Michael Briscoe1, Robert Sykes2,3, Thomas Krystofiak1, Oliver Peck1,3, Kenneth Mangion1,2,3, Colin Berry1,2,3. 1. Department of Cardiology, Queen Elizabeth University Hospital, NHS Greater Glasgow and Clyde Health Board, Glasgow, UK. 2. Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK. 3. West of Scotland Heart and Lung Centre, Golden Jubilee National Hospital, Glasgow, UK.
Abstract
BACKGROUND: The clinical significance of Coronavirus disease 2019 (COVID-19) as an associate of myocardial injury is controversial. HYPOTHESIS: Type 2 MI/Myocardial Injury are associated with worse outcomes if complicated by COVID-19. METHODS: This longitudinal cohort study involved consecutive patients admitted to a large urban hospital. Myocardial injury was determined using laboratory records as ≥1 hs-TnI result >99th percentile (male: >34 ng/L; female: >16 ng/L). Endotypes were defined according to the Fourth Universal Definition of Myocardial Infarction (MI) and COVID-19 determined using PCR. Outcomes of patients with myocardial injury with and without COVID-19 were assessed. RESULTS: Of 346 hospitalized patients with elevated hs-TnI, 35 (10.1%) had laboratory-confirmed COVID-19 (median age [IQR]; 65 [59-74]; 64.8% male vs. COVID-19 negative: 74 [63-83] years; 43.7% male). Cardiac endotypes by COVID-19 status (yes vs. no) were: Type 1 MI (0 [0%] vs. 115 [100%]; p < .0005), Type 2 MI (13 [16.5%] vs. 66 [83.5%]; p = .045), and non-ischemic myocardial injury (cardiac: 4 [5.8%] vs. 65 [94.2%]; p = .191, non-cardiac:19 [22.9%] vs. 64 [77.%]; p < .0005). COVID-19 patients had less comorbidity (median [IQR] Charlson Comorbidity Index: 3.0 [3.0] vs. 5.0 [4.0]; p = .001), similar hs-TnI concentrations (median [IQR] initial: 46 [113] vs. 62 [138]; p = .199, peak: 122 [474] vs. 79 [220] ng/L; p = .564), longer admission (days) (median [IQR]: 14[19] vs. 6[12]; p = .001) and higher in-hospital mortality (63.9% vs. 11.3%; OR = 13.2; 95%CI: 5.90, 29.7). CONCLUSIONS: Cardiac sequelae of COVID-19 typically manifest as Non-cardiac myocardial injury/Type 2MI in younger patients with less co-morbidity. Paradoxically, the admission duration and in-hospital mortality are increased.
BACKGROUND: The clinical significance of Coronavirus disease 2019 (COVID-19) as an associate of myocardial injury is controversial. HYPOTHESIS: Type 2 MI/Myocardial Injury are associated with worse outcomes if complicated by COVID-19. METHODS: This longitudinal cohort study involved consecutive patients admitted to a large urban hospital. Myocardial injury was determined using laboratory records as ≥1 hs-TnI result >99th percentile (male: >34 ng/L; female: >16 ng/L). Endotypes were defined according to the Fourth Universal Definition of Myocardial Infarction (MI) and COVID-19 determined using PCR. Outcomes of patients with myocardial injury with and without COVID-19 were assessed. RESULTS: Of 346 hospitalized patients with elevated hs-TnI, 35 (10.1%) had laboratory-confirmed COVID-19 (median age [IQR]; 65 [59-74]; 64.8% male vs. COVID-19 negative: 74 [63-83] years; 43.7% male). Cardiac endotypes by COVID-19 status (yes vs. no) were: Type 1 MI (0 [0%] vs. 115 [100%]; p < .0005), Type 2 MI (13 [16.5%] vs. 66 [83.5%]; p = .045), and non-ischemic myocardial injury (cardiac: 4 [5.8%] vs. 65 [94.2%]; p = .191, non-cardiac:19 [22.9%] vs. 64 [77.%]; p < .0005). COVID-19 patients had less comorbidity (median [IQR] Charlson Comorbidity Index: 3.0 [3.0] vs. 5.0 [4.0]; p = .001), similar hs-TnI concentrations (median [IQR] initial: 46 [113] vs. 62 [138]; p = .199, peak: 122 [474] vs. 79 [220] ng/L; p = .564), longer admission (days) (median [IQR]: 14[19] vs. 6[12]; p = .001) and higher in-hospital mortality (63.9% vs. 11.3%; OR = 13.2; 95%CI: 5.90, 29.7). CONCLUSIONS: Cardiac sequelae of COVID-19 typically manifest as Non-cardiac myocardial injury/Type 2MI in younger patients with less co-morbidity. Paradoxically, the admission duration and in-hospital mortality are increased.
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