Fulminant Viral Myocarditis Research Articles

Self-recruited neutrophils trigger over-activated innate immune response and phenotypic change of cardiomyocytes in fulminant viral myocarditis

Fulminant myocarditis (FM) is a life-threatening inflammatory disease. However, the mechanisms underlying its acute onset are unknown. By dynamic cardiac function measurement, we discovered that the initiation of sudden hemodynamic collapse was on day 4 in the mouse model of FM. Single-cell RNA-sequencing study revealed that healthy cardiomyocytes (CMs) lost their contractile and metabolic function and differentiated into pro-angiogenic and pro-inflammatory CMs. Meanwhile, neutrophils, the most expanded immune cells, exhibited a unique developmental trajectory only after migrating to the heart, where they continuously attracted peripheral neutrophils via Cxcl2/Cxcl3, resulting in the acute accumulation of neutrophils in the heart. Well-differentiated cardiac-infiltrating neutrophils, rather than viruses, induced phenotypic changes in CMs. Moreover, neutrophils could amplify cytokine storm by recruiting and activating pro-inflammatory monocytes. Blockade of the self-recruiting loop of neutrophils by targeting the Cxcl2/Cxcl3-Cxcr2 axis substantially alleviated FM in mice. Collectively, we provide a comprehensive single-cell atlas of immune cells and CMs in FM, elucidate the disease pathogenesis, and suggest potential therapeutic strategies.

Fulminant Myocarditis Associated With Parvovirus B19 and Epstein-Barr Virus Coinfection

Abstract Parvovirus B19 (PVB19) and Epstein-Barr virus (EBV) commonly cause infection worldwide, with most persons infected during childhood. Their disease courses are usually mild and brief; however, PVB19 and EBV have been implicated as etiologies of viral myocarditis. We report a case of PVB19 and EBV coinfection associated with fulminant lymphocytic myocarditis. We address the implications of the case, including the differential diagnosis, immunomodulatory treatment considerations, and evidence for the pathologic roles of PVB19, EBV, and coinfection in myocarditis. Although the pathogenic roles of PVB19 or EBV alone in myocarditis are not well established, coinfection of PVB19 and EBV may unlock their pathogenic roles causing fulminant myocarditis. Treatment with steroids and intravenous immunoglobulin G in a patient with rapid clinical deterioration despite the presence of active infection on endomyocardial biopsy by polymerase chain reaction can result in a safe and quick recovery of fulminant viral myocarditis. Early and aggressive intervention, including both mechanical circulatory support and immunomodulatory therapy, may be key to improved outcomes in cases of fulminant myocarditis.

Retrospective Analysis of ECMO for Acute Fulminant Viral Myocarditis

Background The inflammation or degeneration of the heart muscle myocarditis may be fatal. This disease often goes undetected. It may also disguise itself as ischemic valvular or hypertensive heart disease. Here we report eight cases of acute fulminant viral myocarditis suffering from low cardiac output ARDS Acute respiratory distress syndrome formation and successfully treated with ECMO Extra corporeal membrane oxygenation.Methodology All the cases were admitted in the emergency coronary care unit with severe respiratory distress poor hemodynamics and ECHO examination revealed low Left ventricle Ejection Fraction LVEF15-20. Veno - Arterial ECMO was initiated with femoro-femoral cannulation with distal limb perfusion. On ECMO support the hemodynamics were stabilized with no inotropic support. The heart and lungs were given adequate rest time for recovery by maintaining total cardiac output on ECMO. The average ECMO support was 84.2 plusmn 4 hours. Maquet Quadrox PLS Sorin Dideco ECMO oxygenators with rotaflow centrifugal pump were used. Delta pressure pre-pump pressures were continuously monitored.Results Out of the eight cases put on VA ECMO for viral myocarditis seven were successfully weaned off and were discharged success rate of 87.5. Soon after the initiation of ECMO the arterial saturation reached the normal levels. The serum lactate levels which were high gt6 mmolL prior to initiation of ECMO remarkably came down to lt2 mmolL after 24 hours. Seven patients were weaned off and decannulated in the operating room. One patient required LV decompression by Balloon Atrial Septostomy in the Hybrid OR and was successfully weaned off after 48 hours. One patient succumbed due to continuous low cardiac output which was irreversible with full blown septicemia and was not responding to ECMO and medications.Conclusion Peripheral VA-ECMO support is very effective in optimizing myocardial recovery for the treatment of refractory acute fulminant viral myocarditis when maximal conventional supports are ineffective.

Extracorporeal membrane oxygenation in intensive care unit: About the first moroccan experience

Circulatory support and particularly extracorporeal membrane oxygenation (ECMO) has become a possible therapeutic measure to treat children and adults with potentially reversible respiratory and/or heart failure who do not respond to conventional treatment. This technique was introduced recently in Morocco, where the first ECMO was performed in our study. This is a retrospective descriptive monocentric study of 5 patients hospitalized in the mother and child reanimation department at the Hassan II University Hospital in Fez. All patients benefited from ECMO during the period from January 2016 to March 2017. We performed 4 VA ECMO and 1 VV ECMO.40% of our patients survived after the introduction of ECMO, while 60% died. Our first case concerns a 12-year-old child suffering from rheumatic fever in whom a VV ECMO was put in place for acute respiratory distress syndrome complicating a mitro-aortic valve replacement surgery for an infective endocarditis. Observation 2 is the experience of a central VA ECMO placed in a 2 years old child, post-cardiotomy of a complex congenital heart disease surgery combining a double outlet right ventricle, interventricular communication and pulmonary arterial hypertension. The 3rd case is a 45-year-old patient carrying a dilated cardiomyopathy with severe biventricular dysfunction and multivisceral failure who benefited from a VA ECMO for a refractory cardiogenic shock as a “bridge to heart transplant”. The 4th patient is an 8-month-old infant with ALCAPA syndrome in whom a VA ECMO was implanted after cardiac coronary reimplantation surgery ( Fig. 1 ). The last case concerns a 56-year-old patient in whom VA ECMO was indicated for cardiogenic shock secondary to fulminant viral myocarditis due to the H3N2 influenza virus. Despite the limited number of patients in our study, the introduction of ECMO in Morocco constitutes a major technical advance announcing significant therapeutic progress in the future.

Effect of Acute Immunosuppression on Left Ventricular Recovery and Mortality in Fulminant Viral Myocarditis: A Case Series and Review of Literature

BackgroundFulminant viral myocarditis (FVM) is a rare cause of cardiogenic shock associated with high morbidity and mortality rates. An inappropriately activated immune system results in severe myocardial inflammation. Acute immunosuppressive therapy for FVM therefore gained in popularity and was described in numerous retrospective studies. MethodsWe conducted an extensive review of the literature and compared it with our single-centre retrospective review of all cases of FVM from 2009-2019 to evaluate the possible effect of acute immunosuppression with intravenous immunoglobulins and/or high dose corticosteroids in patients with FVM. ResultsWe report on 17 patients with a mean age of 46 ± 15 years with a mean left ventricular ejection fraction (LVEF) of 15 ± 9% at admission. Fourteen (82%) of our patients had acute LVEF recovery to ≥ 45% after a mean time from immunosuppression of 74 ± 49 hours (3.1 days). Extracorporeal membrane oxygenation (ECMO) was required in 35% (6/17) of our patients for an average support of 126 ± 37 hours. Overall mortality was 12% (2/17). No patient needed a long-term left ventricular assist device or heart transplant. All surviving patients achieved complete long-term LVEF recovery. ConclusionsOur cohort of 17 severely ill patients received acute immunosuppressive therapy and showed a rapid LVEF recovery, short duration of ECMO support, and low mortality rate. Our suggested scheme of investigation and treatment is presented. These results bring more cases of successfully treated FVM with immunosuppression and ECMO to the literature, which might stimulate further prospective trials or a registry.

Impact of Immunosuppression on Acute Left Ventricular Function Recovery and ECMO Use in Patients with Fulminant Viral Myocarditis: An “All-In” Strategy

Fulminant viral myocarditis (FVM) is a rare cause of cardiogenic shock due to severe myocardial inflammation induced by inappropriately activated immune system. For years, a biased study with 15 patients has maintained the myth that FVM has an excellent prognosis but recent literature clearly shows a high morbidity with need for mechanical circulatory support (MCS) up to 60% and mortality rates between 12 to 45%. Owing to this high mortality, acute immunosuppressive therapy for FVM gained in popularity and was described in numerous retrospective studies, with a combined overall mortality under 5%. Retrospective review of consecutive cases from 2009 to 2019 at IUCPQ. FVM was defined by LVEF < 40%, evidence of active inflammation, positive myonecrosis biomarkers and need for hemodynamic support after a infectious prodrome and new onset heart failure symptoms <2 weeks. 81% (13/16) of our patients had acute LVEF recovery to ≥ 45% with a mean delay of 69 hours (2.9 days) after immunosuppression. ECMO was required for 31% (5/16) of our patients with a mean delay from hemodynamic instability of 32 hours and for a mean duration of 120 hours. The vast majority of patients showed good tolerance to therapy with only 3 possible adverse effects: aseptic meningitis, immune-mediated hemolysis and intensive care myopathy. Our local experience suggests that acute immunosuppressive therapy with IVIG and/or high dose methylprednisolone may influence the natural evolution of FVM by promoting rapid LVEF recuperation and lessen the need and duration of ECMO support.

Fulminant Myopericarditis Complicated by Tamponade Due to Influenza A Infection in a Healthy Young Female

SESSION TITLE: Other Infections SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Viral myocarditis should be strongly considered in any previously healthy patient who presents with new symptoms of chest pain, shortness of breath and fevers. CASE PRESENTATION: A 37-year-old healthy female presented to outpatient clinic and was diagnosed with an upper respiratory infection. Three days later she presented to an emergency department after continued escalation of shortness of breath, fevers, and chest pain. She was found to be tachycardic and hypotensive. Laboratory evaluation revealed WBC 16.7 mcL with Troponin T 0.06 ng/dL and NT-Pro BNP 1209 pg/mL. CT angiography showed no evidence of pulmonary embolism but revealed a new pericardial effusion and bilateral pleural effusion. Echocardiography revealed a left ventricular ejection fraction (LVEF) of 57% and 1.1cm pericardial effusion. Influenza A PCR nasal swab returned positive and the patient was initiated on oseltamivir and intravenous steroids. Over the next 24 hours, the patient continued to deteriorate with worsening tachycardia and hypotension despite aggressive fluid resuscitation and vasopressor support. She was initiated on broad spectrum antibiotics despite negative bacterial respiratory and blood cultures throughout her hospitalization. Troponin T peaked at 0.77 ng/mL. Repeat echocardiography was concerning for tamponade physiology and ultimately an urgent pericardial window operation was performed. This failed to significantly stabilize the patient and she was transferred to a transplant capable center given concern for fulminant viral myocarditis. She underwent right ventricular biopsy under echo guidance, during which LVEF was noted as 42%. Biopsy returned without evidence of myocarditis. Supportive care was continued and gradually the patient’s tachycardia and hypotension improved. MRI was performed on hospital day 8 which showed patchy diffuse myocardial edema and sub-epicardial delayed enhancement with pericardial edema and effusion concerning for myopericarditis. DISCUSSION: Influenza myocarditis is a severe complication of influenza infection. The clinical course is variable, with cardiac sequela typically visible within seven days of infection. Complications are severe with approximately 37% of requiring advanced cardiac support therapy and mortality 25% in available case reports. CONCLUSIONS: During peak influenza season each winter patients presenting with symptoms of chest pain, shortness of breath and fevers should be evaluated for myocarditis given severe potential complications and mortality. Reference #1: Estabragh, Zahra Raisi, and Mamas A. Mamas. “The cardiovascular manifestations of influenza: a systematic review.” International journal of cardiology 167.6 (2013): 2397-2403. Reference #2: Sellers, Subhashini A., and William A. Fischer. “Myocarditis In Severe Influenza Infection: A Review Of The Literature.” D40. CRITICAL CARE: DIAGNOSING AND TREATING BACTERIAL AND VIRAL INFECTIONS IN THE ICU. American Thoracic Society, 2016. A6906-A6906. DISCLOSURE: The following authors have nothing to disclose: Conor Senecal, Thomas Tilbury No Product/Research Disclosure Information

PO14-57 - The interest of antiviral treatment in fulminant viral myocarditis in children

PO14-57 - The interest of antiviral treatment in fulminant viral myocarditis in children

両心補助で救命し得た重症多臓器不全を来たした劇症型心筋炎の1例

劇症型心筋炎はPCPSなどの補助循環を導入し，急性期を乗り切る治療が行われるが，さらに重症な場合補助人工心臓が必要となる．今回，術前にPCPS，IABPを装着していたが臓器障害が進んだ劇症型心筋炎に対し，両心補助人工心臓（BiVAD）を装着し，合併症なく救命できた1例を経験したので報告する．症例は46歳男性．熱発で発症し前医に入院となり，発症3日目に突然の胸痛，循環不全からPCPS，IABPが装着された．心機能は著しく低下し，ほぼ無収縮状態となった．内科的治療を一週間続けていたが心機能の回復を認めず，また臓器障害の進行，肺うっ血の増悪，下肢の阻血が出現し，補助人工心臓装着目的に当院に転院となった．入院時血液生化学所見ではT-Bil 6.9 mg/dl，Cre 1.14 mg/dl，BNP 571 pg/dl，血小板3.3万/μlであった．経食道心エコー検査で両心室ともに高度に拡大，無収縮状態であったため，BiVAD装着の方針とした．上行送血，左室脱血で遠心ポンプに装着し左心補助人工心臓（LVAD）とし，肺動脈送血，右房脱血で遠心ポンプを装着し右心補助人工心臓（RVAD）とした．両心補助にて循環も安定しPCPSを離脱した．術後，徐々に心機能，肺うっ血，臓器障害が改善し，特に合併症を認めることなくBiVAD装着12日目に問題なく離脱した．離脱後10日目に抜管，心機能は正常化し，神経症状などの合併症も認めず，51日目に独歩退院となった．

Use of the Impella 5.0 Device as a Bridge to Recovery in Adult Fulminant Viral Myocarditis

Use of the Impella 5.0 Device as a Bridge to Recovery in Adult Fulminant Viral Myocarditis

0344: Why levosimendan should be considered for the treatment of viral myocarditis in children

Animal studies showed that levosimendan protects cardiomyocytes against apoptotic cell death in acute viral myocarditis. In addition to its inotropic properties, levosimendan seems to prevent the detrimental effects of oxidative stress and to limit cardiomyocyte loss. To analyze the outcome of children who received levosimendan for acute or fulminant viral myocarditis. Retrospective single center study covering the period 2007- 2013. All children (<18 years) with viral myocarditis were treated, in association with epinephrine and/or milrinone, with a 24-hours infusion of levosimendan. Clinical, biological and echocardiographic evolutions were analyzed. Between 2007 and 2013, 18 successive children were treated, 9 for acute myocarditis and 9 for fulminant myocarditis (according to the international clinicopathological classification). Median age was 4 years (1.1-11) and median weight was 15kg (10-40). BNP level significantly decreased 48 hours after the beginning of the infusion (4599ng/L [2698-9266] vs 1928ng/L [848-4557], p=0.05). No dialysis was necessary. Among the fulminant myocarditis group, 1 patient (11%) required early mechanical circulatory support with a limitation of care due to severe neurologic complications. 13 patients (72%) recovered a LVEF >55% (100% for the acute myocarditis group). 1 patient had heart transplantation 18 months later. In our experience, levosimendan was efficient for the inotropic support of acute and fulminant viral myocarditis. We believe that its cardioprotective effect enabled us to limit the use of mechanical assistance (only 11% of the fulminant forms) and allowed a recovering of the cardiac function for the majority of the patients. Although further clinical studies are needed to confirm these data, levosimendan should be systematically considered for the treatment of these critical patients.

Fulminant viral myocarditis after rituximab therapy in pediatric nephrotic syndrome

We report a 7-year-old boy with high-degree steroid-dependent idiopathic nephrotic syndrome (SDNS) who went into remission with rituximab (RTX) maintenance therapy. Four months after this patient received his first RTX infusion, there was a progressive and sustained decrease of immunoglobulin (Ig)G and IgM levels. Thirteen months after the initiation of RTX therapy he was in sustained remission without any steroid or oral immunosuppressive therapy; however, B cell depletion was still present. At this time he developed a fulminant myocarditis due to enterovirus. Despite aggressive treatment and the administration of intravenous polyvalent immunoglobulins there was no clinical improvement. He successfully underwent heart transplant surgery. We conclude that B cell depletion with RTX is efficacious in the treatment of paediatric SDNS but that it may be associated with severe infectious complications. Therefore, we recommend a close monitoring of Ig levels in children who have received RTX therapy and a supplementation with intravenous Ig as soon as the Ig levels fall below the lower limit of the normal range.

Contemporary Experience with Percutaneous and Surgical Right Ventricular Assist Devices

Purpose Significant uncertainty exists regarding the deployment of the recently developed percutaneous right ventricular assist device (pRVAD) in the context of high mortality from right ventricular failure. We compare our initial institutional experience with pRVAD with our contemporary experience with surgical right ventricular assist device (sRVAD). Methods and Materials Percutaneous RVAD was accomplished in the Hybrid operating room. The right internal jugular vein was accessed percutaneously and a 17F Medtronic cannula was passed over a guidewire into the main pulmonary artery. Position was verified using TEE. A long 21F or 25F multistage venous cannula was used for inflow from the femoral vein. sRVAD implantation was performed using standard Thoratec cannulae from the right atrium to the pulmonary artery. An oxygenator was utilized in-line for 2/3 pRVAD patients and 7/17 sRVAD patients. Results Between January 2009 and September 2012, 17 patients underwent placement of sRVAD. During that contemporaneous period, 3 patients underwent pRVAD placement. Indications for pRVAD were RV infarct, RV failure s/p LVAD, and fulminant viral myocarditis. All 3 patients with pRVAD implant survived, 11/17 patients with sRVAD survived. All 3 pRVADs were removed at the bedside without complication. Mean duration of pRVAD support was 4 days. No patient with pRVAD required subsequent re-operation, whereas all sRVAD survivors required at least one further sternotomy. Conclusions pRVAD ease of insertion and removal may lower resistance to RVAD deployment. Support comparable to sRVAD may allow pRVAD use for both early deployment, critical for survival, and as the final procedure after anticipated RV recovery. Also, pRVAD remains flexible to support an in-line oxygenator for the impaired lungs.

First therapeutic use of Artesunate in treatment of human herpesvirus 6B myocarditis in a child

BackgroundHuman herpesvirus 6 (HHV-6) is an important cause of fulminant or acute viral myocarditis. However, insufficiency of standard antiviral treatment against HHV-6 is an emerging problem. ObjectivesTo describe the case of child with HHV-6 myocarditis who was treated by unloading with a left ventricular assist device and Artesunate. Study designCase report supported by histological and viral diagnoses via a combination of histology/immunohistochemistry and polymerase chain reaction techniques performed on cardiac tissues before and after treatment. ResultsFollowing therapeutic intervention, the clinical status and heart function improved. Endomyocardial biopsies revealed decreased levels of HHV-6B DNA in the myocardium and the disappearance of histological findings in support of lymphocytic myocarditis. Left ventricular assist device could be explanted. No adverse effects of Artesunate were noted. ConclusionsIn addition to existing heart failure treatments, Artesunate can be considered as an effective candidate for clinical use in cases of HHV-6B associated myocarditis.

Expanding the Availability of Extracorporeal Cardiopulmonary Resuscitation

A healthy 14-year-old presented to an emergency department in Alaska, complaining of shortness of breath, chest pain, and 72 hours of malaise and headache. On admission, her blood pressure was 80/50 mm Hg, and she had cool extremities. Electrocardiography revealed wide-complex ventricular tachycardia. She underwent synchronized electrical cardioversion. Although she initially converted to sinus rhythm, she subsequently became pulseless, with electrocardiographic evidence of ventricular tachycardia. Despite cardiopulmonary resuscitation, she failed to achieve a perfusing rhythm. Cardiovascular surgery consultation was obtained, and she was placed on partial cardiopulmonary bypass during 2 hours of ongoing chest compressions. Cardiopulmonary bypass flow was limited by the small size of her femoral arteries. She remained in refractory ventricular tachycardia. The cardiopulmonary bypass circuit was modified for transportation of the patient via air ambulance 1500 miles to a tertiary medical center that specializes in pediatric heart failure and mechanical cardiopulmonary support. Upon arrival at the tertiary medical center, she underwent carotid artery cannulation to improve total cardiopulmonary support and percutaneous balloon atrial septostomy to facilitate left ventricular decompression. Intravenous immunoglobulin and steroids were administered to treat presumed acute fulminant viral myocarditis. Extracorporeal life support was support was successfully discontinued after 14 days, but she experienced a thromboembolic stroke. The patient was discharged on hospital day 65 with moderate generalized left-sided weakness, but she was able to ambulate with minimal assistance. She subsequently returned to school and is progressing appropriately with her peers. Cardiac function has normalized, and she remains in normal sinus rhythm.

Diverse stage-dependent effects of glucocorticoids in a murine model of viral myocarditis

BackgroundThe effects of glucocorticoids on viral myocarditis are contentious. The aim of the present study was to determine whether there is a “window of opportunity” for glucocorticoid treatment in a mouse model of acute viral myocarditis induced by Coxsackie group B3 virus (CVB3). MethodsA/J (H-2a) mice were randomly assigned to one of four experimental groups: (1) viral infection without dexamethasone (DEX) treatment; (2) treatment with 0.75mg/kg, i.p., DEX each day for 5 days prior to viral infection; (3) 0.75mg/kg, i.p., DEX treatment for 5 days immediately after viral infection; and (4) 0.75mg/kg, i.p., DEX treatment for 5 days starting on day 7 after infection. ResultsDEX administration before or immediately after viral infection improved survival and attenuated left ventricular dilatation, systolic dysfunction, fibrosis, and infiltration of immune cells in the post-infectious heart. In contrast, late administration of DEX reduced survival (as determined on day 14), and was associated with sustained increases in cardiac tumor necrosis factor-α and interferon-γ levels. The beneficial effects of early DEX administration on survival were completely abrogated by coadministration of a selective cyclooxygenase (COX)-2 inhibitor (NS-398; 5mg/kg per day, p.o.). Notably, the virus titer in the post-infectious heart was significantly suppressed by DEX, but coadministration of NS-398 at the time of viral infection abolished the suppressive effects of DEX and, in fact, increased virus titers. ConclusionsEarly administration of DEX is beneficial in the treatment of fulminant viral myocarditis, whereas late administration of DEX is harmful. The beneficial effects of DEX on survival were completely abolished by simultaneous administration of a selective COX-2 inhibitor. Hence, we speculate that a direct action of DEX on cardiomyocytes, rather than anti-inflammatory effects of DEX on immune cells, confers resistance to myocardial damage induced by viral infection.

Over 2-year disease-free survival after multimodality therapy of a primary cardiac lymphoma

This comment deals with our study regarding the innovative, sequential therapy of a primary cardiac lymphoma. Primary cardiac T-cell lymphoma is defined as a non-Hodgkin lymphoma (NHL) involving only the heart and/or the pericardium, or as an NHL with the main bulk of the tumor located on the heart. It is an extremely rare disease with a typical heterogeneous clinical manifestation and 100% mortality if left untreated. Herein we describe a clinical follow-up of 26 months in a young female patient with eventful heart failure due to the uncommon diagnosis of a primary cardiac T-cell lymphoma. The patient underwent emergent veno-arterial extracorporeal membrane oxygenation (ECMO) implantation with the suspicion of a fulminant viral myocarditis. When rapidly complete contractile cardiac arrest and an almost complete obliteration of the ventricular lumen occurred within 1 day of emergency cardiectomy, implantation of a custom-made biventricular assist device (BVAD) was done and 12 days later successful heart transplantation was performed. In addition, she underwent chemotherapy (CHOP regime) and reduced immunosuppression, always maintained in the subtherapeutic range. The first myocardial biopsy, 2 weeks after transplantation, the patient showed single tumor cells within the graft, but all consecutive biopsies confirmed complete resolution of T-cell infiltration. Six months after transplantation endomyocardial biopsies revealed mild rejection, which was successfully treated with bolus steroids. At 1 year, heart catheterization showed no transplant vasculopathy and a normal ejection fraction of 65%. Severe facial actinomycotic infection occurred on a single occasion, which was treated successfully with surgery, antibiotics and antimycotics. Most recently, more than 2 years later, routine staging, including clinical examination, computed tomography (CT) scans, ultrasound evaluation and endomyocardial biopsy, indicated no evidence of tumor recurrence. The last endomyocardial biopsy showed no rejection (A0, ISHLT 0R). Except for persistently impaired renal function, without the

A fatal case of Human Herpesvirus 6 chronic myocarditis in an immunocompetent adult

Background Human Herpesvirus 6 (HHV-6) is an important cause of fulminant or acute viral myocarditis in immunocompromised or immunocompetent patients. However the physiopathological mechanisms of HHV-6 related acute myocarditis and the involvement of subsequent HHV-6 reactivation phases in the development of chronic cardiomyopathies remain to be assessed. Objectives To describe a case of fatal HHV-6 chronic myocarditis in an immunocompetent adult. Study design Case report and detailed histological and viral diagnoses by combination of histology/immunohistochemistry and polymerase chain reaction techniques on cardiac tissues. Results Histopathological analysis of ventricular tissues showed large interstitial and scarring fibrotic areas with a moderate mononuclear cell infiltrate compatible with histological aspect of chronic myocarditis. Detection of both HHV-6 by real-time PCR and viral glycoproteins in mononuclear and endothelial cells by immunohistochemistry evidenced an ongoing cardiac HHV-6 replication with viral late protein synthesis activity. Conclusions This case report indicates that HHV-6 can establish a chronic active myocarditis leading to heart failure in immunocompetent subjects.

Fulminant myocarditis associated with novel H1N1 influenza A

Myocarditis secondary to H1N1 influenza has been described in children, but only very rarely in adults. We describe a 36-year-old man with no significant medical history who presented with flu-like symptoms of 3-week duration. When he sought medical attention, he was already manifesting heart failure secondary to fulminant myocarditis, along with multiorgan failure. Despite aggressive management, including circulatory support with a catheter-based mechanical cardiac assist device (Impella 2.5 Cardiac Assist Device, Abiomed, Danvers, MA) as a bridge to cardiac transplant, and aggressive antiviral and antibacterial therapy, the patient died of cardiac arrest. An H1N1 polymerase chain reaction postmortem assay produced positive results, and a diagnosis of fulminant viral myocarditis and multiorgan system failure was established.

Circulating cardiac troponins levels and cardiac dysfunction in children with acute and fulminant viral myocarditis

To study the correlation between cardiac troponins blood levels and degrees of cardiac dysfunction in children with acute and fulminant viral myocarditis and to study their prognostic role in predicting the outcomes and risk of having dilated cardiomyopathy. Troponin I & T blood levels were measured in 65 children with acute or fulminant viral myocarditis. The cardiac functions of RV & LV were assessed by Doppler echocardiography. The levels of cTnI & CTnT were significantly higher in patients with fulminant myocarditis than in controls and children with acute myocarditis (p < 0.05 & <0.001* respectively). The cardiac functions were significantly impaired in fulminant myocarditis than in acute myocarditis (p < 0.001*). There were negative correlations between the cardiac troponins levels and the cardiac functions measured by echocardiography in children with acute and fulminant myocarditis. There were 3 deaths (7.5%), and 10 (25%) children developed dilated cardiomyopathy in acute myocarditis while there were eight deaths (32%) and one patient (4%) who developed dilated cardiomyopathy in fulminant myocarditis group. Cardiac troponins levels can predict the severity of myocarditis and the prognosis on the short-term level. Fulminant myocarditis was associated with higher levels of both cTn I & cTn T than acute myocarditis. Despite that fulminant myocarditis has a more aggressive course, the risk of developing cardiomyopathy was less than in acute myocarditis.