Spectrum of Cardiac Involvement in COVID-19

Gill, Gauravpal S.; Vlacancich, Raymond; Mehta, Neil; Chaturvedi, Mansi; Papolos, Alexander

doi:10.7759/cureus.8638

Cited by 9 publications

(12 citation statements)

References 11 publications

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“…Echocardiography revealed that the heart was enlarged and the LVEF was significantly decreased. Bedside chest radiographs showed typical ground-glass changes indicative of viral pneumonia [ 78 – 83 ]. Although no direct data are available showing the presence of NETs in the heart, increased levels of cell-free DNA, MPO-DNA complex, and citH3 in the blood and involvement of NETs in lung autopsy indicate that COVID-19 activates NETosis [ 84 – 86 ].…”

Section: Netosis In Diseases Inducing Hfmentioning

confidence: 99%

NETosis as a Pathogenic Factor for Heart Failure

Ling

2021

Oxidative Medicine and Cellular Longevity

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Heart failure threatens the lives of patients and reduces their quality of life. Heart failure, especially heart failure with preserved ejection fraction, is closely related to systemic and local cardiac persistent chronic low-grade aseptic inflammation, microvascular damage characterized by endothelial dysfunction, oxidative stress, myocardial remodeling, and fibrosis. However, the initiation and development of persistent chronic low-grade aseptic inflammation is unexplored. Oxidative stress-mediated neutrophil extracellular traps (NETs) are the main immune defense mechanism against external bacterial infections. Furthermore, NETs play important roles in noninfectious diseases. After the onset of myocardial infarction, atrial fibrillation, or myocarditis, neutrophils infiltrate the damaged tissue and aggravate inflammation. In tissue injury, damage-related molecular patterns (DAMPs) may induce pattern recognition receptors (PRRs) to cause NETs, but whether NETs are directly involved in the pathogenesis and development of heart failure and the mechanism is still unclear. In this review, we analyzed the markers of heart failure and heart failure-related diseases and comorbidities, such as mitochondrial DNA, high mobility box group box 1, fibronectin extra domain A, and galectin-3, to explore their role in inducing NETs and to investigate the mechanism of PRRs, such as Toll-like receptors, receptor for advanced glycation end products, cGAS-STING, and C-X-C motif chemokine receptor 2, in activating NETosis. Furthermore, we discussed oxidative stress, especially the possibility that imbalance of thiol redox and MPO-derived HOCl promotes the production of 2-chlorofatty acid and induces NETosis, and analyzed the possibility of NETs triggering coronary microvascular thrombosis. In some heart diseases, the deletion or blocking of neutrophil-specific myeloperoxidase and peptidylarginine deiminase 4 has shown effectiveness. According to the results of current pharmacological studies, MPO and PAD4 inhibitors are effective at least for myocardial infarction, atherosclerosis, and certain autoimmune diseases, whose deterioration can lead to heart failure. This is essential for understanding NETosis as a therapeutic factor of heart failure and the related new pathophysiology and therapeutics of heart failure.

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Section: Netosis In Diseases Inducing Hfmentioning

confidence: 99%

NETosis as a Pathogenic Factor for Heart Failure

Ling

2021

Oxidative Medicine and Cellular Longevity

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“…Due to the ST-segment elevation in some cases, suspicion of myocardial ischemia was raised, and many patients underwent a conventional coronary angiography or a coronary computed tomography angiography to rule out coronary stenosis. In all cases, there was no coronary narrowing [14,16,19,33] except for one case which had mild luminal irregularities [29]. Other patients' ECGs showed non-specific ischemic changes such as T-wave inversions [11,26].…”

Section: Diagnostic Testing A) Ecg Findingsmentioning

confidence: 85%

“…In the 29 cases reported, only 2 were found to have right ventricular dysfunction [29,30]. Both cases were in cardiogenic shock and on inotropic and vasoactive support.…”

Section: Echocardiographymentioning

confidence: 99%

“…The first case underwent pericardiocentesis yielding around 300 mL of serous fluid, but with worsening status, she was escalated to veno-arterial extracorporeal membrane oxygenation (VA-ECMO). She later recovered and was discharged successfully [29]. The second case also had to undergo pericardiocentesis which yielded 600 mL of serosanguinous fluid.…”

Section: Echocardiographymentioning

confidence: 99%

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COVID-19 Myocarditis Clinical Presentation, Diagnosis and Management: A Narrative Review

Zaghrini¹,

Emmanuel²,

Zibara³

et al. 2021

Int J Clin Res

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Objective: The purpose of this article is to review the cases of myocarditis in COVID-19 patients and synthesize the current understanding regarding the presentation, diagnosis, and management of myocarditis in the setting of COVID-19 disease. Background: The novel coronavirus disease has shown serious implications for the cardiovascular system, including acute myocardial injury, arrhythmias, venous thromboembolism, and myocarditis. Several cases of myocarditis in COVID-19 patients have been reported since the disease's emergence at the end of 2019. The diagnostic approach and management have been variable. The purpose of this narrative review is to gather the most reliable published material regarding myocarditis in COVID-19 and present it as an overview to simplify the current understanding we have of this disease. Methods: We screened PubMed, Scopus, and Embase. We then selected peer-reviewed and pre-print articles published in English that were related to the involvement of the cardiovascular system in COVID-19, with a focus on myocarditis. We included case reports describing myocarditis in COVID-19 patients and summarized their clinical presentation, diagnosis, and management. References of the selected articles were also screened, and some were included when relevant. Discussion: This article is subdivided into sections that discuss the clinical presentation of COVID-19 myocarditis and move on to various diagnostic approaches and management options. Each subsection presents a brief literature review followed by a summary and interpretation of what was found in the reported cases. Conclusion: After noticing the involvement of the cardiovascular system in COVID-19 patients, specifically through myocarditis, we present this narrative review to provide the medical community with a unified article regarding the current understanding of myocarditis in COVID-19 patients. This article further stresses the necessity of establishing proper treatment guidelines for COVID-19 myocarditis.

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“…While the primary concern of this virus is its potentially devastating pulmonary disease, it was quickly determined that there were numerous extra-pulmonary manifestations of this virus, including renal, gastrointestinal, liver, cardiac, mediastinal, neurologic, hematologic, vascular, cutaneous, reproductive, and ocular complications [ 2 ]. A wide variety of pathologies related to cardiac involvement in COVID-19 have been reported [ 3 , 4 ]. In particular, the pericardial disease has been increasingly recognized to complicate the course of illness, given very little direction on management strategies.…”

Section: Introductionmentioning

confidence: 99%

Challenges in Managing Pericardial Disease Related to Post Viral Syndrome After COVID-19 Infection

Sollie¹,

Vallepu²,

Jagadeesan³

et al. 2021

Cureus

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Although primarily a respiratory illness, coronavirus disease 2019 (COVID-19) has been associated with cardiac involvement with reported cases of myocardial ischemia, arrhythmia, myocarditis, pericarditis, and pericardial effusion leading to cardiac tamponade. Most cases of pericardial disease in this setting have been during the acute infection. Here, we present a patient who developed pericarditis leading to cardiac tamponade after the resolution of the acute COVID-19 infection. Her course of illness was further complicated by poor response to initial medical therapy with non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine which could possibly be related to early exposure to steroids. It is often difficult to establish an underlying etiology for acute pericarditis. Similarly, in our case, although there is no definitive test to prove the causal relationship, this effusion is highly suspicious of being secondary to post viral sequelae after COVID-19 infection when considering the clinical course. It is important to consider pericardial disease as a late complication of COVID-19 even after apparent resolution of the acute infection and be mindful of the therapeutic challenges that we might face while managing such patients.

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Spectrum of Cardiac Involvement in COVID-19

Cited by 9 publications

References 11 publications

NETosis as a Pathogenic Factor for Heart Failure

NETosis as a Pathogenic Factor for Heart Failure

COVID-19 Myocarditis Clinical Presentation, Diagnosis and Management: A Narrative Review

Challenges in Managing Pericardial Disease Related to Post Viral Syndrome After COVID-19 Infection

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