etc.After discharge, the patient was given oral Digoxin, Betaloc, Captopril and diuretics, and hypoglycemia-controlling agents.The patient was followed up every 3-6 months.After more than 2 years of follow-up, the heart function and heart enlargement gradually returned to normal.During the Corona Virus Disease 2019 outbreak, self-withdrawal continued for 2 months.Re-examinations showed decreased cardiac function and enlarged left ventricle again.Medications were resumed again, and the patient was followed up closely.This case report suggested that CDG-Ia may be associated with dilated cardiomyopathy, and the cardiac phenotype may be improved by symptomatic supportive treatment.Copyright © 2021 by the Chinese Medical Association.
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Background Dilated cardiomyopathy (DCM) is caused by many conditions, including ischemia, genetics, infection, chemotherapy, or idiopathic. Clinical suspicion is needed to identify reversible etiologies. Case A middle-aged truck-driver presents with exertional dyspnea, cough, lower extremity edema, and low-grade fever for 2 weeks. He had 20-pack-year smoking history and 3-4 alcoholic drinks weekly. Chest x-ray showed pulmonary congestion. BNP was elevated. ECHO showed severely dilated ventricles with LVEF < 10% and no wall abnormalities. Decision-making Perfusion stress test showed no inducible ischemia. Coronary angiogram showed no epicardial disease. Cardiac MRI (CMR) showed severely dilated biventricular failure, pericardial thickening, circumferential pericardial effusion, epicardial involvement suggestive of subacute myopericardial inflammation and scarring with delayed gadolinium-enhancement and RVEF < 5%. Liver ultrasound showed no cirrhosis. Viral PCR was positive for rhinovirus, negative COVID-19. He was treated medically requiring inotropes then transferred to heart failure center for assist device evaluation. Conclusion Our patient reported moderate alcohol use, which alone would not explain the myopericardial changes seen on CMR. Given the findings, his DCM was attributed to alcohol complicated by possible subacute rhinovirus myocarditis. Our association is further supported by recent respiratory viral prodrome along with exclusion of other etiologies. [Formula presented]Copyright © 2023 American College of Cardiology Foundation
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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
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The proceedings contain 67 papers. The topics discussed include: role of endomyocardial biopsy in differential diagnosis of non- -ischemic cardiomyopathy;metformin treatment is associated with improved quality of life and outcome in patients with diabetes and advanced heart failure (HFREF);translational research in the field of inherited arrhythmias;same day discharge via a dedicated radial lounge - results of 1-year experience during the COVID-19 pandemic;functional assessment of microcirculation in takotsubo cardiomyopathy - a pilot study;an interplay of genetics and inflammation affecting left ventricular reverse remodeling in dilated cardiomyopathy;sildenafil inhibits pulmonary hypertension induced by left heart pressure overload in rats;predicting long-term survival after an ischemic stroke;and longitudinal trends in blood pressure, prevalence, awareness, treatment, and control of hypertension in the Czech population. are there any sex differences?.
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Background Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is an extremely rare disorder. Case A 20-year-old, 36-week pregnant female (G1P0) presented with acute shortness of breath, sharp chest pain and fever. She was COVID-19 positive and required BiPAP. Echocardiogram showed 40% EF, dilated LV with global hypokinesis and moderate mitral regurgitation (MR). She was hypotensive and on oxygen despite diuresis, emergent cesarean and COVID-19 treatment. Left heart catheterization showed anomalous takeoff of the left main coronary artery (LCA) from the dilated pulmonary artery (PA) with coronary steal (Figure 1). She had ALCAPA repair with LIMA to LAD bypass grafting. Decision-making Differential diagnoses included peripartum cardiomyopathy, Covid-myocarditis, pulmonary embolism, and spontaneous coronary artery dissection. LHC was performed only when symptoms failed to improve and troponin kept rising. ALCAPA has two major clinical subtypes - Infantile type and adult type. Adult type presents as dyspnea, chest pain, reduced exercise ability, and sudden cardiac death. Despite having good RCA to LCA collaterals, adult patients can still have ongoing ischemia of the LV myocardium, causing ischemic MR, malignant ventricular dysrhythmias. Diagnosis was delayed due to pregnancy and COVID-19 infection. Conclusion ALCAPA is a lethal coronary disorder. Elevated troponin and dilated cardiomyopathy with acute MR should raise suspicion of ALCAPA in young adults. [Formula presented]Copyright © 2023 American College of Cardiology Foundation
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Background Phospholamban (PLN), an inhibitor of sarcoplasmic reticulum (SR) Ca2+-ATPase, is a regulator of Ca2+ release during excitation-contraction coupling. We present a case of recurrent polymorphic ventricular tachycardia (PMVT)/ventricular fibrillation (VF) due to a PLN mutation. Case 38 year-old male presents after resuscitation following VF arrest. An ICD was implanted. Seven years later, he presented with VF storm requiring ventricular assist device support and he underwent catheter ablation of PVC triggers of VF arising from the moderator band. Because he had an ECG that was concerning for early repolarization syndrome, he was placed on quinidine and metoprolol. After an episode of VT in 2020 in the setting of COVID infection, whole genome sequencing was obtained and identified a pathogenic PLN mutation. PLN L39Ter has been associated with dilated and hypertrophic cardiomyopathy as well as sudden death. The patient has a history of normal left ventricular function and wall thickness by echocardiography. Decision-making Given the involvement of PLN on SR handling of Ca2+, flecainide may be a more effective therapy for the treatment of PMVT/VF in this patient. Conclusion PLN mutations have been associated with cardiomyopathies. This case illustrates a patient with the pathogenic PLN L39X variant with short-coupled PMVT with no imaging evidence of structural heart disease. Whether a more targeted therapy such as flecainide may be more effective in this patient remains to be determined. [Formula presented]Copyright © 2023 American College of Cardiology Foundation
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The international standard treatment for mucopolysaccharidosis type I - Hurler syndrome (MPS1H) is haemopoietic stem cell transplant (HSCT) preceded by intravenous enzyme replacement therapy (ERT), with HSCT ideally undertaken before 18 months age to achieve best outcome. The invasive nature and high risk of morbidity and mortality associated with HSCT, in addition to a complex patient cohort, demands an extensive pre-transplant work-up to minimise risks where avoidable. This is achieved by collaboration between transplant and specialist paediatric LD-metabolic services. Transplant may be delayed due to clinical complications pre-transplant, but non-clinical disruptions have also been encountered in practice causing delays from time of diagnosis to transplantation. This work aimed to identify clinical complications and non-clinical disruptions in this process, and to identify areas of improvement for clinical practice, ultimately to achieve timely intervention and optimise clinical outcomes. A single-centre prospective clinical and procedural analysis of 7 MPS1H patients undergoing HSCT between April 2020 - January 2021 was completed. Age at diagnosis (median(range)) was 10 (1.5–25) months. Time from diagnosis to starting ERT (median(range)) was 10 (3–26) days. Time from diagnosis to transplant (median(range)) was 158 (101–189) days, with age at transplant 14 (6.5–30) months. Multiple reasons causing delay were identified. Clinical factors included presence of dilated cardiomyopathy, requirement for adenotonsillectomy to treat obstructive sleep apnoea, Covid-19 infection, vascular device infection, and acute neurosurgical issues including hydrocephalus requiring ventriculoperitoneal shunt and cervical spine stenosis requiring decompression. Non-clinical factors identified included late cancellation of required investigations, missed clinic appointments, and issues with accessing HSCT donors due to UK/European political situation and Covid-19 restrictions. Clear communication between teams was found to be a key identifying factor in ensuring timely completion of the pre-HSCT.
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Background and Aim: Since December 2019 the novel coronavirus disease 2019 (COVID-19) has been burdening all health systems worldwide. However, cardiopulmonary repercussions in paediat-ric patients with congenital heart disease (CHD) are unknown. The aim of this study is to compare changes in cardiopulmonary exercise test (CPET) in this patients before and after COVID-19. Method(s): Prospective observational study was lead comparing CPET results after COVID-19 in paediatric patients with stable CHD who had a previous routine CPET. All underwent for stand-ardised CPET, using Godfrey ramp protocol as recommended by the European Society of Cardiology (ESC). Measured variables, expressed by predicted values, were: forced vital capacity (FVC), forced expiratory volume (FEV1), ratio of minute venti-lation to carbon dioxide production (VE/VO2 slope), peak oxy-gen consumption (peak VO2), oxygen uptake efficiency slope (OUES), oxygen pulse (O2 pulse) and peak heart rate (pHR). Wilcoxon test was used to compare continuous variables for related samples. Result(s): Ten patients (6 boys, 60%;mean age 11,4 +/- 2,4 years) with hemodynamically stable CHD (3 Tetralogy of Fallot, 30%;2 trans-position of the great arteries, 20%;2 dilated cardiomyopathy, 20%;2 Kawasaki disease, 20%;1 cardiac tumor, 10%) were selected to repeat a post-COVID CPET. All of them had mild COVID and could follow ambulatory treatment. Comparing before/post COVID tests, there were no significantly changes in predicted res-piratory parameters: FVC (90,6 +/- 7,4 vs 98,1 +/- 23,9%;p = 0,799), FEV1 (89,5 +/- 13,8 vs 94,5 +/- 8,8%;p = 0,475), VE/CO2 slope (31,6 +/- 3,7 vs 30,6 +/- 3,9degree, p = 0,203). In the same way, no significantly changes were seen in cardiovascular predicted parameters: oxygen pulse (97,3 +/- 19,2 vs 98,5 +/- 17,4%, p = 0,798), peak VO2 (82,4 +/- 19,4 vs 76,8 +/- 13,7;p = 0,123) and OUES (1,79 +/- 0,4 vs 2,01 +/- 0,6;p = 0,066). Respect peak VO2, there was a non-significant slightly decrease in post-COVID test (82,4 +/- 19,4 vs 76,8 +/- 13,7;p = 0,123). Conclusion(s): In our series, post-COVID CPET results showed that paediatric patients with hemodynamically stable CHD had no impairment in their functional capacity in relation to Sars-CoV-2 disease. Contrary to adults with previous cardiovascular disease, children should have mild infections without sequelae in cardio-pulmonary function.
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SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Acute myocarditis from COVID-19 has been well documented, but there are few cases of COVID -19 patients developing dilated cardiomyopathy (3). We present a case of COVID-19 induced dilated cardiomyopathy leading to cardiogenic shock. CASE PRESENTATION: A 49-year-old African-American female presented to the emergency department (ED) with shortness of breath. She was diagnosed with COVID-19 infection four weeks prior to presentation, and since that time she experienced continuously worsening dyspnea, congestion, and weakness. In the ED, the patient was found to have pulmonary edema and bilateral pleural effusions on chest x-ray, as well as acute kidney injury with a creatinine level of 2.85 mg/dL. An echocardiogram revealed a new diagnosis of dilated cardiomyopathy with reduced ejection fraction of 10-15% with a large left ventricular thrombus. Heparin infusion was initiated and intravenous furosemide was administered for diuresis. Her renal function continued to worsen, which was attributed to cardiorenal syndrome. She became hypotensive and was found to be in cardiogenic shock, which required intensive care unit admission with the initiation of continuous renal replacement therapy (CRRT). The patient improved with CRRT, however her renal function did not recover and she continued to require hemodialysis. She was able to be transferred out of the intensive care unit, and the heparin was bridged to warfarin. Goal-directed medical therapy was initiated for her heart failure. She was eventually discharged home with an external cardioverter-defibrillator vest. A follow-up echocardiogram three months later revealed the left ventricular thrombus had resolved, however, her ejection fraction had improved to only 15-20% despite medication compliance. An implantable cardioverter-defibrillator (ICD) was placed and the patient continues to be followed closely by cardiology. DISCUSSION: Viral infection is a well-documented cause of myocarditis with some patients developing dilated cardiomyopathy (1). Inflammatory dilated cardiomyopathy occurs most commonly in patients infected with Coxsackie B virus, Human Parvovirus B19, Adenovirus, Human Immunodeficiency Virus, Hepatitis C Virus, Cytomegalovirus, Epstein-Barr Virus, and Human Herpes Virus 6 (1). The proposed mechanism of inflammatory cardiomyopathy includes infection of the myocytes, incomplete viral elimination, and persistent retained viral components in the myocytes(2). This may cause direct viral injury or chronic myocardial inflammation leading to remodeling (2). It is documented in the literature that COVID-19 can lead to myocarditis and various types of acute cardiomyopathy (3). However, there have been only a few reported cases of COVID - 19 induced dilated cardiomyopathy (3). CONCLUSIONS: While rarely reported thus far, it should be established that COVID-19 alone can cause dilated cardiomyopathy and lead to heart failure (3). Reference #1: Schultheiss H-P, Baumeier C, Pietsch H, Bock C-T, Poller W, Escher F. Cardiovascular consequences of viral infections: from COVID to other viral diseases. Cardiovascular Research. Published online October 5, 2021. doi:10.1093/cvr/cvab315 Reference #2: Kühl U, Pauschinger M, Seeberg B, et al. Viral Persistence in the Myocardium Is Associated With Progressive Cardiac Dysfunction. Circulation. 2005;(13):1965-1970. doi:10.1161/circulationaha.105.548156 Reference #3: Komiyama M, Hasegawa K, Matsumori A. Dilated Cardiomyopathy Risk in Patients with Coronavirus Disease 2019: How to Identify and Characterise it Early? European Cardiology Review. Published online May 27, 2020. doi:10.15420/ecr.2020.17 DISCLOSURES: No relevant relationships by Amanda Cecchini No relevant relationships by Austin Richardson No relevant relationships by Krupa Solanki
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Aims and objectives: To establish that non-invasive ventilation (NIV) can be substituted by high flow nasal cannula (HFNC) for respiratory support during oral feeding of a patient with COVID-19 patients. Materials and methods: This prospective case series was conducted after taking informed and written consent from the patients. Ten patients with severe COVID-19 disease requiring NIV with inspiratory pressure of <10 cm H2O, positive end-expiratory pressure of <6 cm H2O and FiO2 <0.6 were included in this study. Patients with altered consciousness, circulatory failure, or worsening acidosis were not included in the study. Patients underwent HFNC trial for 10 minutes and were screened for risk of dysphagia and aspiration using a 3-ounce water swallowing test. The patients were given a trial of HFNC for 10 minutes with a flow of 60 L/minute and FiO2 of 0.1 more than their requirement on NIV. The patients were observed for hypoxemia (SpO2 <88%) or signs of respiratory distress, e.g., increase in respiratory rate (>35/minute), laboured breathing pattern, use of accessory muscle of respiration, heart rate (>20% change), blood pressure (>20% change), perspiration, and anxiety. Then, HFNC was used for supporting respiration during oral feeding for up to 20 minutes. Feeding was started with a hypocaloric target on starting day and was increased progressively as per European Society for Clinical Nutrition and Metabolism guidelines to the target estimated caloric requirement. Results: The HFNC support for oral feeding was successful with adequate diet intake in eight patients without desaturation/respiratory distress during oral feeding. Other than COVID-19, co-morbidities in these eight patients included diabetes mellitus, obesity, chronic obstructive pulmonary disease, coronary artery disease, and dilated cardiomyopathy. Six patients, previously on enteral nutrition using the nasogastric tube, were successfully switched to oral feeding with help of HFNC. Four patients were directly started on the oral diet with help of HFNC support. HFNC could not support respiration adequately in two of these four patients. The initial trial was successful for one of the patients and HFNC support for oral feeding was used for 3 days, but a progressive increase in ventilatory requirements resulted in failure of HFNC trial subsequent days and the patient was switched to nasogastric feeding. In another patient, the initial trial of HFNC failed due to rapid desaturation within a few minutes of the trial. The eight patients in whom HFNC was used successfully for feeding were switched to HFNC completely and discharged from the hospital after weaning off from oxygen support. The patients who failed the HFNC support for feeding required higher ventilatory requirements and needed endotracheal intubation. Conclusion: Based on our case series, using daily screening trial of oral feeds with HFNC support in selected patients of severe COVID-19 pneumonia on NIV seems thought-provoking and should be explored for its potential in improving patient's nutrition with a positive impact on the outcome.
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BACKGROUND Vaccination against COVID-19 is crucial for controlling this scourge. COVID/vaccination deniers often rationalise their unfounded fears by citing rare vaccination side-effects. One of the most frequently cited side effects is myocarditis, especially in younger persons. Malta has very high vaccination rates. This study was carried out to ascertain whether admissions to hospital for myocarditis changed during the vaccination rollout, up to October 2021, when 83.4% of Malta’s population of circa half a million had had their first 1st dose. METHODS Malta is served by one large regional hospital (Mater Dei Hospital). Anonymous data for admissions with a diagnosis of myocarditis (ICD I40, I41, I51.4) were obtained for 01/2016-10/2021. Myocarditis discharges and 95% confidence intervals were plotted for 2016-2020. Myocarditis discharges for Jan-Oct 2021 were plotted separately. RESULTS There were no outlier values for myocarditis discharges in either direction for any age for either sex. CONCLUSION Myocarditis, independent of vaccination, is commonest in young males, half resolving and some developing dilated cardiomyopathy, possibly leading to transplantation or death. The ongoing mass vaccination with novel messenger RNA vaccines resulted in reports of myocarditis in male teens, this being a rare side effect. The lack of significantly increased rates of myocarditis admission in any age age/sex group in Malta confirms that only rarely, myocarditis may be temporally associated with COVID vaccination which almost invariably runs a benign course and that this risk is very low, far lower than myocarditis due to actual COVID infection.
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CASE: A 51-year-old man without significant past medical history presented to our hospital with dyspnea on exertion. SARS-CoV-2 was detected on routine occupational screening 2 months prior to admission. He subsequently reported a 100lb weight loss, during which time he experienced dysgeusia and ate primarily cereal, sandwiches, and potatoes and consumed nearly no fruits or vegetables. Three weeks prior to admission he developed postprandial nausea and vomiting and anorexia. A week later he developed progressive epigastric pain, lower extremity edema, and dyspnea while walking around the college campus where he worked as a security guard, and sought medical attention. He did not have fever, chills, night sweats, cough, orthopnea, paroxysmal nocturnal dyspnea, rash, or diarrhea. He had not seen a doctor in 20 years and took no medications. He did not drink alcohol, smoke cigarettes, or use illicit substances. Vital signs were T 36.6°F HR 104 BP 149/111 RR 20 and SpO2 97%. Physical examination revealed a cachectic man with bitemporal wasting, sunken orbits, poor dentition, and severe periodontal disease. JVP was 14cm of H2O at 45°. An S3 was present. The abdomen was tender to palpation in the mid epigastrium. The extremities were cool with 3+ pitting edema. Pancreatitis was diagnosed after discovery of markedly elevated lipase levels and peripancreatic fat stranding on abdominal CT. TTE showed biventricular systolic dysfunction with LVEF 15%. He developed cardiogenic shock complicated by oliguric renal failure, congestive hepatopathy and obtundation, requiring ICU transfer for diuresis and inotropic support. Further workup revealed deficiencies of thiamine, zinc, and vitamins A, C, and D. A regadenoson myocardial perfusion PET/CT showed no flow-limiting coronary artery disease, and workup for inflammatory, infectious, and toxic-metabolic causes of heart failure was unrevealing. While COVID myocarditis and multisystem inflammatory syndrome in adults (MIS-A) were considered, ultimately, a diagnosis of wet beriberi was made. After 5 months of aggressive nutritional supplementation via percutaneous gastrostomy tube and initiation of guideline-directed medical therapy, LVEF improved to 53% and weight increased by 35lbs. IMPACT/DISCUSSION: Wet beriberi is a potentially underrecognized cause of dilated cardiomyopathy in resource-rich areas. Within 3 months, thiamine deficiency can cause high-output heart failure due to impaired myocardial energy metabolism and dysautonomia. Risk factors include alcohol use disorder, prolonged vomiting, and history of bariatric surgery. CONCLUSION: The laboratory evaluation of non-ischemic dilated cardiomyopathy should include measurement of serum thiamine, carnitine, and selenium levels in select patients, alongside iron studies, ANA, screening for HIV, Chagas disease, and viral myocarditis, and genetic testing in patients with a suggestive family history. Empiric thiamine repletion should be considered in all critically ill patients with evidence of malnutrition.
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Background. Coronavirus infection (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with cardiovascular disease especially patients with advanced heart failure are at particularly high risk of morbidity and mortality. Patients with left ventricular assist device (LVAD) represent a unique population at risk because of comorbidities and functionally compromised immunity. Аim of this article was to analyze clinical cases of COVID-19 among LVAD patients of the Republic of Kazakhstan. Material and methods. Characteristics of LVAD patients of the Republic of Kazakhstan who developed COVID-19 between March 2020 and August 2021, initial manifestations of the disease, comorbidities, complications and clinical outcomes were collected and analyzed. Results. A total of 177 patients with LVAD who were supported and registered by the NAO “National Scientific Cardiac Surgery Center” were interviewed. 41 (23.2%) patients had classic COVID-19 symptoms. The mean age of the patients was 55 years (interquartile range, 17-75), and 9 (21.9%) patients were female. The majority of patients (n=36, 87.8%) were implanted with LVAD HeartMate 3. The largest number, 19 (46%) patients, were patients with dilated cardiomyopathy (DCM). The time of LVAD support ranged from 1 month to 83 months before the onset of symptoms and diagnosis of COVID-19. 13 (31.7%) patients required hospitalization due to decreased oxygen saturation (less than 94%) and oxygen deprivation. 3 patients (1.7% among 177 supported patients and 7.3% among patients with COVID-19) required care and treatment in an intensive care unit. Conclusion. We presented an analysis of clinical cases in LVAD patients with COVID-19 in Kazakhstan. To note, there are no guidelines for management and treatment, no data related to the clinical course of COVID-19 in patients on LVAD support to date. Close monitoring of clinical status, anticoagulation and frequent collection of device parameters and DL exit site images, precautionary measures consideration, early diagnosis, timely initiated treatment, supportive psychological care, multidisciplinary approach and rigorous follow-up are crucial in the management of LVAD patients with COVID-19.
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Development of endomyocardial biopsy for acute rejection monitoring in the early Seventies, and above all use of cyclosporine in the clinical practice starting from 1980, introduced the modern era of heart transplantation. Following the initial positive outcomes, the first Italian transplant was performed in Padua by V.Gallucci on November 15th 1985. This pioneering success was rapidly repeated in Pavia, where M.Viganò performed the second transplant on Novembre 17th. Recipient was 20 years old man, suffering from dilated cardiomyopathy, on urgent transplant list. Cardiac index was 1.38 l/min/m2 and pulmonary vascular resistance 1.6 WU. Donor was a 14 years old boy died of brain injury. Total ischemic time was 125 minutes. Induction immunosuppression consisted of horse anti-lymphocyte immunoglobulins, whereas maintenance therapy included cyclosporine, azathioprine and steroids. Postoperative course was complicated by pericardial effusion and cholestatic jaundice. Later pulmonary aspergillosis occurred and due to the profound immunodepression was complicated by fungal localization at L2 vertebral body. The infection was treated with surgical removal of the secondary localization and amphotericin B administration. On December 6th severe acute rejection was found at biopsy and treated with i.v. steroid pulse. Length of ICU and hospital stay was 28 and 72 days, respectively. In 1998 HCV infection was detected and eradicated in 2017 with elbasvir/grazoprevir therapy. Complications of long term immunosuppressive treatment included dyslipidemia, myeloma and basal cell carcinoma. Due to long-term calcineurin inhibitors therapy progressive chronic renal failure occurred, leading to replacement therapy in 2015 and kidney transplantation in 2016. In 2015 the patient underwent percutaneous coronary intervention with stents implantation in two marginal branches and in the anterior descending artery in 2021. Everolimus was introduced to slow down progression of cardiac allograft vasculopathy. In 2020 he suffered from Covid-19, but the course of infection was uneventful being cough the only symptom. We report the eldest survivor after heart transplant in Europe. Our case demonstrates that despite early and long-term complications of immunosuppressive therapy, a careful and patient tailored management allowed an amazing outcome. Nowadays heart transplant remains the best treatment for end stage heart failure and allows to resume a nearly normal quality of life.
ABSTRACT
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.