New-onset Dilated Cardiomyopathy Research Articles

Cardiac damage in an adolescent patient with COVID-19: a case report

COVID-19 has been found to affect the cardiovascular system leading to myocardial damage. A study of 41 patients in Wuhan, China, found that 12% of COVID-19 patients experienced virus-related acute cardiac damage.Subsequent bigger Chinese studies also found acute cardiac damage in 7.2% to 27.8% of hospitalized patients. As a chronicsequela, this condition may result in cardiomyopathy. We report acase of an adolescent COVID-19 survivor with dilated cardiomyopathy with no underlying heart disease. A male patient aged 16 years old was admitted to our outpatient clinic with the primary symptom of exhaustion and had recovered frommild to moderate COVID-19 one month prior to the visit. No previous history of heart disease was documented. Physical examination showed no abnormalities. Laboratory results revealed substantially elevated NT-proBNP (7705 pg/mL) and D-dimer (1850 ng/mL). ECG presented normal sinus rhythm with poorR wave progression. Echocardiography revealed all chamber dilatation, eccentric left ventricular hypertrophy, globalhypokinetic, moderate mitral regurgitation, and reduced ejection fraction (22%). We diagnosed the patient with new-onset dilated cardiomyopathy and began treatment with candesartan, bisoprolol, furosemide, spironolactone, rivaroxaban, and trimetazidine. The recovery was steady at three-month follow-up visit. The emergence of new-onset cardiomyopathy in this previously healthy adolescent raisesthepossibility of COVID-19 acting asthe sole cause of myocardial injuryin the absence of underlying heart disease. To avoid further complications, comprehensive evaluation and effective therapy should be implemented during hospitalization and post-discharge. Additional tests such as cardiac magnetic resonance imaging and endomyocardial biopsies shouldbe performed to support final proof.

C74. Post covid-19 cardiomyopathy in an adolescent patient: a case report

Abstract Background Myocardial injury caused by viral myocarditis may occur during COVID-19 infections. This condition may lead to cardiomyopathy as the chronic sequela. We report a case of an adolescent COVID-19 survivor without underlying heart disease presented with dilated cardiomyopathy. Case Summary A 16-year-old male patient was referred to Cardiology Outpatient Clinic, Indonesian Army Central Hospital Gatot Soebroto. The patient presented with a chief complaint of fatigue and just recovered from mild to moderate COVID-19 one month before the visit. There was no prior history of heart disease. Physical examination was within normal limit, but laboratory findings showed highly elevated NT-proBNP (7705 pg/mL) and D-dimer (1850 ng/mL). ECG revealed normal sinus rhythm with poor R wave progression. Echocardiography detected all chamber dilatation, eccentric left ventricular hypertrophy, global hypokinetic, moderate mitral regurgitation, and reduced ejection fraction (22%). The patient was diagnosed with new-onset dilated cardiomyopathy as a COVID-19 sequela and we initiated treatment with ARB (candesartan), beta-blocker (bisoprolol), diuretics (furosemide and spironolactone), rivaroxaban, and trimetazidine. During a follow-up visit three months later, the patient’s recovery was stable. Discussion The occurrence of new-onset cardiomyopathy in our previously healthy young patient highlights the possible mechanism of COVID-19 as a single cause of myocardial injury without underlying heart disease. Comprehensive evaluation and optimal treatment should be taken during hospitalization and post-discharge period to prevent further complications. Additional examinations such as cardiac magnetic resonance and endomyocardial biopsy should be done to provide definitive confirmation.

C74. Post covid-19 cardiomyopathy in an adolescent patient: a case report

BackgroundMyocardial injury caused by viral myocarditis may occur during COVID-19 infections. This condition may lead to cardiomyopathy as the chronic sequela. We report a case of an adolescent COVID-19 survivor without underlying heart disease presented with dilated cardiomyopathy. Case SummaryA 16-year-old male patient was referred to Cardiology Outpatient Clinic, Indonesian Army Central Hospital Gatot Soebroto. The patient presented with a chief complaint of fatigue and just recovered from mild to moderate COVID-19 one month before the visit. There was no prior history of heart disease. Physical examination was within normal limit, but laboratory findings showed highly elevated NT-proBNP (7705 pg/mL) and D-dimer (1850 ng/mL). ECG revealed normal sinus rhythm with poor R wave progression. Echocardiography detected all chamber dilatation, eccentric left ventricular hypertrophy, global hypokinetic, moderate mitral regurgitation, and reduced ejection fraction (22%). The patient was diagnosed with new-onset dilated cardiomyopathy as a COVID-19 sequela and we initiated treatment with ARB (candesartan), beta-blocker (bisoprolol), diuretics (furosemide and spironolactone), rivaroxaban, and trimetazidine. During a follow-up visit three months later, the patient’s recovery was stable.Discussion The occurrence of new-onset cardiomyopathy in our previously healthy young patient highlights the possible mechanism of COVID-19 as a single cause of myocardial injury without underlying heart disease. Comprehensive evaluation and optimal treatment should be taken during hospitalization and post-discharge period to prevent further complications. Additional examinations such as cardiac magnetic resonance and endomyocardial biopsy should be done to provide definitive confirmation.

Relationships between circulating galectin-3, extracellular matrix fibrosis and outcomes in dilated cardiomyopathy.

Galectin-3 is an emerging biomarker in cardiovascular disease. Myocardial galectin-3 is involved in the pathology of cardiac fibrosis; however, the role of circulating galectin-3 is not yet established. To assess the relationships between circulating galectin-3, fibrosis and outcomes in dilated cardiomyopathy (DCM). We included 70 patients (age: 48 ±12.1 years, ejection fraction (EF) 24.4 ±7.4%) with new-onset DCM (n = 35, ≤6 months). Galectin-3 and procollagen type I and III (PICP, PINP, PIIICP, and PIIINP), transforming growth factor β (TGF-β), connective tissue growth factor (CTGF), osteopontin (OPN), matrix metalloproteinases (MMP-2 and -9), and tissue inhibitor (TIMP-1) were determined in serum at baseline and after 3 and 12 months. Patients underwent endomyocardial biopsy. The endpoint was a combination of death and urgent hospitalization at 12 months. Galectin-3 did not correlate with biopsy-determined fibrosis. Baseline galectin-3 correlated with OPN,, TIMP-1, PIIICP, and MMP-2. In new-onset DCM, galectin-3 levels at baseline were higher than at 3 and 12 months, whereas in chronic DCM there was no difference. Galectin-3 was a predictor of the endpoint (hazard ratio (HR) = 1.115; 95% confidence interval (95% CI) = 1.009-1.231; p < 0.05). The best cut-off value was 14.54 ng/mL (area under the curve (AUC) = 0.67). Patients with galectin-3 ≥14.54 ng/mL had an increased risk of events (HR = 2.569; 95% CI = 1.098-6.009; p < 0.05). Circulating galectin-3 is unrelated to fibrosis. Serial measurements of galectin-3 correlated with markers of fibrosis, including markers of collagen synthesis and OPN. Circulating galectin-3 was independently associated with cardiovascular (CV) outcomes in DCM.

Fulminant Lymphocytic Myocarditis Possibly Secondary to Rhinovirus Infection in an Adolescent Female

Introduction Rhinovirus is responsible for a large number of upper respiratory tract infections annually. While viral infection is a well-known cause of dilated cardiomyopathy (DCM), rhinovirus-associated myocarditis is not well understood. This is a case of a young woman who suffered cardiogenic shock due to fulminant lymphocytic myocarditis and diagnostic testing noting the presence of rhinovirus, suggesting potential causation. Case Description During late autumn, a healthy 19 year old woman noted 1 week of progressive exertional dyspnea associated with a non-productive cough and epigastric pain. She was diagnosed with a new-onset DCM at a community hospital and transferred to our tertiary center for further management. Urgent echocardiography demonstrated severe biventricular systolic dysfunction and chamber dilation but normal wall thickness. Severe tricuspid valve insufficiency was present secondary to torn chordea tendinae causing a flail septal leaflet Cardiac magnetic resonance imaging revealed diffuse biventricular sub-endocardial delayed enhancement concerning for fulminant myocarditis. Viral respiratory testing was positive for rhinovirus alone. Other laboratory diagnostic data was unremarkable. Cardiac catheterization was conducted, demonstrating the absence of coronary artery disease, but severely impaired cardiac output with an index of 1.65 L/min/m2 and moderately elevated left sided filling pressures. An endomyocardial biopsy confirmed lymphocytic myocarditis with extensive necrosis and fibrosis and CD68 positivity indicating macrophage predominate infiltrate. On the night of hospital day 3, hemodynamic instability was noted with an accelerating frequency of ventricular ectopy. Dobutmaine was started and the initiation of temporary mechanical support was attempted with Impella, However, this was aborted due to catheter occlusion of a small diameter femoral artery given her small stature. Therefore, central VA ECMO was placed. An expedited heart transplant evaluation was begun which she received 8 days later. Gross pathology of the explanted heart confirmed the diagnosis, with a mixed T-cell and B-cell lymphocytic infiltrate. Several months post-transplant, she is thriving. In the absence of other compelling causes of DCM, rhinovirus remains a possible culprit. Viral myocarditis is typically characterized by direct myocyte damage causing necrosis and host immune system upregulation leading to molecular mimicry. However, rhinovirus direct cardiac toxicity has not been identified. To date, two other reported cases of unexplained DCM in a 4 and 27 year-old showed the presence of rhinovirus on nasal swab however, myocardial biopsy was not performed. Conclusion This case presents a missed opportunity for confirming the link between rhinovirus and DCM. Confirmatory viral PCR on biopsy tissue should become a practice standard in any suspected cases and as a standard investigation in cases with unclear etiology.

Myocarditis Associated With COVID-19.

Coronavirus disease 2019 (COVID-19) has rapidly evolved into a global pandemic, with affecting to-date over 23 million people and causing over 800,000 deaths around the globe. The major pathogenetic mechanisms include inflammation, vasoconstriction and thrombogenesis. Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) typically manifests as fever, cough, shortness of breath, and exhibits radiographic evidence of bilateral pneumonic infiltrates. Recent meta-analyses have shown that myocardial injury, including viral myocarditis, is prevalent among infected patients, especially in patients requiring ICU level care. Diagnosis of viral myocarditis is multifactorial and involves detection of elevated cardiac biomarkers and echocardiographic evidence of cardiomyopathy, in the absence of diseased coronary arteries. Endomyocardial biopsy with histopathologic examination provides definitive confirmation. We present a case of a previously healthy 52-year-old male who presented clinically with suspected myocarditis with new-onset dilated cardiomyopathy (DCM) and systolic dysfunction as a sequela of infection with SARS-CoV-2. In this report we highlight the clinical presentation of echocardiographic findings and proposed pathogenetic mechanisms of myocarditis associated with COVID-19 which has a varied presentation, ranging from clinically silent to life-threatening arrhythmias with hemodynamic compromise.

Twelve-month kinetics of circulating fibrosis-linked microRNAs (miR-21, miR-29, miR-30, and miR-133a) and the relationship with extracellular matrix fibrosis in dilated cardiomyopathy.

IntroductionA single measurement of any biomarker may not reflect its full biological meaning. The kinetics of fibrosis-linked microRNAs and their relationship with extracellular matrix (ECM) fibrosis in dilated cardiomyopathy (DCM) have not been explored.Material and methodsWe evaluated 70 consecutive DCM patients (48 ±12.1 years, left ventricular ejection fraction 24.4 ±7.4%). All patients underwent right ventricular endomyocardial biopsy in order to quantify ECM fibrosis and measure collagen volume fraction (CVF). Circulating microRNAs (miR-21-5p, miR-29b, miR-30c-5p, and miR-133a-3p) were measured with quantitative polymerase chain reaction (PCR) at baseline and at 3 and 12 months.ResultsBased on the biopsy results, two groups of patients were identified: with (n = 24, 34.3%) and without (n = 46, 65.7%) ECM fibrosis. Except for a single measurement of miR-29b at 3 months (DCM with fibrosis: 6.03 ±0.72 vs. DCM without fibrosis: 6.4 ±0.75 ΔCq; p < 0.05), baseline, 3- and 12-month kinetics of microRNAs did not differ between the two groups. Moreover, 12-month microRNA kinetics did not differ in patients with new-onset DCM (duration < 6 months; n = 35) and chronic DCM (> 6 months; n = 35). Only miR-29 at 3 months correlated with CVF (r = –0.31; p < 0.05), whereas other microRNAs did not correlate with CVF either at 3 or at 12 months.ConclusionsRegardless of ECM fibrosis status or duration of the disease, 12-month patterns of circulating microRNAs are similar in DCM. Correlations between microRNAs, measured at 3 and 12 months, are lower than expected. In this study, regardless of the time point, circulating microRNAs were not able to differentiate between DCM patients with versus without fibrosis.

Reading between the Lyme: isBorrelia burgdorferia cause of dilated cardiomyopathy? The debate continues

Reading between the Lyme: is<i>Borrelia burgdorferi</i>a cause of dilated cardiomyopathy? The debate continues

Ventricular Remodeling and Survival Are More Favorable for Myocarditis Than For Idiopathic Dilated Cardiomyopathy in Childhood

Background— Myocarditis is a cause of a new-onset dilated cardiomyopathy phenotype in children, with small studies reporting high rates of recovery of left ventricular (LV) function. Methods and Results— The presenting characteristics and outcomes of children with myocarditis diagnosed clinically and with biopsy confirmation (n=119) or with probable myocarditis diagnosed clinically or by biopsy alone (n=253) were compared with children with idiopathic dilated cardiomyopathy (n=1123). Characteristics at presentation were assessed as possible predictors of outcomes. The distributions of time to death, transplantation, and echocardiographic normalization in the biopsy-confirmed myocarditis and probable myocarditis groups did not differ ( P ≥0.5), but both groups differed significantly from the idiopathic dilated cardiomyopathy group (all P ≤0.003). In children with myocarditis, lower LV fractional shortening z -score at presentation predicted greater mortality (hazard ratio, 0.85; 95% confidence interval, 0.73 to 0.98; P =0.03) and greater LV posterior wall thickness predicted transplantation (hazard ratio, 1.17; 95% confidence interval, 1.02 to 1.35; P =0.03). In those with decreased LV fractional shortening at presentation, independent predictors of echocardiographic normalization were presentation with an LV end-diastolic dimension z -score &gt;2 (hazard ratio, 0.36; 95% confidence interval, 0.22 to 0.58; P &lt;0.001) and greater septal wall thickness (hazard ratio, 1.16; 95% confidence interval, 1.01 to 1.34; P =0.04). Conclusions— Children with biopsy-confirmed or probable myocarditis had similar proportions of death, transplantation, and echocardiographic normalization 3 years after presentation and better outcomes than those of children with idiopathic dilated cardiomyopathy. In children with myocarditis who had impaired LV ejection at presentation, rates of echocardiographic normalization were greater in those without LV dilation and in those with greater septal wall thickness at presentation. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00005391.

Predicting recovery: Successful explant of a ventricular assist device in a child with dilated cardiomyopathy

A previously healthy, 13-year-old girl presented with new-onset dilated cardiomyopathy, and is placed on a left ventricular assist device (VAD). Herein we describe a unique VAD weaning protocol used to determine the timing and feasibility of a VAD explant.

Intravenous immune globulin in the therapy of myocarditis and acute cardiomyopathy.

Although an autoimmune pathogenesis has been postulated for dilated cardiomyopathy, immunosuppressive therapy has not been shown to be effective in clinical trials. Immune modulatory therapy with immune globulin is an effective therapy for Kawasaki disease in children, and recent data suggest that it improves ventricular function in children with new-onset dilated cardiomyopathies. The role of immune globulin therapy in adults with this disorder has not previously been evaluated. Ten patients were treated with high-dose intravenous immune globulin infusions (2 g/kg). All were hospitalized with NYHA class III to IV heart failure, left ventricular ejection fraction (LVEF) < 0.40, and symptoms for < 6 months at the time of presentation. One patient died before the completion of therapy. The remaining 9 were discharged, and LVEF was reassessed 12 months after therapy. LVEF improved from 0.24 +/- 0.02 (mean +/- SEM) at baseline to 0.41 +/- 0.04 at follow-up (P = .003). All 9 patients improved functionally to NYHA class I to II, and there have been no subsequent hospitalizations for heart failure during the course of follow-up. In this series of patients with new-onset dilated cardiomyopathy treated with high-dose immune globulin, LVEF improved 17 EF units. The effectiveness of intravenous immune globulin therapy in this disorder should be evaluated in a randomized, multicenter trial.

Recently diagnosed idiopathic dilated cardiomyopathy: Incidence of myocarditis and efficacy of prednisone therapy

Fifty-two patients with recently diagnosed idiopathic dilated cardiomyopathy were studied to determine the incidence of myocarditis; patients were randomly assigned to receive either conventional therapy alone or conventional therapy plus prednisone to assess possible therapeutic efficacy with regard to survival. Inflammatory criteria were present in 23% of the population studied with 13% having overt myocarditis according to the Dallas criteria. The addition of prednisone to conventional therapy did not improve survival in a homogeneous population with new-onset dilated cardiomyopathy. Furthermore, the diagnosis of myocarditis by endomyocardial biopsy did not influence 2-year survival once dilated cardiomyopathy had developed. Biopsy-documented myocarditis resolved in all patients, according to results of 3-month follow-up endomyocardial biopsies, regardless of treatment group. There was a trend for patients with a left ventricular ejection fraction less than 20% to show reduced survival at 2 years compared to the group with a higher ejection fraction ( p = 0.07). Right ventricular dysfunction determined at catheterization was present in 20 of 52 patients and was the most significant predictor of survival. Patients with precerved right ventricular function had a 95% 24-month survival rate compared to 47% for patients with right ventricular diastolic dysfunction (right ventricular end-diastolic pressure ≥11 mm Hg) ( p = 0.005).