Complete recovery of fulminant cytotoxic CD8 T‐cell‐mediated myocarditis after ECMELLA unloading and immunosuppression

Jurčová, Ivana; Rocek, Jan; Bracamonte‐Baran, William; Želı́zko, Michael; Netuka, Ivan; Malušková, Jana; Kautzner, Josef; Čiháková, Daniela; Melenovský, Vojtěch; Malý, Jiří

doi:10.1002/ehf2.12697

Cited by 5 publications

(5 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a case report showing the histopathology of fulminant lymphocytic myocarditis (not following COVID-19 vaccination), the myocardium was infiltrated with CD8-J o u r n a l P r e -p r o o f dominant T lymphocytes and macrophages, similar to our case. 6 CD3 and CD68 positive findings are one of the hallmarks of immunostaining for lymphocytic myocarditis, but are not disease-specific. However, it is presumed that T lymphocytes and macrophages are involved in the pathogenic mechanisms.…”

Section: Discussionmentioning

confidence: 97%

Biopsy-Proven Fulminant Myocarditis Requiring Mechanical Circulatory Support Following COVID-19 mRNA Vaccination

et al. 2022

View full text Add to dashboard Cite

A 48-year-old woman suffered from cardiogenic shock with fulminant myocarditis following the second dose of COVID-19 vaccine (mRNA-1273). Venoarterial extracorporeal membrane oxygenation and Impella® support were essential in achieving hemodynamic stability. Endomyocardial biopsy revealed lymphocytic infiltration with predominant immunostaining for CD8 and CD68 positive cells. Left ventricular ejection fraction improved significantly after treatment with mechanical circulatory support. Myocarditis following COVID-19 mRNA vaccination may also occur in middle-aged women; it may be fulminant and require mechanical circulatory support. Although our results suggest the involvement of cytotoxic T lymphocytes and macrophages, further investigations are needed before establishing this pathogenetic mechanisms.

show abstract

Section: Discussionmentioning

confidence: 97%

Biopsy-Proven Fulminant Myocarditis Requiring Mechanical Circulatory Support Following COVID-19 mRNA Vaccination

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Interestingly, except for five cases (AMC = 2, GCMC = 2 and DCMi = 1), the number of CD4 + T lymphocytes was either equal or higher than those of CD8 + T cells. In acute myocarditis, a shift of CD4-to-CD8 ratio towards CD8 + T cells is known [22], explaining the elevated CD8 + cells in AMC and GCMC patients. However, as CD4 + T cells are considered to be the major driver of autoimmune myocarditis [20], our data support the idea that vaccine-induced myocardial inflammation is a consequence of excessive CD4 + T-cell infiltration, and thus, a potential driver of autoimmunological myocardial damage.…”

Section: Discussionmentioning

confidence: 99%

Intramyocardial Inflammation after COVID-19 Vaccination: An Endomyocardial Biopsy-Proven Case Series

Baumeier

Aleshcheva

Harms

et al. 2022

IJMS

View full text Add to dashboard Cite

Myocarditis in response to COVID-19 vaccination has been reported since early 2021. In particular, young male individuals have been identified to exhibit an increased risk of myocardial inflammation following the administration of mRNA-based vaccines. Even though the first epidemiological analyses and numerous case reports investigated potential relationships, endomyocardial biopsy (EMB)-proven cases are limited. Here, we present a comprehensive histopathological analysis of EMBs from 15 patients with reduced ejection fraction (LVEF = 30 (14–39)%) and the clinical suspicion of myocarditis following vaccination with Comirnaty® (Pfizer-BioNTech) (n = 11), Vaxzevria® (AstraZenica) (n = 2) and Janssen® (Johnson & Johnson) (n = 2). Immunohistochemical EMB analyses reveal myocardial inflammation in 14 of 15 patients, with the histopathological diagnosis of active myocarditis according the Dallas criteria (n = 2), severe giant cell myocarditis (n = 2) and inflammatory cardiomyopathy (n = 10). Importantly, infectious causes have been excluded in all patients. The SARS-CoV-2 spike protein has been detected sparsely on cardiomyocytes of nine patients, and differential analysis of inflammatory markers such as CD4+ and CD8+ T cells suggests that the inflammatory response triggered by the vaccine may be of autoimmunological origin. Although a definitive causal relationship between COVID-19 vaccination and the occurrence of myocardial inflammation cannot be demonstrated in this study, data suggest a temporal connection. The expression of SARS-Cov-2 spike protein within the heart and the dominance of CD4+ lymphocytic infiltrates indicate an autoimmunological response to the vaccination.

show abstract

“…ECMELLA/ECPELLA) has recently gained strong attention. 30 , 31 , 32 , 33 , 34 In most of these studies, the mortality risk was reduced when unloading was added, yet the high rates of complications make its routine applicability dubious. At present, there is still a lack of a randomized controlled trial (RCT) comparing these strategies to define the time of implantation and the ideal clinical scenario.…”

Section: Discussionmentioning

confidence: 99%

“…However, there exists up to seven different methods of unloading, 6,8,30 from which the combination of VA‐ECMO and Impella (i.e. ECMELLA/ECPELLA) has recently gained strong attention 30–34 . In most of these studies, the mortality risk was reduced when unloading was added, yet the high rates of complications make its routine applicability dubious.…”

Section: Discussionmentioning

confidence: 99%

Time course, factors related to, and prognostic impact of venoarterial extracorporeal membrane flow in cardiogenic shock

et al. 2022

View full text Add to dashboard Cite

Aims Venoarterial extracorporeal membrane oxygenation (VA‐ECMO) is currently one of the most used devices in refractory cardiogenic shock. However, there is a lack of evidence on how to set the ‘optimal’ flow. We aimed to describe the evolution of VA‐ECMO flows in a cardiogenic shock population and determine the risk factors of ‘high‐ECMO flow’. Methods and results A 7 year database of patients supported with VA‐ECMO was used. Based on the median flow during the first 48 h of the VA‐ECMO run, patients were classified as ‘high‐flow’ or ‘low‐flow’, respectively, when median ECMO flow was ≥3.6 or <3.6 L/min. Outcomes included rates of ventilator‐associated pneumonia, ECMO‐related complications, days on ECMO, days on mechanical ventilation, intensive care unit and hospitalization lengths of stay, and in‐hospital and 60 day mortality. Risk factors of high‐ECMO flow were assessed using univariate and multivariate cox regression. The study population included 209 patients on VA‐ECMO, median age was 51 (40–59) years, and 78% were males. The most frequent aetiology leading to cardiogenic shock was end‐stage dilated cardiomyopathy (57%), followed by acute myocardial infarction (23%) and fulminant myocarditis (17%). Among the 209 patients, 105 (50%) were classified as ‘high‐flow’. This group had a higher rate of ischaemic aetiology (16% vs. 30%, P = 0.023) and was sicker at admission, in terms of worse Simplified Acute Physiology Score II score [40 (26–58) vs. 56 (42–74), P < 0.001], higher lactate [3.6 (2.2–5.8) mmol/L vs. 5.2 (3–9.7) mmol/L, P < 0.001], and higher aspartate aminotransferase [97 (41–375) U/L vs. 309 (85–939) U/L, P < 0.001], among others. The ‘low‐flow’ group had less ventilator‐associated pneumonia (40% vs. 59%, P = 0.007) and less days on mechanical ventilation [4 (1.5–7.5) vs. 6 (3–12) days, P = 0.009]. No differences were found in lengths of stay or survival according to the ECMO flow. The multivariate analysis showed that risk factors independently associated with ‘high‐flow’ were mechanical ventilation at cannulation [odds ratio (OR) 3.9, 95% confidence interval (CI) 2.1–7.1] and pre‐ECMO lactate (OR 1.1, 95% CI 1.0–1.2). Conclusions In patients with refractory cardiogenic shock supported with VA‐ECMO, sicker patients had higher support since early phases, presenting thereafter higher rates of ventilator‐associated pneumonia but similar survival compared with patients with lower flows.

show abstract

Complete recovery of fulminant cytotoxic CD8 T‐cell‐mediated myocarditis after ECMELLA unloading and immunosuppression

Cited by 5 publications

References 13 publications

Biopsy-Proven Fulminant Myocarditis Requiring Mechanical Circulatory Support Following COVID-19 mRNA Vaccination

Biopsy-Proven Fulminant Myocarditis Requiring Mechanical Circulatory Support Following COVID-19 mRNA Vaccination

Intramyocardial Inflammation after COVID-19 Vaccination: An Endomyocardial Biopsy-Proven Case Series

Time course, factors related to, and prognostic impact of venoarterial extracorporeal membrane flow in cardiogenic shock

Contact Info

Product

Resources

About