Association of COVID-19 with impaired endothelial glycocalyx, vascular function and myocardial deformation 4 months after infection
Association of COVID-19 with impaired endothelial glycocalyx, vascular function and myocardial deformation 4 months after infection
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DOI：
10.1002/ejhf.2326
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发表时间：
2021-09-13
影响因子：
18.2
通讯作者：
Ikonomidis, Ignatios
中科院分区：
文献类型：
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作者：
Lambadiari, Vaia;Mitrakou, Asimina;Ikonomidis, Ignatios
目的SARS-CoV-2感染可能导致内皮和血管功能障碍。我们研究了COVID-19感染后4个月动脉硬度、内皮冠状动脉和心肌功能标志物的变化。方法和结果在一项病例对照前瞻性研究中，我们纳入了70名COVID-19感染后4个月的患者，70名年龄和性别匹配的未经治疗的高血压患者（阳性对照）和70名健康个体。我们测量了（i）舌下动脉微血管的灌注边界区（PBR）（增加的PBR指示减少的内皮糖萼厚度），（ii）血流介导的扩张（FMD），（iii）通过多普勒超声心动图的冠状动脉血流储备（CFR），（iv）脉搏波速度（PWV），（v）整体左心室和右心室纵向应变（GLS），和（vi）丙二醛（MDA），氧化应激标志物，血栓调节蛋白和血管性血友病因子作为内皮生物标志物。COVID-19患者的CFR和FMD与高血压患者相似（分别为2.48 ± 0.41 vs. 2.58 ± 0.88，P = 0.562和5.86 ± 2.82% vs. 5.80 ± 2.07%，P = 0.872），但低于对照组（分别为3.42 ± 0.65，P = 0.0135和9.06 ± 2.11%，P = 0.002）。与对照组相比，COVID-19和高血压患者的PBR 5 -25（2.07 +/- 0.15 μ m和2.07 +/- 0.26 μ m，P = 0.8 vs. 1.89 +/- 0.17 μ m，P = 0.001），PWV较高（颈动脉-股动脉PWV 12.09 +/- 2.50 vs. 11.92 +/- 2.94，P = 0.7 vs. 10.04 +/-1.80 m/s，P = 0.036）和左心室和右心室GLS受损（-19.50 +/- 2.56% vs. -19.23 +/-2.67%，P = 0.864 vs. -21.98 +/-1.51%，P = 0.020和-16.99 +/- 3.17% vs. -18.63 +/-3.20%，P = 0.002 vs. -20.51 +/-2.28%，P < 0.001）。MDA和血栓调节蛋白在COVID-19中较高;高血压组和对照组（10.67 ± 0.32 vs 1.76 ± 0.03，P = 0.003 vs 1.01 ± 0.05 nmol/L，P = 0.001和3716.63 ± 188.36 vs 3114.46 ± 179.18 pg/mL，P = 0.017对比2590.02 +/- 156.51 pg/mL，P < 0.001）。残留的心血管症状在4个月与氧化应激和内皮功能障碍marker.Conclusions SARS-CoV-2可能会导致内皮和血管功能障碍与受损的心脏功能4个月后感染。
Aims SARS-CoV-2 infection may lead to endothelial and vascular dysfunction. We investigated alterations of arterial stiffness, endothelial coronary and myocardial function markers 4 months after COVID-19 infection.Methods and results In a case-control prospective study, we included 70 patients 4 months after COVID-19 infection, 70 age- and sex-matched untreated hypertensive patients (positive control) and 70 healthy individuals. We measured (i) perfused boundary region (PBR) of the sublingual arterial microvessels (increased PBR indicates reduced endothelial glycocalyx thickness), (ii) flow-mediated dilatation (FMD), (iii) coronary flow reserve (CFR) by Doppler echocardiography, (iv) pulse wave velocity (PWV), (v) global left and right ventricular longitudinal strain (GLS), and (vi) malondialdehyde (MDA), an oxidative stress marker, thrombomodulin and von Willebrand factor as endothelial biomarkers. COVID-19 patients had similar CFR and FMD as hypertensives (2.48 +/- 0.41 vs. 2.58 +/- 0.88, P = 0.562, and 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, and 9.06 +/- 2.11%, P = 0.002, respectively). Compared to controls, both COVID-19 and hypertensives had greater PBR5-25 (2.07 +/- 0.15 mu m and 2.07 +/- 0.26 mu m, P = 0.8 vs. 1.89 +/- 0.17 mu m, P = 0.001), higher PWV (carotid-femoral PWV 12.09 +/- 2.50 vs. 11.92 +/- 2.94, P = 0.7 vs. 10.04 +/- 1.80m/s, P = 0.036) and impaired left and right ventricular 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 +/- 0.32 vs 1.76 +/- 0.03, P = 0.003 vs. 1.01 +/- 0.05 nmol/L, P = 0.001 and 3716.63 +/- 188.36 vs. 3114.46 +/- 179.18 pg/mL, P = 0.017 vs. 2590.02 +/- 156.51 pg/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 4 months after infection.