Wenjia Bai, Betty Raman, Steffen E Peterson, Stefan Neubauer, Zahra Raisi-Estabragh, Nay Aung, Nicholas C Harvey, Naomi Allen, Rory Collins,
Abstract
Case studies conducted after recovery from acute infection with SARS-CoV-2 have frequently identified abnormalities on CMR imaging, suggesting the possibility that SARS-CoV-2 infection commonly leads to cardiac pathology. However, these observations have not been able to distinguish between associations that reflect pre-existing cardiac abnormalities (that might confer a greater likelihood of more severe infection) from those that arise as consequences of infection. To address this question, UK Biobank volunteers (n=1285; 54.5% women; mean age at baseline, 59.8 years old; 96.3% white) who attended an imaging assessment including cardiac magnetic resonance (CMR) before the start of the COVID-19 pandemic were invited to attend a second imaging assessment in 2021. Cases with evidence of previous SARS-CoV-2 infection were identified through linkage to PCR-testing or other medical records, or a positive antibody lateral flow test; n=640 in data available on 22 Sep 2021) and were matched to controls with no evidence of previous infection (n=645). The majority of these infections were milder and did not involve hospitalisation. Measures of cardiac and aortic structure and function were derived from the CMR images obtained on the cases before and after SARS-CoV-2 infection from images for the controls obtained over the same time interval using a previously validated, automated algorithm. Cases and controls had similar cardiac and aortic imaging phenotypes at their first imaging assessment. Changes between CMR imaging measures in cases before and after infection were not significantly different from those in the matched control group. Additional adjustment for comorbidities made no material difference to the results. While these results are preliminary and limited to imaging metrics derived from automated analyses, they do not suggest clinically significant persistent cardiac pathology in the UK Biobank population after generally milder (non-hospitalised) SARS-CoV-2 infection.
Competing Interest Statement
PMM acknowledges consultancy fees from Novartis, Bristol Myers Squibb, Celgene and Biogen He has received honoraria or speakers honoraria from Novartis, Biogen and Roche and has received research or educational funds from Biogen, Novartis, GlaxoSmithKline and Nodthera.
Funding Statement
PMM acknowledges generous personal and research support from the Edmond J Safra Foundation and Lily Safra, a National Institute for Health Research (NIHR) Senior Investigator Award, the UK Dementia Research Institute and the NIHR Biomedical Research Centre at Imperial College London. WB acknowledges support from EPSRC SmartHeart Programme (EP/P001009/1). SEP acknowledges support from the National Institute for Health Research Barts Biomedical Research Centre. NA and ZRE acknowledge support from the NIHR through Academic Clinical Lecturer funding. ZRE was supported by British Heart Foundation Clinical Research Training Fellowship No. FS/17/81/33318. BR and SN acknowledge support from the Oxford NIHR Biomedical Research Centre and the British Heart Foundation. BR is also supported by the British Heart Foundation Oxford Centre of Research Excellence Transition Clinical Intermediate Fellowship (RE/18/3/34214). NCH acknowledges support from the UK Medical Research Council (MRC MC_UU_12011/1), and NIHR Southampton Biomedical Research Centre, University of Southampton, and University Hospital Southampton. RC Is a British Heart Foundation Chairholder.
https://www.medrxiv.org/content/10.1101/2021.11.04.21265918v1
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