Impact of Cardiovascular Diseases on COVID-19: A Systematic Review

Cao, Qingtai; Lei, Hanyu; Yang, Minghong; Le, Wei; Dong, Yinmiao; Nasser, M; Liu, MengQi; Zhu, Ping; Xu, Lei; Zhao, Mingyi

doi:10.12659/msm.930032

Cited by 6 publications

(9 citation statements)

References 92 publications

(102 reference statements)

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“…Alternatively, the existence of a high mortality risk in untreated cancer patients with COVID-19 indicates that cancer alone, without its associated treatments, may affect the immune system ( 109 ). Patients with COVID-19 also depicted elevated levels of IL-6, whereas increased IL-6 is associated with cardiac dysfunction and can further increase the risk of cardiovascular incidents such as heart failure and myocardial infraction ( 110 ). In addition to its function as an indicator of cardiovascular events, IL-6 also serves as a potent reference in its signaling pathways and pathophysiology.…”

Section: Covid-19 and The Most Common Comorbiditiesmentioning

confidence: 99%

“…In cardiac patients, ACE-2 levels and expression are low in fibroblasts as compared to the healthy control, but high in endothelial cells and cardiomyocytes, whereas the same increase is found in patients with heart failure and aortic stenosis ( 120 ). It may seem oxymoronic that ACE-2 can contribute to healthy cardiovascular function while worsening SARS-CoV-2 infection through ACE-2 dysregulation ( 110 ). Viral infection can cause endothelial cell dysfunction resulting in microvascular dysfunction, which is correlated with pericytes injury ( 121 ).…”

Section: Covid-19 and The Most Common Comorbiditiesmentioning

confidence: 99%

“…Nox2 levels can be correlated with troponin elevation and instances of heart failure, presenting a possible link between Nox2 activation and cardiovascular issues as a result of COVID-19. Therefore, it can be suggested that Nox2 levels could potentially serve as biomarker for COVID-19 infection ( 110 ). ACE-2 is also downregulated in older people, which intensifies the severity of their COVID-19 infection and may explains why age is a risk factor.…”

Section: Covid-19 and The Most Common Comorbiditiesmentioning

confidence: 99%

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COVID-19 and Preexisting Comorbidities: Risks, Synergies, and Clinical Outcomes

et al. 2022

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its associated symptoms, named coronavirus disease 2019 (COVID-19), have rapidly spread worldwide, resulting in the declaration of a pandemic. When several countries began enacting quarantine and lockdown policies, the pandemic as it is now known truly began. While most patients have minimal symptoms, approximately 20% of verified subjects are suffering from serious medical consequences. Co-existing diseases, such as cardiovascular disease, cancer, diabetes, and others, have been shown to make patients more vulnerable to severe outcomes from COVID-19 by modulating host–viral interactions and immune responses, causing severe infection and mortality. In this review, we outline the putative signaling pathways at the interface of COVID-19 and several diseases, emphasizing the clinical and molecular implications of concurring diseases in COVID-19 clinical outcomes. As evidence is limited on co-existing diseases and COVID-19, most findings are preliminary, and further research is required for optimal management of patients with comorbidities.

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Section: Covid-19 and The Most Common Comorbiditiesmentioning

confidence: 99%

Section: Covid-19 and The Most Common Comorbiditiesmentioning

confidence: 99%

Section: Covid-19 and The Most Common Comorbiditiesmentioning

confidence: 99%

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COVID-19 and Preexisting Comorbidities: Risks, Synergies, and Clinical Outcomes

et al. 2022

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“…cTn1 is increased in patients suffering from severe COVID-19 disease versus those with moderate disease. [ 24 ],[ 25 ],[ 26 ],[ 27 ],[ 28 ],[ 29 ],[ 30 ],[ 31 ],[ 32 ],[ 33 ],[ 34 ],[ 35 ],[ 36 ] Tajbakhsh et al . reported 11.8% of deceased COVID-19 patients with no preexisting CVD experienced heart damage accompanied by a greater level of cTn1 or cardiac arrest during hospitalization.…”

Section: Resultsmentioning

confidence: 99%

COVID-19-Induced Cardiovascular Damage Differs from other Prevalent Viruses

et al. 2021

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Viral infections persist globally, among all ages, gender, and ethnicity. Of particular importance is COVID-19, associated with asymptomatic to severe symptoms, including complications/mortality. Cardiovascular disease (CVD) involves heart and blood vessel disorders including coronary heart disease, cerebrovascular disease, peripheral artery disease, thrombosis, and more. CVD associated with severe COVID-19 includes heart failure, coronary artery disease, cardiomyopathy, hypertension, and cerebrovascular disease/stroke. Data were acquired from PubMed, Google Scholar, Centers for Disease Prevention and Control, and Lexi-Comp using the search terms “COVID-19 and cardiovascular pathology;” “COVID-19 induced CVD;” “Viral infection induced CVD;” and “Viral infection induced heart damage.” COVID-19-induced CVD mechanisms include direct viral entry, inflammation, cytokine storm, hypoxia, interferon-mediated immune response, plaque destabilization, stress, and drug-induced causes. Other viral pathologies causing CVD include atherosclerosis, inflammation, cytokine storm, and plaque destabilization. Individual parameters, such as old age, males, and higher body mass index (BMI), are more likely to experience viral-associated complications, possibly explained by patient risk factors or comorbidities. Populations at higher risk include older males with an elevated BMI. Viral mechanisms associated with CVD are similar but differ in disease severity, potentially explained by diverse cytokine profiles where COVID-19 activates different types at higher quantities.

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“…The cardiac manifestations that may occur during COVID-19 infection include acute cardiac injury, myocarditis, acute myocardial infarction (AMI), heart failure, arrhythmia, cardiomyopathy, hypotension, shock, and cardiac arrest (18,23,24). An echocardiographic study of patients with COVID-19 documented pre-existing abnormalities, which prompted the authors to suggest caution with regard to attributing such abnormalities to acute COVID-19 infection (25).…”

Section: The Clinical Aspects Of Covid-19 and Cardiovascular Diseasementioning

confidence: 99%

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury

et al. 2022

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Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.

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Impact of Cardiovascular Diseases on COVID-19: A Systematic Review

Cited by 6 publications

References 92 publications

COVID-19 and Preexisting Comorbidities: Risks, Synergies, and Clinical Outcomes

COVID-19 and Preexisting Comorbidities: Risks, Synergies, and Clinical Outcomes

COVID-19-Induced Cardiovascular Damage Differs from other Prevalent Viruses

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury

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