Annals of clinical and laboratory science · 2021
COVID-19 Cardiac Injury: An Important Cause of COVID-19 Related Morbidityand Mortality.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ricks Elizabeth, Wahed Amer, Dasgupta Amitava, Buja L Maximilian
Аннотация
OBJECTIVE: Although coronavirus disease 2019 (COVID-19) typically presents as a respiratory illness, co-existent cardiovascular symptomatology associated with an elevated serum troponin level has been identified as a risk factor for adverse outcomes. Our study addressed the need to correlate serum cardiovascular biomarkers with tissue pathology based on autopsy.
MATERIALS AND METHODS: In 13 patients, we reviewed the clinical history and measurements of serum troponin and other biomarkers and correlated them with autopsy findings.
RESULTS: At autopsy, the 13 COVID-19 patients exhibited evidence of diffuse alveolar damage (DAD) and cardiomegaly (heart weights ranged from 380 to 1170 grams). Of the 13 patients, three had elevated troponin I and evidence of severe coronary artery disease (CAD) (cases 4, 5, and 11), while six had elevated troponin I without evidence of severe CAD (cases 1, 3, 6, 7, 8, and 9), and four had no clinical or pathological evidence of CAD. Of note, cases 7 and 9 had significantly elevated troponin I levels (8.84 ng/mL and 4.94 ng/mL, respectively). Several cases showed focal degenerative change or damage of cardiomyocytes. However, none of the cases had evidence of lymphocytic myocarditis.
CONCLUSION: Although we observed elevated biomarkers of heart failure in some cases, it was not a consistent finding and did not correlate with evidence of myocarditis. The elevated biomarkers may reflect non-ischemic heart damage as a consequence of COVID-19 infection.
MATERIALS AND METHODS: In 13 patients, we reviewed the clinical history and measurements of serum troponin and other biomarkers and correlated them with autopsy findings.
RESULTS: At autopsy, the 13 COVID-19 patients exhibited evidence of diffuse alveolar damage (DAD) and cardiomegaly (heart weights ranged from 380 to 1170 grams). Of the 13 patients, three had elevated troponin I and evidence of severe coronary artery disease (CAD) (cases 4, 5, and 11), while six had elevated troponin I without evidence of severe CAD (cases 1, 3, 6, 7, 8, and 9), and four had no clinical or pathological evidence of CAD. Of note, cases 7 and 9 had significantly elevated troponin I levels (8.84 ng/mL and 4.94 ng/mL, respectively). Several cases showed focal degenerative change or damage of cardiomyocytes. However, none of the cases had evidence of lymphocytic myocarditis.
CONCLUSION: Although we observed elevated biomarkers of heart failure in some cases, it was not a consistent finding and did not correlate with evidence of myocarditis. The elevated biomarkers may reflect non-ischemic heart damage as a consequence of COVID-19 infection.