Numbers and phenotype of non-classical CD14dimCD16+ monocytes are predictors of adverse clinical outcome in patients with coronary artery disease and severe SARS-CoV-2 infection

COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection likely ranks among the deadliest diseases in human history. As with other coronaviruses, SARS-CoV-2 infection damages not only the lungs but also the heart and many other organs that express angiotensin-converting enzyme 2 (ACE2), a receptor for SARS-CoV-2. COVID-19 has upended lives worldwide. Dietary behaviors have been altered such that they favor metabolic and cardiovascular complications, while patients have avoided hospital visits because of limited resources and the fear of infection, thereby increasing out-hospital mortality due to delayed diagnosis and treatment. Clinical observations show that sex, age, and race all influence the risk for SARS-CoV-2 infection, as do hypertension, obesity, and pre-existing cardiovascular conditions. Many hospitalized COVID-19 patients suffer cardiac injury, acute coronary syndromes, or cardiac arrhythmia. SARS-CoV-2 infection may lead to cardiomyocyte apoptosis and necrosis, endothelial cell damage and dysfunction, oxidative stress and reactive oxygen species production, vasoconstriction, fibrotic and thrombotic protein expression, vascular permeability and microvascular dysfunction, heart inflammatory cell accumulation and activation, and a cytokine storm. Current data indicate that COVID-19 patients with cardiovascular diseases should not discontinue many existing cardiovascular therapies such as ACE inhibitors, angiotensin receptor blockers, steroids, aspirin, statins, and PCSK9 inhibitors. This review aims to furnish a framework relating to COVID-19 and cardiovascular pathophysiology.

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“…Decreased numbers of these cells were positively associated with ICU admission, respiratory failure, and use of mechanical ventilation. [ 279 ]…”

Section: Inflammation and The Cytokine Storm In Covid-19 Patientsmentioning

confidence: 99%

COVID-19, the Pandemic of the Century and Its Impact on Cardiovascular Diseases

Zhang

Wang

Zhang

et al. 2021

Cardiology Discovery

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“… 30 There is accumulating evidence that SARS-CoV-2 associated respiratory distress is associated with a hyper-thrombotic state and hyper-inflammation. 38 , 39 Further, platelets exhibit local and systemic thrombo-inflammatory activities and are able to alter immune cell functions inducing plaque formation in CAD. They function as connection between local inflammatory responses at vascular wall and development of an atherogenetic milieu.…”

mentioning

confidence: 99%

Platelet Activation and Plasma Levels of Furin Are Associated With Prognosis of Patients With Coronary Artery Disease and COVID-19

Langnau

Rohlfing

Gekeler

et al. 2021

ATVB

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Objective: Patients with coronary artery disease (CAD) are at increased risk for cardiac death and respiratory failure following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Platelets are crucially involved in pathogenesis of CAD and might also contribute to pathophysiology of SARS-CoV-2 infection. Approach and Results: We enrolled a cohort of 122 participants from February 2020 to July 2020 including 55 patients with preexisting CAD and acute SARS-CoV-2 infection (CAD-SARS-CoV-2 positive ), 28 patients with CAD and without SARS-CoV-2 (CAD-SARS-CoV-2 negative ), and 39 healthy controls. Clinical and cardiac examination of the CAD-SARS-CoV-2 positive group included blood sampling, echocardiography, and electrocardiography within 24 hours after hospital admission. Phenotyping of platelets was performed by flow cytometry; plasma levels of chemokines were analyzed by ELISA. Respiratory failure of patients was stratified by the Horovitz index as moderately/severely impaired when Horovitz index <200 mm Hg. The clinical end point was defined as Horovitz index <200 mm Hg with subsequent mechanical ventilation within a follow-up of 60 days. CAD-SARS-CoV-2 positive patients display a significant enhanced platelet activation and hyper-inflammation early at time of hospital admission. Circulating platelet/leukocyte co-aggregates correlate with plasma levels of cytokines/chemokines like IL (interleukin)-6, CCL2, and CXCL10 as well as activation of platelets is associated with CCL5 and elevation of pulmonary artery pressure. Furthermore, furin is stored and released from activated platelets. High furin plasma levels are associated with poor clinical prognosis in CAD-SARS-CoV-2 positive patients. Conclusions: Patients with CAD and SARS-CoV-2 infection exhibit elevated systemic platelet activation and enhanced plasma levels of the subtilisin-like proprotein convertase furin, which may contribute to an unfavorable clinical prognosis.

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“…Another trial revealed, that the amount of CD14 dim CD16 þ monocytes in peripheral blood of COVID-19 patients with severe coronary artery disease is remarkably decreased. 28 These so-called nonclassical monocytes normally trigger cytokine release, which leads to systemic inflammation. The authors conclude that the decreased number of these nonclassical monocytes is due to migration into the heart and lung tissue, which in turn triggers tissue destruction and consecutively organ failure.…”

Section: Resultsmentioning

confidence: 99%

COVID-19 and Cardiac Arrhythmias

Duckheim

Schreieck

2021

Hamostaseologie

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Since the coronavirus disease (COVID-19) pandemic spread unrelentingly all over the world, millions of cases have been reported. Despite a high number of asymptomatic cases, the course of the disease can be serious or even fatal. The affection of the myocardium, called myocardial injury, is caused by multiple triggers. The occurrence of cardiac arrhythmias in COVID-19 patients with myocardial involvement and a critical course is common. In this review, potential mechanisms, incidence, and treatment options for cardiac arrhythmias in COVID-19 patients will be provided by performing a literature research in MESH database and the National Library of Medicine. Common cardiac arrhythmias in COVID-19 patients were sinus tachycardia, atrial fibrillation (AF), ventricular tachycardia (VT), ventricular fibrillation (VF), atrioventricular block, sinusoidal block or QTc prolongation. AF was the most common heart rhythm disorder. About 10% of COVID-19 patients develop new-onset AF and 23 to 33% showed recurrence of AF in patients with known AF. One retrospective trial revealed the incidence of VT or VF to be 5.9% in hospitalized patients. Both AF and VT are clearly associated with worse outcome. Several mechanisms such as hypoxia, myocarditis, myocardial ischemia, or abnormal host immune response, which induce cardiac arrhythmias, have been described. The effect of QT-prolonging drugs in inducing cardiac arrhythmias has become mitigated as these medications are no longer recommended. Acute management of cardiac arrhythmias in COVID-19 patients is affected by the reduction of exposure of health care personnel. More prospective data are desirable to better understand pathophysiology and consecutively adapt management.

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Numbers and phenotype of non-classical CD14dimCD16+ monocytes are predictors of adverse clinical outcome in patients with coronary artery disease and severe SARS-CoV-2 infection

Cited by 19 publications

References 31 publications

COVID-19, the Pandemic of the Century and Its Impact on Cardiovascular Diseases

COVID-19, the Pandemic of the Century and Its Impact on Cardiovascular Diseases

Platelet Activation and Plasma Levels of Furin Are Associated With Prognosis of Patients With Coronary Artery Disease and COVID-19

COVID-19 and Cardiac Arrhythmias

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