natriuretic-peptide--brain has been researched along with Cytokine-Release-Syndrome* in 4 studies
1 review(s) available for natriuretic-peptide--brain and Cytokine-Release-Syndrome
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Biomarkers of Cardiac Stress and Cytokine Release Syndrome in COVID-19: A Review.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in the coronavirus 2019 (COVID-19) global pandemic. While primarily a respiratory virus, SARS-CoV-2 can cause myocardial injury. The pattern of injury, referred to as acute COVID-19 cardiovascular syndrome (ACovCS), is defined by cardiac troponin leak in the absence of obstructive coronary artery disease. Although the etiology of the injury is unknown, many speculate that a cytokine release syndrome (CRS) may be an important factor. We aim to review recent data concerning markers of cardiac injury in ACovCS and its relation to the CRS.. Cardiac injury was common in patients hospitalized for COVID-19, with both cardiac troponin and B-type natriuretic peptide (BNP) being elevated in this population. Biomarkers were correlated with illness severity and increased mortality. Cytokines such as IL-6 were more often elevated in patients with ACovCS. Myocarditis evident on cardiac MR following COVID-19 may be associated with cardiac troponin levels. The impact of dexamethasone and remdesivir, two therapies shown to have clinical benefit in COVID-19, on myocardial injury is unknown. Biomarkers of cardiac stress and injury in COVID-19 may be used to stratify risk in the future. Currently, there is no evidence that inhibition of cytokine release will reduce myocardial injury in patients with COVID-19. Topics: Biomarkers; Cardiomyopathies; COVID-19; Cytokine Release Syndrome; Humans; Natriuretic Peptide, Brain; SARS-CoV-2; Troponin | 2021 |
3 other study(ies) available for natriuretic-peptide--brain and Cytokine-Release-Syndrome
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Scientific hypothesis and rational pharmacological for the use of sacubitril/valsartan in cardiac damage caused by COVID-19.
On March 11, 2020 the World Health Organization (WHO) declared the state of global pandemic caused by the new SARS-CoV-2 (COVID-19). To date, no antivirals directed against SARS-CoV-2 or effective vaccines to combat the viral infection are available. Severe acute respiratory syndrome caused by SARS-CoV-2 is treated empirically with antivirals, anti-inflammatory, anticoagulants. The approval of an effective vaccine still takes time. In this state, it may be useful to find new therapeutic solutions from drugs already on the market. Recent hypotheses suggest that the use of AT-1 receptor antagonists (ARB) in combination with neprilisin inhibitors (NEPi) could indirectly provide clinical benefits to patients with SARS-CoV-2 and cardiac involvement. In this article we investigate and describe a possible innovative pharmacological approach for the treatment of the most severe stages of COVID-19 infection. Topics: Aminobutyrates; Angiotensin-Converting Enzyme Inhibitors; Antiviral Agents; Biphenyl Compounds; COVID-19 Drug Treatment; Cytokine Release Syndrome; Cytokines; Drug Combinations; Heart Failure; Homeostasis; Humans; Inflammation; Models, Theoretical; Natriuretic Peptide, Brain; Neprilysin; Peptide Fragments; Receptor, Angiotensin, Type 2; Tetrazoles; Valsartan; World Health Organization | 2021 |
Cardiovascular biomarkers in COVID-19.
Topics: Biomarkers; C-Reactive Protein; Cardiovascular Diseases; COVID-19; Cytokine Release Syndrome; Fibrin Fibrinogen Degradation Products; Humans; Interleukin-6; Natriuretic Peptide, Brain; SARS-CoV-2; Severity of Illness Index; Troponin | 2021 |
COVID-19 and myocardial injury: is there a role for interleukin-1 inhibition?
Topics: Betacoronavirus; C-Reactive Protein; Coronavirus Infections; COVID-19; Cytokine Release Syndrome; Endothelium, Vascular; Humans; Interleukin-1; Macrophage Activation; Multiple Organ Failure; Myocardial Ischemia; Natriuretic Peptide, Brain; Pandemics; Peptide Fragments; Pneumonia, Viral; SARS-CoV-2; Troponin I | 2020 |