Myocardial Work in Patients Hospitalized With COVID-19: Relation to Biomarkers, COVID-19 Severity, and All-Cause Mortality
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › fagfællebedømt
Forlagets udgivne version, 4,18 MB, PDF-dokument
BACKGROUND: COVID-19 infection has been hypothesized to affect left ventricular function; however, the underlying mechanisms and the association to clinical outcome are not understood. The global work index (GWI) is a novel echocardiographic measure of systolic function that may offer insights on cardiac dysfunction in COVID-19. We hypothesized that GWI was associated with disease severity and all-cause death in patients with COVID-19. METHODS AND RESULTS: In a multicenter study of patients admitted with COVID-19 (n=305), 249 underwent pressure-strain loop analyses to quantify GWI at a median time of 4 days after admission. We examined the association of GWI to cardiac biomarkers (troponin and NT-proBNP [N-terminal pro-B-type natriuretic peptide]), disease severity (oxygen requirement and CRP [C-reactive protein]), and all-cause death. Patients with elevated troponin (n=71) exhibited significantly reduced GWI (1508 versus 1707 mm Hg%; P=0.018). A curvilinear association to NT-proBNP was observed, with increasing NT-proBNP once GWI decreased below 1446 mm Hg%. Moreover, GWI was significantly associated with a higher oxygen requirement (relative increase of 6% per 100– mm Hg% decrease). No association was observed with CRP. Of the 249 patients, 37 died during follow-up (median, 58 days). In multivariable Cox regression, GWI was associated with all-cause death (hazard ratio, 1.08 [95% CI, 1.01–1.15], per 100– mm Hg% decrease), but did not increase C-statistics when added to clinical parameters. CONCLUSIONS: In patients admitted with COVID-19, our findings indicate that NT-proBNP and troponin may be associated with lower GWI, whereas CRP is not. GWI was independently associated with all-cause death, but did not provide prognostic information beyond readily available clinical parameters. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04377035.
|Tidsskrift||Journal of the American Heart Association|
|Status||Udgivet - 2022|
Dr Biering-Sørensen is a Steering Committee member of the Amgen-financed Global Approach to Lowering Adverse Cardiac Outcomes through Improving Contractility in Heart Failure (GALACTIC-HF) trial; is part of the Steering Committee of the Boston Scientific–financed LUX-Dx Heart Failure Sensors in an Insertable Cardiac Monitor System Clinical Study (LUX-Dx TRENDS); is on the Advisory Board of Sanofi Pasteur and Amgen; received speaker honorarium from Novartis and Sanofi Pasteur; and received research grants from GE Healthcare and Sanofi Pasteur. Dr Smiseth is coinventor of the “Method for Myocardial Segment Work Analysis,” which was used to calculate myocardial work. Dr Svendsen is on the Advisory Board for Medtronic; received a research grant from Medtronic; and received speaker honorarium from Medtronic. Dr Kirk reports fees for consultation, lectures, and travel by Gilead, Janssen, Merck, and Viiv, outside the submitted work. The remaining authors have no disclosures to report.
The ECHOVID-19 study was financed by the Novo Nordisk Foundation (grant NFF20SA0062835). Europcar provided a vehicle for transportation between hospitals. Dr Olsen was financed by the Danish Heart Foundation (grant 18-R125-A8534-22083), Herlev and Gentofte Hospital’s Research Council, Kong Christian den Tiendes Fond, and Fru Asta Florida Boldings Mindelegat. Dr Biering-Sørensen was funded by Herlev and Gentofte Hospital, Fondsbørsvekselerer Henry Hansen og Hustrus Hovedlegat, the Lundbeck Foundation, and the Novo Nordisk Foundation.
© 2022 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is a.