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Post COVID ‐19 syndrome with impairment of flow‐mediated epicardial vasodilation and flow reserve
Author(s) -
Verma Amanda,
Ramayya Tarun,
Upadhyaya Anand,
Valenta Ines,
Lyons Maureen,
Marschall Jonas,
Dehdashti Farrokh,
Gropler Robert J.,
Woodard Pamela K.,
Schindler Thomas Hellmut
Publication year - 2022
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.13871
Subject(s) - vasodilation , medicine , cardiology , ventricle , blood flow , coronary circulation , endothelial dysfunction , circulatory system
Abstract Aims The aim of this study is to evaluate whether post‐acute sequelae of COVID‐19 cardiovascular syndrome (PASC‐CVS) is associated with alterations in coronary circulatory function. Materials and Methods In individuals with PASC‐CVS but without known cardiovascular risk factors ( n = 23) and in healthy controls (CON, n = 23), myocardial blood flow (MBF) was assessed with 13 N‐ammonia and PET/CT in mL/g/min during regadenoson‐stimulated hyperemia, at rest, and the global myocardial flow reserve (MFR) was calculated. MBF was also measured in the mid and mid‐distal myocardium of the left ventricle (LV). The Δ longitudinal MBF gradient (hyperemia minus rest) as a reflection of an impairment of flow‐mediated epicardial vasodilation, was calculated. Results Resting MBF was significantly higher in PASC‐CVS than in CON (1.29 ± 0.27 vs. 1.08 ± 0.20 ml/g/min, p ≤ .024), while hyperemic MBFs did not differ significantly among groups (2.46 ± 0.53 and 2.40 ± 0.34 ml/g/min, p = .621). The MFR was significantly less in PASC‐CVS than in CON (1.97 ± 0.54 vs. 2.27 ± 0.43, p ≤ .031). In addition, there was a Δ longitudinal MBF gradient in PASC‐CVS, not observed in CON (−0.17 ± 0.18 vs. 0.04 ± 0.11 ml/g/min, p < .0001). Conclusions Post‐acute sequelae of COVID‐19 cardiovascular syndrome may be associated with an impairment of flow‐mediated epicardial vasodilation, while reductions in coronary vasodilator capacity appear predominantly related to increases in resting flow in women deserving further investigations.