Key result
Six months after acute COVID-19, patients with prior myocardial injury exhibited significantly higher average E/e' ratio (10.1 vs 7.3, P=0.01) and systolic pulmonary artery pressure during exercise.
Why the study?
There was limited information on late cardiac sequelae and myocardial functional alterations in patients who recovered from acute COVID-19 hospitalization.
Does myocardial injury during acute COVID-19 infection lead to long-term echocardiographic functional alterations at 6 months compared to patients without acute injury?
Observational (n=48)
Does myocardial injury during acute COVID-19 infection lead to long-term echocardiographic functional alterations at 6 months compared to patients without acute injury?
Absolute Event Rate: 10.1% vs 7.3%
p-value: p=0.01
Patients with myocardial injury during acute COVID-19 hospitalization demonstrate significant exercise-induced diastolic abnormalities at 6 months compared to those without acute cardiac involvement.
Exercise unmasks diastolic changes 6 months after COVID myocardial injury; hypothesis-generating and requires prospective validation before guiding follow-up.
AIMS: Myocardial injury is frequently observed in patients hospitalized with coronavirus disease 2019 (COVID-19) pneumonia. Different cardiac abnormalities have been reported during the acute COVID-19 phase, ranging from infra-clinic elevations of myocardial necrosis biomarkers to acute cardiac dysfunction and myocarditis. There is limited information on late cardiac sequelae in patients who have recovered from acute COVID-19 illness. We aimed to document the presence and quantify the extent of myocardial functional alterations in patients hospitalized 6 months earlier for COVID-19 infection. METHODS AND RESULTS: We conducted a prospective echocardiographic evaluation of 48 patients (mean age 58 ± 13 years, 69% male) hospitalized 6 ± 1 month earlier for a laboratory-confirmed and symptomatic COVID-19. Thirty-two (66.6%) had pre-existing cardiovascular risks factors (systemic hypertension, diabetes, or dyslipidaemia), and three patients (6.2%) had a known prior myocardial infarction. Sixteen patients (33.3%) experienced myocardial injury during the index COVID-19 hospitalization as identified by a rise in cardiac troponin levels. Six months later, 60.4% of patients still reported clinical symptoms including exercise dyspnoea for 56%. Echocardiographic measurements under resting conditions were not different between patients with versus without myocardial injury during the acute COVID-19 phase. In contrast, low-level exercise (25W for 3 min) induced a significant increase in the average E/e' ratio (10.1 ± 4.3 vs. 7.3 ± 11.5, P = 0.01) and the systolic pulmonary artery pressure (33.4 ± 7.8 vs. 25.6 ± 5.3 mmHg, P = 0.02) in patients with myocardial injury during the acute COVID-19 phase. Sensitivity analyses showed that these alterations of left ventricular diastolic markers were observed regardless of whether of cardiovascular risk factors or established cardiac diseases indicating SARS-CoV-2 infection as a primary cause. CONCLUSIONS: Six months after the acute COVID-19 phase, significant cardiac diastolic abnormalities are observed in patients who experienced myocardial injury but not in patients without cardiac involvement.
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Fayol et al. (2021) conducted an observational in COVID-19 (n=48). Myocardial injury during acute COVID-19 vs. No myocardial injury during acute COVID-19 was evaluated on Average E/e' ratio during low-level exercise (25W for 3 min) (p=0.01). Six months after acute COVID-19, patients with prior myocardial injury exhibited significantly higher average E/e' ratio (10.1 vs 7.3, P=0.01) and systolic pulmonary artery pressure during exercise.
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