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COVID-19 and myocardial injury: Targeting elevated biomarkers for potential novel therapies
Pengyang Li1, Qun Chen1, Ion S Jovin1
1Virginia Commonwealth University, Richmond VA; McGuire VA Medical Center, Richmond VA.
Insights
COVID-19 is a significant cause of elevated troponin in hospitalized patients. Age, troponin, and C-reactive protein levels predict poor outcomes, suggesting targeted therapies for myocardial injury.
Area of Science:
- Cardiology
- Infectious Diseases
- Critical Care Medicine
Background:
- The COVID-19 pandemic has seen an increase in myocardial injury among hospitalized patients.
- Elevated oxidant stress and inflammatory biomarkers are implicated in COVID-19-related myocardial injury.
- Novel therapies targeting these biomarkers may improve outcomes.
Purpose of the Study:
- To investigate the prevalence of COVID-19 as a primary diagnosis in patients with myocardial injury.
- To identify predictors of mortality in COVID-19 patients with elevated troponin.
- To explore the role of cardiac biomarkers in COVID-19-associated myocardial injury.
Main Methods:
- Analysis of troponin assays from emergency room patients between January 1 and December 31, 2021.
- Categorization of ICD-10 diagnoses and recording of biomarker elevations for admitted patients with elevated troponin.
- Determination of independent predictors of death at a 6-month follow-up for COVID-19 patients.
Main Results:
- COVID-19 was the primary diagnosis in 10% of admitted patients with myocardial injury.
- Independent predictors of death in COVID-19 patients included age, peak troponin level, and peak C-reactive protein (CRP) level.
- 42% of COVID-19 patients with myocardial injury died within 6 months.
Conclusions:
- Newly diagnosed COVID-19 is a common cause of elevated troponin in hospitalized patients without Type 1 Myocardial Infarction.
- Age, peak troponin, and peak CRP levels are independent predictors of adverse outcomes.
- Targeting cardiac biomarkers with antioxidant or anti-inflammatory therapies may be beneficial.
Background:
The prevalence of COVID-19 as the primary diagnosis among hospitalized patients with myocardial injury has increased during the pandemic and targeting elevated oxidant stress and inflammatory biomarkers may offer a potential role for novel therapies to improve outcomes.
Methods:
At a single VA Medical Center from January 1 through December 31, 2021, troponin assays from patients being evaluated in the Emergency Room for consideration of admission were analyzed and peak levels from each patient were considered abnormal if exceeding the Upper Reference Limit (URL). Among admitted patients with an elevated troponin level, ICD-10 diagnoses were categorized, biomarker elevations were recorded, and independent predictors of death in patients with COVID-19 were determined at a median of 6-months following admission.
Results:
Of 998 patients, 399 (40 %) had a negative troponin and were not included in the analysis. Additional patients with an elevated troponin were also excluded, either because they were not admitted (n = 68) or had a final diagnosis of Type 1 MI (n = 117). Of the remaining 414 patients with an elevated peak troponin, COVID-19 was the primary diagnosis in 43 patients (10 %) and was the 4th most common diagnosis of patients admitted with myocardial injury behind congestive heart failure, sepsis, and COPD or pneumonia. At a median of 6-months following admission, 18 (42 %) of the COVID-19 patients had died and independent predictors of death (Odd Ratio: Confidence Intervals) were age (1.18: 1.06‒1.37), Troponin level (Log 10 transformed) (16.54: 2.30‒266.65) and C-Reactive Protein (CRP) (1.30: 1.10‒1.65).
Conclusions:
Newly diagnosed COVID-19 during the pandemic was a common cause of elevated troponin in hospitalized patients without a Type 1 MI. Age, peak troponin level and peak CRP level were independent predictors of poor outcomes and suggest a need to target these cardiac biomarkers, potentially with novel antioxidant or anti-inflammatory therapies.
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