Suspected subclinical myocarditis detected by cardiac magnetic resonance imaging late post COVID-19 recovery

Ghugre, Nilesh R.; Orbach, Ady; Biswas, Labonny; Connelly, Kim A.; Chan, Adrienne K.; Strauss, Bradley H.; Wright, Graham A.; Roifman, Idan

doi:10.1016/j.jccase.2021.04.014

Cited by 7 publications

(4 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These have the potential to mirror or act like the original antigen itself, and anti-idiotype responses against the enterovirus coxsackievirus B3 can cause autoimmune myocarditis in mice [ 70 ]. Ultimately, this mechanism may be involved in the persistent myocardial inflammation described in earlier reports of long COVID-19 [ 71 ] and the implications of cardiac injury in the subacute and chronic COVID-19 forms have been evaluated by CMR which represents the standard reference of cardiac involvement assessment [ 72 ].…”

Section: Imaging For the Detection Of Covid-19 Cardiovascular Injurymentioning

confidence: 99%

Advanced Imaging Supports the Mechanistic Role of Autoimmunity and Plaque Rupture in COVID-19 Heart Involvement

Laino

Ammirabile

Motta

et al. 2022

Clinic Rev Allerg Immunol

View full text Add to dashboard Cite

The cardiovascular system is frequently affected by coronavirus disease-19 (COVID-19), particularly in hospitalized cases, and these manifestations are associated with a worse prognosis. Most commonly, heart involvement is represented by myocarditis, myocardial infarction, and pulmonary embolism, while arrhythmias, heart valve damage, and pericarditis are less frequent. While the clinical suspicion is necessary for a prompt disease recognition, imaging allows the early detection of cardiovascular complications in patients with COVID-19. The combination of cardiothoracic approaches has been proposed for advanced imaging techniques, i.e., CT scan and MRI, for a simultaneous evaluation of cardiovascular structures, pulmonary arteries, and lung parenchyma. Several mechanisms have been proposed to explain the cardiovascular injury, and among these, it is established that the host immune system is responsible for the aberrant response characterizing severe COVID-19 and inducing organ-specific injury. We illustrate novel evidence to support the hypothesis that molecular mimicry may be the immunological mechanism for myocarditis in COVID-19. The present article provides a comprehensive review of the available evidence of the immune mechanisms of the COVID-19 cardiovascular injury and the imaging tools to be used in the diagnostic workup. As some of these techniques cannot be implemented for general screening of all cases, we critically discuss the need to maximize the sustainability and the specificity of the proposed tests while illustrating the findings of some paradigmatic cases.

show abstract

Section: Imaging For the Detection Of Covid-19 Cardiovascular Injurymentioning

confidence: 99%

Advanced Imaging Supports the Mechanistic Role of Autoimmunity and Plaque Rupture in COVID-19 Heart Involvement

Laino

Ammirabile

Motta

et al. 2022

Clinic Rev Allerg Immunol

View full text Add to dashboard Cite

show abstract

“…Given the current knowledge, it seems that also low-level troponin changes are associated with an increased risk for cardiovascular disease during the later course ( 37 ). Our study evidences that such changes can start early on after mild to moderate COVID-19; and can continue to be detectable for multiple months thereafter.…”

Section: Discussionmentioning

confidence: 99%

Mild COVID-19 induces early, quantifiable, persistent troponin I elevations in elder men

Bürgi¹,

Rösslein²,

Nolte³

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

ImportanceElderly patients, especially men, are at risk of increased morbidity from coronavirus disease 2019 (COVID-19). Long-term data on troponin I levels in longitudinal observational studies of outpatients with mild to moderate COVID-19 are scarce.ObjectiveThis controlled cohort study aimed to evaluate the course of troponin I concentrations over a long period in convalescent COVID-19 outpatients with mild to moderate symptoms.Setting and participantsIn this cohort study, individuals with PCR-confirmed, mild to moderate SARS-CoV-2 infection as well as control individuals with confirmed negative PCR and negative SARS-CoV-2 serology were included. Study visits were performed from April 2020 through July 2021 (initialized during the first wave of the corona pandemic in Switzerland). A study visit in patients comprised blood draws every week in the first month and additionally after 8 weeks. This course was repeated in patients observed long-term.ResultsThis study enrolled 278 individuals from the Canton of St. Gallen, Switzerland, aged 12–92 years (59.5% women), who had mild to moderate COVID-19 symptoms (outpatients only) and a diagnosis confirmed by positive RT-PCR. Fifty-four of the participants with confirmed SARS-CoV-2 infection were followed for 14 months with repeat cycles of the testing protocol. In addition, 115 symptomatic patients that were PCR and serology negative were enrolled in the same time period as a control group. In COVID-19 patients, low-level troponin I concentrations (cTnI) were significantly increased from baseline until week 9 after positive RT-PCR diagnosis in men older than 54 years [ΔcTnI = 5.0 ng/L (median); 95% CI 4.1–6.0; p = 0.02]. The troponin I concentration remained elevated throughout 14 months in men older than 54 years within the cohort with a prolonged observation period. This statistically significant change in troponin I concentration was not dependent on co-morbidities in this group. ALT, Creatinine, BNP, and D-Dimer values after convalescence did not differ in comparison to the control cohort.ConclusionIn this analysis of individuals with confirmed SARS-CoV-2 infection, hs troponin I levels of men aged 54 or older significantly increased after infection. They remained elevated for at least 14 months after diagnosis. This suggests the possibility of an ongoing, long-term, low-grade myocardial injury. Further studies with focus on elderly patients and a prolonged observational period are necessary to elucidate whether the phenomenon observed is associated with detectable structural changes to the heart muscle or is without further clinical consequences.

show abstract

“…For myocarditis diagnosis, the updated 2018 LLC require a T1-based criterion (increased T1 relaxation time, extracellular volume, or late gadolinium enhancement (LGE)) and a T2-based criterion (increased T2 relaxation time, myocardial edema, increased T2 signal intensity) [35,36]. These findings are observed in post-COVID myocarditis including LGE and increased T1 relaxation time [31,37,38]. The prevalence of cardiac MR findings in patients with clinically suspected post-COVID myocarditis varies between 2% and 10% with a higher percentage showing localized edema [27,[38][39][40][41].…”

Section: Imaging and Laboratory Testingmentioning

confidence: 99%

Presentations, Diagnosis, and Treatment of Post-COVID Viral Myocarditis in the Inpatient Setting: A Narrative Review

Sayegh¹,

Goins²,

Hall³

et al. 2023

Cureus

View full text Add to dashboard Cite

While coronavirus disease 2019 (COVID-19) infection rates have declined, and mortality outcomes have improved with vaccines, targeted antiviral therapies, and improved care practices over the course of the pandemic, post-acute sequelae of SARS CoV-2 infection (PASC, also referred to as "long COVID") has emerged as a significant concern, even among individuals who appear to have fully recovered from their initial infection. Acute COVID-19 infection is associated with myocarditis and cardiomyopathies, but the prevalence and presentation of post-infectious myocarditis are unclear. We provide a narrative review of post-COVID myocarditis, including symptoms and signs, physical exam findings, diagnosis, and treatment strategies.Post-COVID myocarditis has a wide range of presentations, from very mild symptoms to severe ones that can include sudden cardiac death. Several studies have noted what appears to be a bimodal distribution of affected patients, with individuals under age 16 (particularly males) most affected, followed by those over age 50. The gold standard of diagnosis for myocarditis is endomyocardial biopsy and cardiac magnetic resonance imaging with a confirmed diagnosis of COVID-19. However, if these are not available, other studies such as electrocardiogram, echocardiography, and inflammatory markers can guide clinicians to diagnose post-COVID myocarditis when appropriate. Treatment is largely supportive and may include oxygen therapy, intravenous hydration, diuretics, steroids, and antivirals. Post-COVID myocarditis is rare but important to recognize as more patients present with this condition in the inpatient setting.

show abstract

Suspected subclinical myocarditis detected by cardiac magnetic resonance imaging late post COVID-19 recovery

Cited by 7 publications

References 6 publications

Advanced Imaging Supports the Mechanistic Role of Autoimmunity and Plaque Rupture in COVID-19 Heart Involvement

Advanced Imaging Supports the Mechanistic Role of Autoimmunity and Plaque Rupture in COVID-19 Heart Involvement

Mild COVID-19 induces early, quantifiable, persistent troponin I elevations in elder men

Presentations, Diagnosis, and Treatment of Post-COVID Viral Myocarditis in the Inpatient Setting: A Narrative Review

Contact Info

Product

Resources

About