tetano
Editor, Senior Moderator
Curr Heart Fail Rep
. 2021 Mar 5.
doi: 10.1007/s11897-021-00505-2. Online ahead of print.
Biomarkers of Cardiac Stress and Cytokine Release Syndrome in COVID-19: A Review
Jonathan S Gordon[SUP] 1 [/SUP], Mark H Drazner[SUP] 2 [/SUP]
Affiliations
Abstract
Purpose of 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.
Recent findings: 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.
Keywords: BNP; COVID-19; cardiac biomarkers; coronavirus; cytokine release syndrome; troponin.
. 2021 Mar 5.
doi: 10.1007/s11897-021-00505-2. Online ahead of print.
Biomarkers of Cardiac Stress and Cytokine Release Syndrome in COVID-19: A Review
Jonathan S Gordon[SUP] 1 [/SUP], Mark H Drazner[SUP] 2 [/SUP]
Affiliations
- PMID: 33666855
- DOI: 10.1007/s11897-021-00505-2
Abstract
Purpose of 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.
Recent findings: 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.
Keywords: BNP; COVID-19; cardiac biomarkers; coronavirus; cytokine release syndrome; troponin.