Jitka Starekova¹, David A Bluemke^1,2, William S Bradham^1,3, Thomas M Grist^1,2,4, Mark L Schiebler¹, and Scott B Reeder^1,2,3,4,5
1Radiology, University of Wisconsin-Madison, Madison, WI, United States, ²Medical Physics, University of Wisconsin-Madison, Madison, WI, United States, ³Medicine, University of Wisconsin-Madison, Madison, WI, United States, ⁴Biomedical Engineering, University of Wisconsin-Madison, Madison, WI, United States, ⁵Emergency Medicine, University of Wisconsin-Madison, Madison, WI, United States

Mass immunization campaigns continue in attempts to contain the ongoing COVID-19 pandemic. COVID-19 vaccines authorized for use in the United States include BNT162b2 (Pfizer-BioNTech), mRNA-1273 (Moderna), and JNJ-78436735 (Johnson & Johnson). 

To date multiple cases of vaccine-associated inflammation of the heart have been reported. In this work, we describe cardiac MRI findings in 9 patients (adults and children) with clinical and imaging-based diagnosis of myocarditis and/or pericarditis diagnosed shortly after COVID-19 mRNA vaccination at our institution. 

 

Vlad G Zaha¹, Junjie Ma¹, Jae Mo Park¹, Munes Fares¹, Nicholas Hendren¹, Spencer Carter¹, Anjali Rao¹, Ravi Vamsee¹, Madhusudan Ganigara¹, Mohamed Nagiub¹, Mohammad Tarique Hussain¹, Ricardo La Hoz¹, James Cutrell¹, Pradeep Mammen¹, Mark Drazner¹, James de Lemos¹, Craig Malloy¹, and Justin Grodin^1
1University of Texas Southwestern Medical Center, Dallas, TX, United States

Noninvasive detection of myocardial inflammation can be challenging. Up to 73% of patients recovered from COVID-19 had increased native T1 on cardiac MRI¹  representing inflammation or edema. Therefore, we tested whether hyperpolarized (HP) [1-13C]pyruvate detectis post-COVID-19 inflammation in the myocardium. HP [1-13C]lactate has been suggested as a surrogate imaging marker of inflammation in the heart^2,3, attributed to increased glycolytic activity in infiltrating white cells plus a possible increase in activity of lactate dehydrogenase. We demonstrate the feasibility of imaging with HP [1-13C]pyruvate as noninvasive method to detect metabolic changes that may identify cardiac inflammation in the convalescent stage after COVID-19.

Jed Wingrove^1,2, Janine Makaronidis^1,2, Ferran Prados^2,3,4, Baris Kanber^2,3,4, Marios C Yiannakas³, Gloria Castellazzi^3,5,6, Claudia AM Gandini Wheeler-Kingshott^3,7,8, and Rachel Batterham^1,2
1Centre for Obesity Research, University College London, London, United Kingdom, ²Biomedical Research Centre at UCLH and UCL, National Institute for Health Research, London, United Kingdom, ³NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London, United Kingdom, ⁴Centre for Medical Image Computing, Department of Medical Physics and Biomedical Engineering, University College London, London, United Kingdom, ⁵Department of Electrical, Computer and Biomedical Engineering, University of Pavia, Pavia, Italy, ⁶IRCCS C., Mondino Foundation, Pavia, Italy, ⁷Brain Connectivity Centre, IRCCS Mondino Foundation, Pavia, Italy, ⁸Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy

Anosmia or loss of smell is a common COVID-19 symptom. We studied a group of individuals with persistent anosmia and those who had recovered olfactory function following COVID-19 infection as well as healthy volunteers. Using resting state EPI and seed based analysis we found significant differences in connectivity between olfactory nodes and prefrontal regions known to be involved in smell processing. Furthermore, our analysis also identified connectivity differences between olfactory regions and brain areas involved in appetite control, highlighting areas of the brain that may be affected by COVID-19 related anosmia. 

Linda Chang^1,2,3, Meghann C. Ryan⁴, Huajun Liang¹, Xin Zhang¹, Eric Cunningham¹, Eleanor Wilson⁵, Andrea Levine⁶, Shyamasundaran Kottilil⁵, and Thomas M. Ernst^1,2
1Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore, MD, United States, ²Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States, ³Neurology, University of Maryland School of Medicine, Baltimore, MD, United States, ⁴Program in Neuroscience, University of Maryland School of Medicine, Baltimore, MD, United States, ⁵Medicine, Division of Infectious Disease, University of Maryland School of Medicine, Baltimore, MD, United States, ⁶Medicine, Critical Care Medicine, University of Maryland School of Medicine, Baltimore, MD, United States

Post-acute sequelae of COVID-19 is highly prevalent after the acute infection. Neuropsychiatric symptoms are particularly common; however, the pathophysiology of how the brain is affected remains unclear. This study aimed to evaluate whether convalescent COVID-19 participants have abnormal brain activation that is related to quantitative neurobehavioral measures. 21 COVID-19 participants and 20 healthy controls were evaluated with the NIH-Toolbox® and blood-oxygenation level dependent-functional MRI (BOLD-fMRI), using the N-back tasks. Despite similar performance on the NIH-Toolbox-cognitive battery, COVID-19 participants had greater brain activation than controls in the precuneus and dorsal anterior cingulate cortex, which also predicted poorer dexterity, endurance, and locomotion.

Lily McCarthy¹, Oleksandr Khegai², Jonathan Goldstein³, Puneet Belani⁴, Puneet Pawha⁴, Shingo Kihira⁴, Brian Mathew³, Kapil Gururangan³, Qing Hao³, Anuradha Singh³, Allison Navis³, Bradley Delman⁴, Nathalie Jette³, and Priti Balchandani^2
1Icahn School of Medicine at Mount Sinai, New York, NY, United States, ²BioMedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States, ³Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, United States, ⁴Radiology, Icahn School of Medicine at Mount Sinai, New York, NY, United States

COVID-19 is known to result in neurological manifestations which sometimes correlate with neuroimaging abnormalities. Understanding these abnormalities requires further systematic study. We undertook a retrospective analysis of 60 MRIs from hospitalized COVID-19 patients (20 intubated, 20 non-brain cancer, and 20 non-intubated/non-cancer) with neurological manifestations. Neuroimaging showed non-infarct parenchymal T2/FLAIR signal hyperintensities (26.7%), acute/subacute infarcts (25%), microhemorrhages (21.7%), chronic infarcts (18.3%), chronic macrohemorrhages (10%), and acute macrohemorrhages (6.7%). Common neurological symptoms were confusion/encephalopathy/delirium (70%), generalized weakness (38.3%), and impaired responsiveness/coma (38.3%). Thus, COVID-19 may be associated with neuroimaging abnormalities. Differences in abnormalities were seen based on permutations of cancer and intubation.

Jimmy Zhou Yu^1,2, Tobias Granberg^2,3, Roya Shams², Sven Petersson², Adrian Szum², Magnus Sköld⁴, Sven Nyrén^1,2, and Johan Lundberg^2,3
1Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm Solna, Sweden, ²Radiology department, Karolinska University Hospital, Stockholm, Sweden, ³Department of Neuroscience, Karolinska Institutet, Stockholm Solna, Sweden, ⁴Department of Medicine, Karolinska Institutet, Stockholm Solna, Sweden

Mechanisms underlying dyspnea in non-hospitalized patients with persistent post-COVID is unknown. Lung perfusion abnormalities have been reported in acute COVID-19, and may also be important in post-COVID. Dynamic contrast enhanced (DCE)-MRI [MS1] was applied to study lung perfusion in 28 non-hospitalized patients with persistent dyspnea 4-13 months post-COVID. Time-to-peak (TTP)[MS2]  maps were numerically summarized as normalized as 2 numeric values: mean TTP and TTP ratio. Comparison was made against 22 age and sex matched controls. Perfusion abnormalities were found, with a striking sex difference with men showing more pronounced perfusion abnormalities. Perfusion abnormalities correlated with self-rated dyspnea in men.

Laura C. Saunders¹, Guilhem J. Collier¹, Ho-Fung Chan¹, Paul J. C. Hughes¹, Laurie J. Smith¹, Helen Marshall¹, James A. Eaden¹, Jody Bray¹, David J. Capener¹, Leanne Armstrong¹, Jennifer Rodgers¹, Martin Brook¹, Alberto M. Biancardi¹, James Watson², Zoë Gabriel², Madhwesha R. Rao¹, Graham Norquay¹, Oliver Rodgers¹, Fred Wilson³, Tony Cahn³, Andy Swift¹, Smitha Rajaram², Fergus Gleeson^4,5, James T. Grist⁵, Gary H. Mills^2,6, James Meiring², Lisa Watson², Paul J. Collini⁶, Rod Lawson², Roger Thompson¹, and Jim M. Wild^1
1Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom, ²Sheffield Teaching Hospitals, Sheffield, United Kingdom, ³GlaxoSmithKline, Stevenage, United Kingdom, ⁴Oxford NHS Foundation Trust, Oxford, United Kingdom, ⁵University of Oxford, Oxford, United Kingdom, ⁶University of Sheffield, Sheffield, United Kingdom

This work uses a multinuclear ¹H and ¹²⁹Xe protocol to assess pathophysiological changes in patients with COVID-19 pneumonia, without signs of interstitial lung disease, at 6 and 12 weeks after hospital admission. ¹H and ¹²⁹Xe protocol: ultra-short echo time, dynamic contrast enhanced lung perfusion, ¹²⁹Xe lung ventilation, ¹²⁹Xe diffusion weighted MRI, ¹²⁹Xe 3D spectroscopic imaging. Though significant improvements in lung ventilation homogeneity (decreased low ventilation percentage and ventilation coefficient of variation), gas transfer (increased RBC:TP, decreased TP T₂^*) and perfusion (increased pulmonary blood volume and flow) were seen between 6 and 12 weeks, low RBC:TP ratio persisted for some patients.