1356410 - Patients with post–acute sequelae of Covid-19 presenting as postural orthostatic tachycardia syndrome have lower native T1 stress reactivity during long-term follow-up

Background: Post-acute sequelae of Covid-19 (PASC) is a novel clinical syndrome with diverse symptoms. It has previously been reported that PASC patients can develop postural orthostatic tachycardia syndrome (POTS) and that Covid-19 induce microvascular endothelial dysfunction in acutely ill, hospitalized patients, that persists post discharge. Whether myocardial inflammation and reduced stress reactivity in the microcirculation contributes to POTS pathophysiology in PASC remains unclear. Myocardial inflammation can be detected by cardiovascular magnetic resonance (CMR) imaging using native T1 mapping. Furthermore, native T1 has previously been shown to detect the change in myocardial perfusion during adenosine stress in normal physiology. Therefore, this study aimed to elucidate differences in native T1 and stress reactivity (deltaT1) between patients with PASC, both with and without POTS and healthy subjects.

Methods: Patients with PASC due to prior mild Covid-19 infection (n=26, mean ± SD age 41 ± 11 years, 92 % females) and healthy subjects (n=21, age 37 ± 15 years, 100 % females, p=0.08) underwent 1.5T or 3T CMR (MAGNETOM Aera, or Skyra, Siemens Healthcare, Erlangen, Germany) at least 6 months after the primary Covid-19 infection. 15 of 26 patients with PASC (39 ± 11 years, 87 % females) were diagnosed with POTS. Patients with PASC had no previous cardiac disease or notable comorbidities and were followed in outpatient care for long-term Covid-19 at Karolinska University Hospital, Stockholm Sweden. Native T1 maps were acquired with a prototype 5s(3s)3s modified look-locker inversion recovery sequence before and during adenosine stress. Global native T1 were acquired by carefully delineating endo- and epicardial borders. Delta T1 (%) was calculated as (stress-rest)/rest (%) for native T1.

Results: Patients with PASC had lower delta T1 compared with healthy subjects (3.7 ± 2.4 vs 5.5 ± 2.9 %, p=0.03, Figure 1). Moreover, patients with PASC POTS had lower delta T1 than healthy subjects (3.2 ± 2.7 vs 5.5 ± 2.9 %, p=0.02, Figure 2), however there was no difference in delta T1 in patients with PASC POTS compared with patients with PASC non-POTS (3.2 ± 2.7 vs 4.3 ± 1.8, p=0.23, Figure 2).
There was no difference in native T1 at rest or stress in patients with PASC compared with healthy subjects, neither at 1.5 nor 3 T
(p > 0.05 for all). This remained true for all subgroup analysis of PASC POTS and PASC non-POTS.

Conclusion: Patients with PASC and particularly those with PASC POTS have lower native T1 stress reactivity compared with healthy subjects. These findings suggest presence of microvascular dysfunction as a pathophysiological mechanism in patients with PASC POTS long after initial infection and can be detected using non-contrast stress imaging.