COVID-19 and the Cardiovascular System

Veer, Manik; Kumar, Aarthi Madhana; Ivanova, V F

doi:10.1097/cnq.0000000000000323

Cited by 11 publications

(6 citation statements)

References 27 publications

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“…4,7,12 has been shown to be associated with development of cardiovascular conditions, including myocardial injury, arrhythmia, acute coronary syndrome, and venous thromboembolism. 5,6,10,11,[13][14][15][16][17] Although early data relating to pediatric COVID-19 cases are limited, systematic reviews of cases in children showed that underlying cardiovascular defects were prevalent, with congenital heart disease (CHD) being associated with worse clinical outcomes. 18,19 Congenital heart disease is estimated to occur in 3 to 10 children per 1000 live births in the US, [20][21][22] and this rate is increasing.…”

Section: Introductionmentioning

confidence: 99%

Association of Congenital and Acquired Cardiovascular Conditions With COVID-19 Severity Among Pediatric Patients in the US

et al. 2022

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IMPORTANCEIdentifying the associations between severe COVID-19 and individual cardiovascular conditions in pediatric patients may inform treatment. OBJECTIVE To assess the association between previous or preexisting cardiovascular conditions and severity of COVID-19 in pediatric patients. DESIGN, SETTING, AND PARTICIPANTS This retrospective cohort study used data from a large, multicenter, electronic health records database in the US. The cohort included patients aged 2 months to 17 years with a laboratory-confirmed diagnosis of COVID-19 or a diagnosis code indicating infection or exposure to SARS-CoV-2 at 85 health systems between March 1, 2020, and January 31, 2021.

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Section: Introductionmentioning

confidence: 99%

Association of Congenital and Acquired Cardiovascular Conditions With COVID-19 Severity Among Pediatric Patients in the US

et al. 2022

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“…On the other hand, the severity of SARS infection largely relied on the load of virus as well as immunopathological response of host according to the accumulative evidence [43]. The common imbalance of Th1 and Th2 response easily contributed to cytokine storm which may be linked with myocardial injury [44]. Cardiac troponin T may be a sensitive marker help us discern severe patients.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Troponin T as the Underlying Risk Factor Associated With Disease Severity and Mortality in Patients With Coronavirus Disease 2019

Wei-ping

Liu

Tang

et al. 2020

Preprint

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Backgrounds: To describe the clinical characteristics of coronavirus disease 2019 hospitalized patients and further analyze the potential risk factors related to the severity of the disease and 28-day mortality of patients.Methods: A total of 122 coronavirus disease 2019 patients hospitalized in Wuhan Third Hospital from 26 January 2020 to 16 March 2020 were included in this retrospective study. Clinical data of patients were retrospectively analyzed, and the risk factors associated with disease severity and 28-day mortality were screened by cox regression analysis.Results: Of all 122 patients, the median age was 64 years old (interquartile range, 57- 71 years old).Compared with non-severe patients, severe patients had higher indices like cardiac troponin T and respiratory rate. In cox regression analysis, cardiac troponin T correlated with 28-day mortality most.Conclusions: Abnormal cardiac troponin T value after admission were in strong correlation with 28-day survival status.

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“…While the fundamental mechanism by which SARS-CoV-2 interacts with CD147 in humans is debated in the scientific community [ 13 ], there is a lot of potential rationales supporting the theory that CD147 could still play a role in the COVID-19 clinical course, even if it is not a functional viral entry receptor. For example, compared to ACE2 protein expression, CD147 is expressed in cardiomyocytes and endothelial cells, which may correlate with massive hemodynamic instability and cardiovascular abnormalities during SARS-CoV-2 infection [ 14 , 15 ]. The high expression of CD147 protein, but not ACE2 protein, on erythrocytes and platelets, may also contribute to a "catch and clump” mechanism that increases the risk of thrombosis in various organ systems during SARS-CoV-2 infection [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Development of a novel human CD147 knock-in NSG mouse model to test SARS-CoV-2 viral infection

et al. 2022

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Background An animal model that can mimic the SARS-CoV-2 infection in humans is critical to understanding the rapidly evolving SARS-CoV-2 virus and for development of prophylactic and therapeutic strategies to combat emerging mutants. Studies show that the spike proteins of SARS-CoV and SARS-CoV-2 bind to human angiotensin-converting enzyme 2 (hACE2, a well-recognized, functional receptor for SARS-CoV and SARS-CoV-2) to mediate viral entry. Several hACE2 transgenic (hACE2Tg) mouse models are being widely used, which are clearly invaluable. However, the hACE2Tg mouse model cannot fully explain: (1) low expression of ACE2 observed in human lung and heart, but lung or heart failure occurs frequently in severe COVID-19 patients; (2) low expression of ACE2 on immune cells, but lymphocytopenia occurs frequently in COVID-19 patients; and (3) hACE2Tg mice do not mimic the natural course of SARS-CoV-2 infection in humans. Moreover, one of most outstanding features of coronavirus infection is the diversity of receptor usage, which includes the newly proposed human CD147 (hCD147) as a possible co-receptor for SARS-CoV-2 entry. It is still debatable whether CD147 can serve as a functional receptor for SARS-CoV-2 infection or entry. Results Here we successfully generated a hCD147 knock-in mouse model (hCD147KI) in the NOD-scid IL2Rgammanull (NSG) background. In this hCD147KI-NSG mouse model, the hCD147 genetic sequence was placed downstream of the endogenous mouse promoter for mouse CD147 (mCD147), which creates an in vivo model that may better recapitulate physiological expression of hCD147 proteins at the molecular level compared to the existing and well-studied K18-hACE2-B6 (JAX) model. In addition, the hCD147KI-NSG mouse model allows further study of SARS-CoV-2 in the immunodeficiency condition which may assist our understanding of this virus in the context of high-risk populations in immunosuppressed states. Our data show (1) the human CD147 protein is expressed in various organs (including bronchiolar epithelial cells) in hCD147KI-NSG mice by immunohistochemical staining and flow cytometry; (2) hCD147KI-NSG mice are marginally sensitive to SARS-CoV-2 infection compared to WT-NSG littermates characterized by increased viral copies by qRT-PCR and moderate body weight decline compared to baseline; (3) a significant increase in leukocytes in the lungs of hCD147KI-NSG mice, compared to infected WT-NSG mice. Conclusions hCD147KI-NSG mice are more sensitive to COVID-19 infection compared to WT-NSG mice. The hCD147KI-NSG mouse model can serve as an additional animal model for further interrogation whether CD147 serve as an independent functional receptor or accessory receptor for SARS-CoV-2 entry and immune responses.

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COVID-19 and the Cardiovascular System

Cited by 11 publications

References 27 publications

Association of Congenital and Acquired Cardiovascular Conditions With COVID-19 Severity Among Pediatric Patients in the US

Association of Congenital and Acquired Cardiovascular Conditions With COVID-19 Severity Among Pediatric Patients in the US

Cardiac Troponin T as the Underlying Risk Factor Associated With Disease Severity and Mortality in Patients With Coronavirus Disease 2019

Development of a novel human CD147 knock-in NSG mouse model to test SARS-CoV-2 viral infection

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