Pathological Evidence for SARS-CoV-2 as a Cause of Myocarditis

Kawakami, Rika; Sakamoto, Atsushi; Kawai, Kenji; Gianatti, Andrea; Pellegrini, Dario; Nasr, Ahmed; Kutys, PA Bob; Guo, Liang; Cornelissen, Anne; Mori, Masayuki; Sato, Yu; Pescetelli, Irene; Brivio, Matteo; Romero, Maria; Guagliumi, Giulio; Virmani, Renu; Finn, Aloke V.

doi:10.1016/j.jacc.2020.11.031

Cited by 202 publications

(237 citation statements)

References 43 publications

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“…Four out of five cases with increased cardioinflammatory infiltrate presented without cardiomyocyte necrosis (n = 4) while one case presented as active, lymphohistiocytic myocarditis. These findings are in line with a literature review assessing the autopsy incidence of SARS-CoV-2-associated myocarditis, confirming that clinically relevant cardioinflammatory changes are generally a rare finding in COVID-19 [40,41]. Of note, all these cases were deemed RT-PCR negative.…”

Section: Cardioinflammationsupporting

confidence: 85%

Characterisation of cardiac pathology in 23 autopsies of lethalCOVID‐19

Haslbauer

Tzankov

Mertz³

et al. 2021

The Journal of Pathology CR

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While coronavirus disease 2019 primarily affects the respiratory tract, pathophysiological changes of the cardiovascular system remain to be elucidated. We performed a retrospective cardiopathological analysis of the heart and vasculature from 23 autopsies of COVID-19 patients, comparing the findings with control tissue. Myocardium from autopsies of COVID-19 patients was categorised into severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive (n = 14) or negative (n = 9) based on the presence of viral RNA as determined by reverse transcriptase polymerase chain reaction (RT-PCR). Control tissue was selected from autopsies without COVID-19 (n = 10) with similar clinical sequelae. Histological characteristics were scored by ordinal and/or categorical grading. Five RT-PCR-positive cases underwent in situ hybridisation (ISH) for SARS-CoV-2. Patients with lethal COVID-19 infection were mostly male (78%) and had a high incidence of hypertension (91%), coronary artery disease (61%), and diabetes mellitus (48%). Patients with positive myocardial RT-PCR died earlier after hospital admission (5 versus 12 days, p < 0.001) than patients with negative RT-PCR. An increased severity of fibrin deposition, capillary dilatation, and microhaemorrhage was observed in RT-PCR-positive myocardium than in negatives and controls, with a positive correlation amongst these factors All cases with increased cardioinflammatory infiltrate, without myocyte necrosis (n = 4) or with myocarditis (n = 1), were RT-PCR negative. ISH revealed positivity of viral RNA in interstitial cells. Myocardial capillary dilatation, fibrin deposition, and microhaemorrhage may be the histomorphological correlate of COVID-19-associated coagulopathy. Increased cardioinflammation including one case of myocarditis was only detected in RT-PCR-negative hearts with significantly longer hospitalisation time. This may imply a secondary immunological response warranting further characterisation.

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Section: Cardioinflammationsupporting

confidence: 85%

Characterisation of cardiac pathology in 23 autopsies of lethalCOVID‐19

Haslbauer

Tzankov

Mertz³

et al. 2021

The Journal of Pathology CR

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“…Viral myocarditis (VMC) is one of the common clinical cardiovascular diseases, which is caused by viral infection, especially the localized or diffuse myocardial inflammatory lesions caused by Coxsackie B virus [ 1 ]. The potential pathogenesis was considered to be that the virus-mediated immune response can directly act on cardiomyocytes and intracardiac capillaries, leading to degeneration and necrosis of cardiomyocytes and ultimately injury cardiac dysfunction [ 2 , 3 ]. The prognosis of most cases is good, but a small number of patients can have an acute outbreak leading to heart failure or sudden death, a small number of patients keep the heart cavity enlarged for several months to several years without heart failure, or the condition deteriorates again and evolves into dilated myocarditis [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Establishment of a Nomogram for Predicting Early Death in Viral Myocarditis

Sun

Xie

Guo

et al. 2021

Cardiology Research and Practice

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Objective. This research aimed to establish a nomogram for predicting early death in viral myocarditis (VMC) patients. Method. A total of 362 consecutive VMC patients in Fujian Medical University Affiliated First Quanzhou Hospital between January 1, 2009, and December 31, 2019, were included. A least absolute shrinkage and selection operator (LASSO) regression model was used to detect the risk factors that most consistently and correctly predicted early death in VMC. The performance of the nomogram was assessed by calibration, discrimination, and clinical utility. Result. 9 factors were screened by LASSO regression analysis for predicting the early death of VMC. Combined with the actual clinical situation, the heart failure (HF) (OR: 2.13, 95% CI: 2.76–5.95), electrocardiogram (ECG) (OR: 6.11, 95% CI: 1.05–8.66), pneumonia (OR: 3.62, 95% CI: 1.43–9.85), brain natriuretic peptide (BNP) (OR: 4.66, 95% CI: 3.07–24.06), and lactate dehydrogenase (LDH) (OR: 1.90, 95% CI: 0.19–9.39) were finally used to construct the nomogram. The nomogram’s C-index was 0.908 in the training cohort and 0.924 in the validation cohort. And the area under the receiver operating characteristic curve of the nomogram was 0.91 in the training cohort and 0.924 in the validating cohort. Decision curve analysis (DCA) also showed that the nomogram was clinically useful. Conclusion. This nomogram achieved an good prediction of the risk of early death in VMC patients.

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“…In addition, we consider an advantage that the study population was rather homogenous: we prospectively enrolled consecutive, intubated patients with severe Covid-19, with no obvious preexisting cardiovascular disease in order to eliminate known factors triggering AF. Cardiac Magnetic Resonance tomography was not performed, but its utility in ICU is limited by the out-of-hour availability and the requirement for some breath-holding, while no patients underwent endomyocardial biopsy (caring inherent risks), as it is not suggested due to the low incidence of myocarditis in Covid-19 [12]. Instead, in all patients, troponin levels and a full echocardiographic examination were performed, which seem appropriate to reveal cardiac involvement in Covid-19.…”

Section: Discussionmentioning

confidence: 99%

“…However, there is a lack of clear association of new onset AF (NOAF), to direct myocardial damage depicted with Cardiac Magnetic Resonance (CMR), histopathologic ndings or even echocardiographic ndings. In addition, Covid-19 myocarditis seems to be an uncommon nding [12].…”

mentioning

confidence: 99%

Secondary bacterial infections trigger New Onset Atrial Fibrillation in ICU Covid-19 ARDS patients

Zakynthinos¹,

Tsolaki²,

Karavidas³

et al. 2021

Preprint

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Background Cardiac arrhythmias, mainly atrial fibrillation (AF), is frequently reported in COVID-19 patients, yet causality has not been explored. Intensive Care Unit patients frequently present AF during critical illness. Sepsis is one of the main contributors of AF occurrence in ICU patients. The aim of the study was to explore if Covid-19 myocardial involvement is the only contributor for New Onset Atrial Fibrillation (NOAF) in intubated ICU patients. Methods Consecutive intubated, Covid-19ARDS patients, were prospectively studied for factors triggering NOAF. Demographics, data on Covid-19 infection duration, severity of illness and ARDS are reported. Echocardiographic findings, troponin levels and secondary infection (sepsis/septic shock) data were collected on the day of AF and compared to the preceding days’ and/or ICU admission data. Comparison was also performed between NOAF and control group (no AF) on admission. Results Among 105 patients screened, 79 were eligible; nineteen presented NOAF (24%). Baseline characteristics did not differ between the NOAF and control groups. Troponin levels were mildly elevated upon ICU admission in both groups. NOAF occurred on the 18 ± 4.8 days from Covid-19 symptoms’ onset, and the 8.5 ± 2.1 ICU day. Seventeen patients in the NOAF group (89.5%) presented a septic secondary infection vs 25 (41.6%) in the control group (p < 0.001). In sixteen NOAF patients (84.2%), AF occurred concurrently with a secondary septic episode. Noradrenaline, lactate levels and inflammation biomarkers presented a gradual increase in the days preceding the AF day (all p < 0.05). Troponin increased compared to admission (p = 0.017). AF did not resolve or re-occurred if sepsis persisted. Upon ICU admission left ventricular ejection fraction was rather normal, yet, global longitudinal strain was equally impaired (< 16.5%) in 63% vs 78% in the NOAF and control groups, respectively. The right ventricle was mildly dilated, and 36 (45.6%) patients had pericardial effusion. Echocardiographic findings did not change on NOAF occurrence. Conclusion Secondary infections seem to be major contributors for NOAF in Covid-19 patients, probably playing the role of the “second hit” in an affected myocardium from Covid-19.

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Pathological Evidence for SARS-CoV-2 as a Cause of Myocarditis

Cited by 202 publications

References 43 publications

Characterisation of cardiac pathology in 23 autopsies of lethalCOVID‐19

Characterisation of cardiac pathology in 23 autopsies of lethalCOVID‐19

Establishment of a Nomogram for Predicting Early Death in Viral Myocarditis

Secondary bacterial infections trigger New Onset Atrial Fibrillation in ICU Covid-19 ARDS patients

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