Post by Nadica (She/Her) on Jul 8, 2024 4:08:02 GMT
Myocardial fibrosis occurs in non-hospitalised patients with chronic symptoms after COVID-19 - Published Jan 26, 2022
1. Introduction
Persistent symptoms have been observed in patients recovering from SARS-CoV-2 infection [1], [2], [3], post-acute sequelae of COVID-19 (PASC) [2]. Acute COVID-19 infection is associated with multi-organ sequalae, including pulmonary and cardiac, at short to medium term follow-up especially in those with severe illness [4], [5], [6]. We conducted an observational study to evaluate the prevalence and extent of residual myocardial injury in a group of patients recovering from mild COVID-19, managed in the community, with persistent symptoms post infection, to help determine if PASC may relate to cardiac and pulmonary fibrosis in mild disease.
Twenty patients with positive real time polymerase chain reaction (RT-PCR) for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), who were treated in the community for initial infection, with persistent symptoms at >4 months after COVID-19 infection were evaluated with comprehensive cardiac and pulmonary investigations. Informed consent was obtained for all participants and the study conducted in accordance with the Declaration of Helsinki.
CMR imaging was performed on a 3.0-Tesla scanner (Achieva, Philips Medical Systems, Best, the Netherlands) using institutional standardised imaging protocols. Myocardial T1 and T2 mapping were acquired over a single midventricular short-axis slice using a validated variant of a modified Look-Locker imaging sequence. T2-maps were acquired with a respiratory-navigated black-blood, turbo-spin-echo sequence on a midventricular short-axis slice, sampled at different echo-times to reconstruct a T2-map. Late gadolinium enhancement (LGE) images were acquired with administration of 0.1 mmol/kg of body weight of gadobutrol (Gadovist; Bayer) using a phase-sensitive inversion recovery sequence (PSIR).
CMR images were evaluated using cvi42, v5.2 (Circle Cardiovascular Imaging, Calgary, Canada). The presence or absence of LGE was determined visually and quantified as proportion of total myocardium, with an LGE region being captured if SI > 2 SD’s above the mean SI of the remote reference myocardium.
Complete lung function testing and arterial blood gas analysis was performed at 12–16 weeks’ follow-up. All participants were evaluated with non-contrast computed tomography (CT) of the chest and pathology for high-sensitivity troponin-I (hsTrI), C-reactive protein (CRP) and inflammatory cytokines at 8 months after COVID-19 infection.
In our cohort of recovering patients, managed in the community for initial COVID-19 infection and complaining of persistent symptoms, there is a larger than expected burden of myocardial injury demonstrated by presence of scar on LGE imaging by 12 months.
1. Introduction
Persistent symptoms have been observed in patients recovering from SARS-CoV-2 infection [1], [2], [3], post-acute sequelae of COVID-19 (PASC) [2]. Acute COVID-19 infection is associated with multi-organ sequalae, including pulmonary and cardiac, at short to medium term follow-up especially in those with severe illness [4], [5], [6]. We conducted an observational study to evaluate the prevalence and extent of residual myocardial injury in a group of patients recovering from mild COVID-19, managed in the community, with persistent symptoms post infection, to help determine if PASC may relate to cardiac and pulmonary fibrosis in mild disease.
Twenty patients with positive real time polymerase chain reaction (RT-PCR) for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), who were treated in the community for initial infection, with persistent symptoms at >4 months after COVID-19 infection were evaluated with comprehensive cardiac and pulmonary investigations. Informed consent was obtained for all participants and the study conducted in accordance with the Declaration of Helsinki.
CMR imaging was performed on a 3.0-Tesla scanner (Achieva, Philips Medical Systems, Best, the Netherlands) using institutional standardised imaging protocols. Myocardial T1 and T2 mapping were acquired over a single midventricular short-axis slice using a validated variant of a modified Look-Locker imaging sequence. T2-maps were acquired with a respiratory-navigated black-blood, turbo-spin-echo sequence on a midventricular short-axis slice, sampled at different echo-times to reconstruct a T2-map. Late gadolinium enhancement (LGE) images were acquired with administration of 0.1 mmol/kg of body weight of gadobutrol (Gadovist; Bayer) using a phase-sensitive inversion recovery sequence (PSIR).
CMR images were evaluated using cvi42, v5.2 (Circle Cardiovascular Imaging, Calgary, Canada). The presence or absence of LGE was determined visually and quantified as proportion of total myocardium, with an LGE region being captured if SI > 2 SD’s above the mean SI of the remote reference myocardium.
Complete lung function testing and arterial blood gas analysis was performed at 12–16 weeks’ follow-up. All participants were evaluated with non-contrast computed tomography (CT) of the chest and pathology for high-sensitivity troponin-I (hsTrI), C-reactive protein (CRP) and inflammatory cytokines at 8 months after COVID-19 infection.
In our cohort of recovering patients, managed in the community for initial COVID-19 infection and complaining of persistent symptoms, there is a larger than expected burden of myocardial injury demonstrated by presence of scar on LGE imaging by 12 months.