Association of COVID‐19 with impaired endothelial glycocalyx, vascular function and myocardial deformation four months after infection

Lambadiari, Vaia; Mitrakou, Asimina; Kountouri, Aikaterini; Thymis, John; Katogiannis, Konstantinos; Korakas, Emmanouil; Varlamos, Charalampos; Andreadou, Ioanna; Tsoumani, Maria; Triantafyllidi, Helen; Bamias, Aristotelis; Thomas, Konstantinos; Kazakou, Pinelopi; Grigoropoulou, Sotiria; Kavatha, Dimitra; Antoniadou, Anastasia; Dimopoulos, Meletios A; Ikonomidis, Ignatios

AIMS: SARS‐CoV‐2 infection may lead to endothelial and vascular dysfunction. We investigated alterations of arterial stiffness, endothelial coronary and myocardial function markers four months after COVID‐19 infection. METHODS AND RESULTS: In a case‐control prospective study, we included 70 patients four months after COVID‐19 infection, 70 age‐ and sex‐matched untreated hypertensive patients (positive control) and 70 healthy individuals. We measured a) perfused boundary region (PBR) of the sublingual arterial microvessels (increased PBR indicates reduced endothelial glycocalyx thickness), b) flow‐mediated dilation (FMD), c) coronary Flow Reserve (CFR) by Doppler echocardiography d) pulse wave velocity (PWV) e) global left (LV) and right (RV) ventricular longitudinal strain (GLS) and f) malondialdehyde (MDA), an oxidative stress marker, thrombomodulin and von Willebrand factor (vWF) as endothelial biomarkers. COVID‐19 patients had similar CFR and FMD with hypertensives (2.48±0.41 vs 2.58±0.88, p=0.562, 5.86±2.82% vs 5.80±2.07%, p=0.872 respectively) but lower values than controls (3.42±0.65, p=0.0135, 9.06±2.11%, p=0.002 respectively). Compared to controls, both COVID‐19 and hypertensives had greater PBR5‐25 (2.07±0.15μm and 2.07±0.26μm p=0.8 vs 1.89±0.17μm, p=0.001), higher PWV (PWVc‐f 12.09±2.50 vs 11.92±2.94, p=0.7 vs 10.04±1.80m/sec, p=0.036) and impaired LV and RV GLS (‐19.50 ±2.56% vs −19.23±2.67%, p=0.864 vs −21.98±1.51%, p=0.020 and ‐16.99±3.17% vs ‐18.63±3.20%, p=0.002 vs ‐20.51±2,.28%, p<0.001). MDA and thrombomodulin were higher in COVID‐19 patients than both hypertensives and controls (10.67±2.75 vs 1.76± 0.30, p=0.003 vs 1.01±0.50nmole/L, p=0.001 and 3716.63±188.36 vs 3114.46±179.18, p=0.017 vs 2590.02±156.51pg/ml, p<0.001). Residual cardiovascular symptoms at 4 months were associated with oxidative stress and endothelial dysfunction markers. CONCLUSIONS: SARS‐CoV‐2 may cause endothelial and vascular dysfunction linked to impaired cardiac performance four months after infection.