Miscellaneous

1356079 - Cardiac Magnetic Resonance imaging and 18F-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography evaluation of the cardiopulmonary axis during acute COVID-19

Wednesday, January 25, 2023

Location: E-POSTER

Presenting Author(s)

AE

Ahmed El-Medany, MSc

Cardiology Registrar
North Bristol NHS Trust, United Kingdom

Primary Author(s)

AE

Ahmed El-Medany, MSc

Cardiology Registrar
North Bristol NHS Trust, United Kingdom

Co-Author(s)

KH

Kevin Horn, PhD

Nuclear Medicine PET/CT Acting Instructor and Consultant
Medical University of South Carolina, United States
FM

Florence Mouy, BSc

Internal Medical Trainee
North bristol NHS Trust, England, United Kingdom
RS

Rachel Scott, BSc

Internal Medical Trainee
North Bristol NHS Trust, United Kingdom
SV

Sudhir Vinayak, MD

Radiology Consultant
Aga Khan University Hospital, Kenya
KM

Khalid Makhdomi, MD

Nuclear Medicine Consultant
Aga Khan University Hospital, Kenya
KO

Kevin Onyinkwa, MD

Radiology Consultant
Aga Khan University Hospital, Kenya
MO

Mariah Obino, MD

Fellow
The Ottawa Hospital
Ottawa, Ontario, Canada
EN

Edward Nganga, MD

Radiology Consultant
Aga Khan University Hospital, Kenya
MC

Michael Chung, MD

Professor of Infectious Diseases
Emory University, United States
AS

Anoop Shah

Associate professor of clinical epidemiology
London School of Hygiene and Tropical Medicine, United Kingdom
SG

Samuel Gitau, MD

Radiology Consultant
Aga Khan University Hospital, Kenya
SB

Stephen Bowen, PhD

Associate professor of nuclear medicine
University of Washington, United States
SA

Shirjel Alam, MD, PhD

Cardiology Consultant
North Bristol NHS Trust, United Kingdom

Background:

COVID-19 causes pneumonitis, but is also associated with cardiac injury. The mechanism of cardiac injury could be due to (i) mechanical right ventricular injury due to lung pathology, (ii) left ventricular (LV) injury related to downstream effects of lung inflammation, (iii) cardiac inflammation related to systemic inflammation[1].

Using 18F-fluorodeoxyglucose positron-emission-tomography/computed tomography (18F-FDG-PET/CT) and cardiac magnetic resonance (CMR) imaging, we investigated the associations between: (i) right ventricular (RV) function and lung consolidation/inflammation, (ii) LV oedema/fibrosis and maximum lung inflammation, (iii) Systemic inflammation assessed by reticulo-endothelial system activation (spleen) and cardiac/lung injury in acute SARS-CoV-2 infection.

Methods: Consecutive hospitalised patients with acute COVID-19 were prospectively recruited to undergo 18F-FDG-PET/CT and CMR imaging[1].

RV function by CMR was assessed using tricuspid annular plane systolic excursion (TAPSE), and RV ejection fraction (RVEF)[2]. Left ventricular injury was assess by T1 (mild oedema and fibrosis) and T2 (oedema) values for segments of the anatomical 17-segment model[3].

18F-FDG-PET/CT was used to assess inflammatory cell activity. Standard uptake value (SUV) was measured in the spleen and lungs. For lung analysis, CT and 18F-FDG-PET/CT images were analysed separately for lung consolidation and inflammation respectively. The volumes of consolidated lung and inflamed lung were presented as percentage of total lung volume[1].

Results:

Data were presented by tertile of RVEF for 25 participants (Table 1). Median lung inflammation was 25% [IQR 6.9-38.7%] and 14.6% [1.6-24.5%], for the lowest and highest RVEF tertiles, respectively; and median lung consolidation was 14.6% [8.7-18.1%] and 7.9% [3.3-15.8%], for the lowest and highest RVEF tertiles, respectively (Table 1).

There was no statistically significant correlation between RVEF and lung inflammation (r=0.11, p=0.10) or lung consolidation (r=0.03, p=0.36); and no statistically significant correlation between TAPSE and lung inflammation (r=0.05, p=0.26) or lung consolidation (r=0.01, p=0.7) (Figure 1).

There was no significant correlation between maximum splenic SUV and maximum cardiac T1 and T2 (r=0.001, p=0.77; r=0.01, p=0.72, respectively); and no significant correlation between maximum lung SUV and maximum cardiac T1 and T2 (r=0.01, p=0.73; r=0.02, p=0.57, respectively).

There was significant correlation between maximum splenic SUV and maximum lung SUV (r=0.27, p< 0.01) (Figure 2).

Conclusion:

In acute COVID 19, lung injury is not associated with impairment of right ventricular function. Reticulo-endothelial activation strongly correlates with lung activity, suggesting lung injury is part of a systemic inflammatory process[4]. However cardiac injury did not correlate with lung injury or reticulo-endothelial activation, suggesting this process is multi-factorial.