Clinically Suspected Myocarditis in the Course of Severe Acute Respiratory Syndrome Novel Coronavirus-2 Infection: Fact or Fiction?

Ozierański, Krzysztof; Tymińska, Agata; Jonik, Szymon; Marcolongo, R; Baritussio, Anna; Grabowski, Marcin; Filipiak‬, Krzysztof J.; Opolski, Grzegorz

doi:10.1016/j.cardfail.2020.11.002

Cited by 33 publications

(44 citation statements)

References 34 publications

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“…A review of cardiovascular pathology 108 came to the conclusion that even though 7.2% of patients had histological evidence of myocarditis, most of these cases would likely not be functionally significant, and reduced the true prevalence to less than 2%, suggesting that the patients with autopsy were dying 'with' myocarditis rather than 'of' myocarditis. A similar conclusion was reached by another group of researchers in a review article 111 indicating that distinct European Society of Cardiology criteria should be used before a diagnosis of myocarditis was made The pathogenesis of myocardial dysfunction is probably multifactorial (see below).…”

Section: Cardiovascular Systemsupporting

confidence: 55%

“…99 Although these autopsy series would initially indicate that clinical COVID-19 can have widespread cardiac involvement, a number of review publications published 10 months after the outbreak have pointed out a number of challenges with these reports. 111 The first is a disconnect between autopsy studies and clinical myocarditis, pointing out that the diagnosis of clinical myocarditis is a challenge, requiring a number of distinct and distinguishing investigations including ECG, non-invasive technologies like echocardiography and cardiac MRI. Although a definitive diagnosis of myocarditis needs endomyocardial biopsy (EMB), there have actually been very few published studies in which EMBs have been performed.…”

Section: Cardiovascular Systemmentioning

confidence: 99%

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Pathophysiology of infection with SARS‐CoV‐2—What is known and what remains a mystery

Sridhar

Nicholls

2021

Respirology

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Coronavirus disease 2019 (COVID-19), caused by coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused extensive disruption and mortality since its recent emergence. Concomitantly, there has been a race to understand the virus and its pathophysiology. The clinical manifestations of COVID-19 are manifold and not restricted to the respiratory tract. Extrapulmonary manifestations involving the gastrointestinal tract, hepatobiliary system, cardiovascular and renal systems have been widely reported. However, the pathophysiology of many of these manifestations is controversial with questionable support for direct viral invasion and an abundance of alternative explanations such as pre-existing medical conditions and critical illness. Prior research on SARS-Co-V and NL63 was rapidly leveraged to identify angiotensin-converting enzyme 2 (ACE2) receptor as the key cell surface receptor for SARS-CoV-2. The distribution of ACE2 has been used as a starting point for estimating vulnerability of various tissue types to SARS-CoV-2 infection. Sophisticated organoid and animal models have been used to demonstrate such infectivity of extrapulmonary tissues in vitro, but the clinical relevance of these findings remains uncertain. Clinical autopsy studies are typically small and inevitably biased towards patients with severe COVID-19 and prolonged hospitalization. Technical issues such as delay between time of death and autopsy, use of inappropriate antibodies for paraffin-embedded tissue sections and misinterpretation of cellular structures as virus particles on electron micrograph images are additional problems encountered in the extant literature. Given that SARS-CoV-2 is likely to circulate permanently in human populations, there is no doubt that further work is required to clarify the pathobiology of COVID-19.

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Section: Cardiovascular Systemsupporting

confidence: 55%

Section: Cardiovascular Systemmentioning

confidence: 99%

Pathophysiology of infection with SARS‐CoV‐2—What is known and what remains a mystery

Sridhar

Nicholls

2021

Respirology

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“…Usually, cardiovascular involvement in COVID-19 patients has been described as myocardial injury identified by troponin increase [11][12][13][14], thus a precise morphological and functional characterization of the heart in COVID-19 patients with clinically suspected myocarditis is lacking on a large scale. Nearly all the information about myocarditis in these patients comes from case reports or small series [15][16][17][18][19][20][21], which have been included in 3 systematic reviews so far [15][16][17].…”

Section: Prevalence Characteristics and Prognosis Of Myocarditis Inmentioning

confidence: 99%

Myocarditis in COVID-19 patients: current problems

et al. 2021

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Myocarditis has been reported as a possible clinical presentation or complication in patients with coronavirus disease (COVID)-19 due to SARS-CoV-2. Despite the alarm that this possibility generated among physicians, there is paucity of information about mechanisms, prevalence, prognosis, diagnosis and therapy of myocarditis in the context of COVID-19. This brief review has the goal to revise and summarize current knowledge on myocarditis in COVID-19 patients and underline problems especially related to diagnosis and treatment.

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“…The exact mechanism of myocarditis in COVID patients is not clear. SARS-CoV-2 is not thought to be a cardiotropic virus [ 2 ]. Isolation of the virus from the cardiomyocyte in the autopsy or biopsy specimen has not been possible [ 2 ].…”

Section: Discussionmentioning

confidence: 99%

“…SARS-CoV-2 is not thought to be a cardiotropic virus [ 2 ]. Isolation of the virus from the cardiomyocyte in the autopsy or biopsy specimen has not been possible [ 2 ]. However viral particles have been found in cardiomyocyte in one pediatric patient [ 3 ] and in the myocardial macrophage in another case [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Fulminant Myocarditis: Covid Or Not COVID? Reinfection Or co-infection?

Yeleti¹,

Guglin

Saleem

et al. 2021

Future Cardiol.

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We describe a unique case of fulminant myocarditis in a patient with presumed SARS-CoV-2 reinfection. Patient had initial infection 4 months backand had COVID-19 antibody at the time of presentation. Endomyocardial biopsy showed lymphocytic myocarditis, that is usually seen in viral myocarditis. The molecular diagnostic testing of the endomyocardial biopsy for cardiotropic viruses was positive for Parvovirus and negative for SARS-CoV-2. Authors highly suspect co-infection of SARS-CoV-2 and Parvovirus, that possibly triggered the immune cascade resulting in fulminant myocarditis. Patient was hemodynamically unstable with ventricular tachycardia and was supported on VA ECMO and Impella CP. There was impressive recovery of left ventricular function within 48 hours, leading to decannulation of VA ECMO in 72 h. This unique case was written by the survivor herself.

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Clinically Suspected Myocarditis in the Course of Severe Acute Respiratory Syndrome Novel Coronavirus-2 Infection: Fact or Fiction?

Abstract: Highlights section Myocarditis in the course of SARS-CoV-2 infection is highly over-diagnosed. The term „myocarditis” should be used only for endomyocardial biopsy- and/or autopsy- proven diagnosis. There is still no proof that SARS-CoV-2 can cause direct cardiomyocyte damage.

Cited by 33 publications

References 34 publications

Pathophysiology of infection with SARS‐CoV‐2—What is known and what remains a mystery

Pathophysiology of infection with SARS‐CoV‐2—What is known and what remains a mystery

Myocarditis in COVID-19 patients: current problems

Fulminant Myocarditis: Covid Or Not COVID? Reinfection Or co-infection?

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