Aborted sudden death from Epstein–Barr myocarditis

Farina, Andrea; Maggiolini, Stefano; Sabato, M. Di; Gentile, Gaetano; Meles, Ester; Achilli, Felice

doi:10.2459/jcm.0b013e3283405b04

Cited by 2 publications

(1 citation statement)

References 27 publications

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“…The Epstein–Barr virus has rarely been reported as a cause of acute myocarditis, accounting for approximately 1% of cases, but it has been associated with ventricular arrhythmias and sudden death. [4,5] Myocardial dystrophic calcification is a rare complication of myocarditis. We failed to find any other reports on myocardial calcification in EB viral myocarditis.…”

Section: Discussionmentioning

confidence: 99%

Myocardial calcification found in Epstein–Barr viral myocarditis and rhabdomyolysis

Sui

Tang²,

Wu³

2018

Medicine

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Rationale:The Epstein–Barr (EB) virus has rarely been reported as a cause of fulminant myocarditis. To our knowledge, the present case is the first report on myocardial calcification in EB viral myocarditis and rhabdomyolysis.Patient concerns:A 17-year-old man was admitted to the department with fever, chest tightness, and tachypnea that had been present for 2 days.Diagnoses:The initial investigation showed elevated liver enzyme levels, creatine kinase levels, creatine kinase isoenzyme levels, and elevated serum myoglobin. Echocardiography showed that left ventricular motion amplitude decreased. Test for immunoglobin M and immunoglobin G antibodies against Epstein–Barr virus were positive. These findings were consistent with fulminant myocarditis, cardiogenic shock, and rhabdomyolysis.Interventions:The patient was intensively treated with venoarterial extracorporeal membrane oxygenation (VA-ECMO), continuous renal replacement therapy (CRRT).Outcomes:Myocardial calcification was observed in the left ventricle walls on CT examination 10 days after the admission. Four months later, the patient is still alive and with adequate daily life.Lessons:This case indicates that this rare form of myocardial calcification may be associated with EB viral infection and rhabdomyolysis.

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Section: Discussionmentioning

confidence: 99%

Myocardial calcification found in Epstein–Barr viral myocarditis and rhabdomyolysis

Sui

Tang²,

Wu³

2018

Medicine

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Circulating virome and inflammatory proteome in patients with ST-elevation myocardial infarction and primary ventricular fibrillation

Oliveras

Revuelta‐López

García-García

et al. 2022

Sci Rep

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Primary ventricular fibrillation (PVF) is a life-threatening complication of ST-segment elevation myocardial infarction (STEMI). It is unclear what roles viral infection and/or systemic inflammation may play as underlying triggers of PVF, as a second hit in the context of acute ischaemia. Here we aimed to evaluate whether the circulating virome and inflammatory proteome were associated with PVF development in patients with STEMI. Blood samples were obtained from non-PVF and PVF STEMI patients at the time of primary PCI, and from non-STEMI healthy controls. The virome profile was analysed using VirCapSeq-VERT (Virome Capture Sequencing Platform for Vertebrate Viruses), a sequencing platform targeting viral taxa of 342,438 representative sequences, spanning all virus sequence records. The inflammatory proteome was explored with the Olink inflammation panel, using the Proximity Extension Assay technology. After analysing all viral taxa known to infect vertebrates, including humans, we found that non-PVF and PVF patients only significantly differed in the frequencies of viruses in the Gamma-herpesvirinae and Anelloviridae families. In particular, most showed a significantly higher relative frequency in non-PVF STEMI controls. Analysis of systemic inflammation revealed no significant differences between the inflammatory profiles of non-PVF and PVF STEMI patients. Inflammatory proteins associated with cell adhesion, chemotaxis, cellular response to cytokine stimulus, and cell activation proteins involved in immune response (IL6, IL8 CXCL-11, CCL-11, MCP3, MCP4, and ENRAGE) were significantly higher in STEMI patients than non-STEMI controls. CDCP1 and IL18-R1 were significantly higher in PVF patients compared to healthy subjects, but not compared to non-PVF patients. The circulating virome and systemic inflammation were not associated with increased risk of PVF development in acute STEMI. Accordingly, novel strategies are needed to elucidate putative triggers of PVF in the setting of acute ischaemia, in order to reduce STEMI-driven sudden death burden.

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Aborted sudden death from Epstein–Barr myocarditis

Cited by 2 publications

References 27 publications

Myocardial calcification found in Epstein–Barr viral myocarditis and rhabdomyolysis

Myocardial calcification found in Epstein–Barr viral myocarditis and rhabdomyolysis

Circulating virome and inflammatory proteome in patients with ST-elevation myocardial infarction and primary ventricular fibrillation

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