Coronavirus-induced myocarditis: A meta-summary of cases

Ho, Jamie Sin-Ying; Sia, Ching‐Hui; Chan, Mark Y.; Lin, Weiqin; Wong, Raymond

doi:10.1016/j.hrtlng.2020.08.013

Cited by 128 publications

(140 citation statements)

References 47 publications

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“…Among 143 patients with COVID-19, 31 (21.7%) who had significantly higher mortality. In cardiac injury group, the median duration from illness onset to death was 17.8 [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] days; a figure that is comparable to published data in literature. Shi et al [14] described in a retrospective cohort of patients with COVID-19 that 19.7% had cardiac injury with mortality rate of 51.2% compared with 4.5% in non-cardiac injury group.…”

Section: Discussionsupporting

confidence: 64%

“…The postulated mechanisms include direct damage to the cardiomyocytes, systemic inflammation, myocardial interstitial fibrosis, interferon mediated immune response and exaggerated cytokine response by Type 1 and 2 helper T cells, in addition to coronary plaque destabilization, and hypoxia [6,7]. Cardiac Injury may manifest as severe myocarditis with reduced systolic function, and elevated troponin hs-TNI [10,11]. Patients with pre-existing cardiovascular diseases are more prone to SARS-CoV-2 infection and they are more likely to develop stormy course [12].…”

Section: Introductionmentioning

confidence: 99%

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Myocardial Injury Is Associated with Higher Morbidity and Mortality in Patients with 2019 Novel Coronavirus Disease (COVID-19)

Al-Wahaibi

Al-Wahshi

Elfadil

2020

SN Compr. Clin. Med.

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COVID-19 pandemic, a global health disaster, has resulted in substantial morbidity and mortality across the globe since emerging on December 2019. Studies have shown that cardiovascular manifestations and complications linked to COVID-19 can be attributed to unfavorable clinical outcome and poor prognosis. Adult patients with laboratory-confirmed COVID-19 requiring hospitalization in participating centers between March and June 2020 were included. Data including demographics, laboratory findings, comorbidities, treatments and interventions were collected. Mortality and clinical outcomes in patients with and without cardiac injury were compared. A total of 143 hospitalized patients with confirmed COVID-19 were included (86.7% male; age 49.36 ± 15.32 years). Cardiovascular diseases (CVDs) including hypertension, cardiomyopathy, coronary heart disease, and rhythm disturbances were noted in 34.3% of the study population and 21.7% had cardiac injury. In comparison with patients without cardiac injury, patients with cardiac injury were older (59 [33-89] vs 47 [22-94] years; P < 0.0001) and had more comorbidities and cardiovascular (CV) risk factors (hypertension in 61.3% vs 24.1%; P < 0.0001, chronic heart failure in 16.1% vs 0%; P < 0.00001, diabetes mellitus 54.8% vs 31.3%; P 0.015, COPD/asthma 19.4% vs 3.6%; P 0.002); more patients with cardiac injury required invasive mechanical ventilation (77.4% vs 38.4%; P 0.00012). Complications were more prevalent in patients with cardiac injury than those without cardiac injury and included acute respiratory distress syndrome (87% vs 42.9%; P < 0.00001), acute kidney injury (67.7% vs 11.6%; P < 0.00001), and anemia (38.7% vs 3.6%;P < 0.00001). The need for renal replacement therapy was also higher in patients with cardiac injury (48.4% vs 3.6%; P < 0.00001). Noticeably, patients with cardiac injury had higher mortality than those without cardiac injury (53.3% vs 7.1%; P < 0.00001). In summary, myocardial injury is common among hospitalized patients with COVID-19 in Oman in relation to older patients with more CV risk factors and comorbidities, and is associated with higher risk of in-hospital mortality and unfavorable clinical outcomes. Keywords Cardiac injury. Myocardial injury. COVID-19. Oman This article is part of the Topical Collection on Covid-19

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Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Myocardial Injury Is Associated with Higher Morbidity and Mortality in Patients with 2019 Novel Coronavirus Disease (COVID-19)

Al-Wahaibi

Al-Wahshi

Elfadil

2020

SN Compr. Clin. Med.

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“…Similar to 2009 pandemic H1N1 influenza infection; several cases of myocarditis have been reported in COVID-19 patients. A meta summary analyzed 31 studies with a total of 51 myocarditis cases (159). Out of these, 12 patients were diagnosed based on cardiac magnetic resonance imaging (MRI) or histopathology, and 39 patients were diagnoses based on the inflammatory markers and electrocardiogram (ECG) (159).…”

Section: Comparison Of Cardiovascular Conditions Associated With Sarsmentioning

confidence: 99%

“…A meta summary analyzed 31 studies with a total of 51 myocarditis cases (159). Out of these, 12 patients were diagnosed based on cardiac magnetic resonance imaging (MRI) or histopathology, and 39 patients were diagnoses based on the inflammatory markers and electrocardiogram (ECG) (159). Also, comparable to 2009 H1N1 influenza infection, several fulminant myocarditis cases were observed in COVID-19 patients (160)(161)(162)(163)(164)(165)(166)(167)(168).…”

Section: Comparison Of Cardiovascular Conditions Associated With Sarsmentioning

confidence: 99%

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

2020

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Influenza virus infection causes 3-5 million cases of severe illness and 250,000-500,000 deaths worldwide annually. Although pneumonia is the most common complication associated with influenza, there are several reports demonstrating increased risk for cardiovascular diseases. Several clinical case reports, as well as both prospective and retrospective studies, have shown that influenza can trigger cardiovascular events including myocardial infarction (MI), myocarditis, ventricular arrhythmia, and heart failure. A recent study has demonstrated that influenza-infected patients are at highest risk of having MI during the first seven days of diagnosis. Influenza virus infection induces a variety of pro-inflammatory cytokines and chemokines and recruitment of immune cells as part of the host immune response. Understanding the cellular and molecular mechanisms involved in influenza-associated cardiovascular diseases will help to improve treatment plans. This review discusses the direct and indirect effects of influenza virus infection on triggering cardiovascular events. Further, we discussed the similarities and differences in epidemiological and pathogenic mechanisms involved in cardiovascular events associated with coronavirus disease 2019 (COVID-19) compared to influenza infection.

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“…As indicated in Figure 2, the excessive immune response in patients with severe COVID-19 may lead to various pathological outcomes: coagulopathy with associated venous and arterial thrombosis, subsequent stroke and possible death or disability [57,58]; multi-organ failure, partly due to coagulopathy, and possible death [59][60][61][62]; deleterious effects on vital organs, including acute kidney injury [63,64], myocarditis [65] and pulmonary fibrosis [66][67][68][69].…”

Section: Anti-inflammatory Effects Of At 2 R Activationmentioning

confidence: 99%

Correcting the imbalanced protective RAS in COVID-19 with angiotensin AT2-receptor agonists

Steckelings

Sumners

2020

Clinical Science

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that is responsible for the global corona virus disease 2019 (COVID-19) pandemic enters host cells via a mechanism that includes binding to angiotensin converting enzyme (ACE) 2 (ACE2). Membrane-bound ACE2 is depleted as a result of this entry mechanism. The consequence is that the protective renin–angiotensin system (RAS), of which ACE2 is an essential component, is compromised through lack of production of the protective peptides angiotensin-(1-7) and angiotensin-(1-9), and therefore decreased stimulation of Mas (receptor Mas) and angiotensin AT2-receptors (AT2Rs), while angiotensin AT1-receptors (AT1Rs) are overstimulated due to less degradation of angiotensin II (Ang II) by ACE2. The protective RAS has numerous beneficial actions, including anti-inflammatory, anti-coagulative, anti-fibrotic effects along with endothelial and neural protection; opposite to the deleterious effects caused by heightened stimulation of angiotensin AT1R. Given that patients with severe COVID-19 exhibit an excessive immune response, endothelial dysfunction, increased clotting, thromboses and stroke, enhancing the activity of the protective RAS is likely beneficial. In this article, we discuss the evidence for a dysfunctional protective RAS in COVID and develop a rationale that the protective RAS imbalance in COVID-19 may be corrected by using AT2R agonists. We further review preclinical studies with AT2R agonists which suggest that AT2R stimulation may be therapeutically effective to treat COVID-19-induced disorders of various organ systems such as lung, vasculature, or the brain. Finally, we provide information on the design of a clinical trial in which patients with COVID-19 were treated with the AT2R agonist Compound 21 (C21). This trial has been completed, but results have not yet been reported.

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Coronavirus-induced myocarditis: A meta-summary of cases

Cited by 128 publications

References 47 publications

Myocardial Injury Is Associated with Higher Morbidity and Mortality in Patients with 2019 Novel Coronavirus Disease (COVID-19)

Myocardial Injury Is Associated with Higher Morbidity and Mortality in Patients with 2019 Novel Coronavirus Disease (COVID-19)

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

Correcting the imbalanced protective RAS in COVID-19 with angiotensin AT2-receptor agonists

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