Quantitative Perfusion
Rebecka Steffen Johansson, MD
PhD student
Karolinska Institute, Sweden
Rebecka Steffen Johansson, MD
PhD student
Karolinska Institute, Sweden
Daniel E. Loewenstein, MD
PhD student
Karolinska Institute
Stockholm, Stockholms Lan, Sweden
Judith Bruchfeld, MD, PhD
MD, PhD
Karolinska Institute
Stockholm, Sweden
Michael Runold, MD, PhD
MD, PhD
Karolinska Institute, Sweden
Hui Xue, PhD
Director, Imaging AI Program
National Institutes of Health
Bethesda, Maryland, United States
Peter Kellman, PhD
Senior Scientist
National Institutes of Health, Maryland, United States
Kenneth Caidahl, MD, PhD
Professor
Karolinska Institutet
Stockholm, Stockholms Lan, Sweden
Henrik Engblom, MD, PhD
Professor
Lund University
Lund, Skane Lan, Sweden
Jannike Nickander, MD, PhD
MD, PhD
Karolinska Institute
Stockholm, Stockholms Lan, Sweden
Coronavirus disease 2019 (Covid-19) can affect the heart, and long-term symptoms of dyspnea and chest-pain following severe Covid-19 have been reported. However, the pathophysiological mechanisms of cardiac involvement are not yet fully understood. Coronary microvascular dysfunction (CMD) has emerged as a pathophysiological mechanism in myocardial ischemia even in the absence of obstructive coronary artery disease. Automated pixel-wise adenosine stress cardiac magnetic resonance (CMR) perfusion mapping can quantify myocardial perfusion in rest and stress and identify CMD as a globally reduced stress perfusion or reduced myocardial perfusion reserve (MPR). Covid-19 may induce CMD, but it is unknown if CMD is present long-term after severe Covid-19. Therefore, this study aimed to elucidate whether CMD is present during long-term follow-up in patients hospitalized due to severe Covid-19, using stress CMR perfusion mapping.
Methods:
Patients were identified from the prospective, single-center cohort study “Follow-up of patients with severe Covid-19”, aiming to characterize long-term consequences following hospitalization due to severe Covid-19. Patients with and without cardiac involvement were included. CMR (1.5T Aera, Siemens Healthineers) included cine imaging, native T1 and T2 mapping, and post-contrast T1 mapping following intravenous contrast (total dose 0.2 mmol/kg of gadoteric acid, Gd-DOTA) rendering extracellular volume (ECV) maps. Furthermore, quantitative perfusion maps were acquired during adenosine stress (140 micrograms/kg/min) and in rest, after intravenous contrast (0.05 mmol/kg). By averaging segmental values per patient, global native T1, T2, ECV and rest and stress perfusion values were acquired. MPR was calculated as the ratio of stress perfusion to rest perfusion. CMD was defined as stress perfusion < 1.62 ml/min/g or MPR< 2.04. The Covid-19 patients were compared to previously examined healthy volunteers. Values were presented as mean ± standard deviation and compared with the independent t-test in normally distributed data and the Mann-Whitney U test in non-normally distributed data.
Results:
In total, 37 patients (56±12 years old, 76% male) and 15 healthy volunteers (59±16 years old, 40% male) were included. CMR was performed 292 (158) days following discharge. Compared to healthy volunteers, the Covid-19 patients had greater weight and greater left ventricular mass indexed to body surface area (Table 1). The Covid-19 patients had reduced stress and rest perfusion compared to healthy volunteers (Figure 1), but MPR was unaffected and no other CMR measures differed between the groups (Table 1). CMD was present in 4 (11%) of the Covid-19 patients and in none of the healthy volunteers (p=0.311).
Conclusion:
Patients hospitalized due to severe Covid-19 seem to have an increased prevalence of CMD at long-term follow-up compared to age-matched healthy volunteers. However, if CMD was present in these patients before hospitalization is not known.