Raia Lisa, Urbina Tomas, Gabarre Paul, Bonny Vincent, Hariri Geoffroy, Ehrminger Sebastien, Bigé Naïke, Baudel Jean-Luc, Guidet Bertrand, Maury Eric, Joffre Jeremie, Ait-Oufella Hafid
Medical Intensive Care Unit, Saint Antoine University Hospital, APHP, Sorbonne University, 75012, Paris, France.
Pierre Louis Institute of Epidemiology and Public Health, Sorbonne University, Inserm U1136, Paris, France.
Ann Intensive Care. 2022 Jun 13;12(1):51. doi: 10.1186/s13613-022-01027-3.
Some clinical and histological studies have reported that SARS-CoV-2 infection may damage the endothelium. However, the impact of this virus on endothelial function in vivo remains poorly characterized. In this single-center pilot observational study, we performed iontophoresis of acetylcholine coupled with Laser doppler to investigate microvascular endothelial reactivity in COVID-19 patients compared to patients with non-COVID-19 bacterial pneumonia (NCBP) patients.
During three consecutive months, 32 COVID-19 patients and 11 control NCBP patients with acute respiratory failure were included. The median age was 59 [50-68] and 69 [57-75] years in COVID-19 and NCBP groups, respectively (P = 0.11). There was no significant difference in comorbidities or medications between the two groups, except for body mass index, which was higher in COVID-19 patients. NCBP patients had a higher SAPS II score compared to COVID-19 patients (P < 0.0001), but SOFA score was not different between groups (P = 0.51). Global hemodynamic and peripheral tissue perfusion parameters were not different between groups. COVID-19 patients had significantly lower skin microvascular basal blood flow than NCBP patients (P = 0.02). In addition, endothelium-dependent microvascular reactivity was threefold lower in COVID-19 patients than NCBP patients (P = 0.008).
Both baseline skin microvascular blood flow and skin endothelial-dependent microvascular reactivity were impaired in critically ill COVID-19 patients compared to NCBP patients, despite a lower disease severity score supporting a specific pathogenic role of SARS-CoV-2 on the endothelium.
一些临床和组织学研究报告称，新型冠状病毒2（SARS-CoV-2）感染可能会损害内皮细胞。然而，这种病毒对体内内皮功能的影响仍未得到充分描述。在这项单中心试点观察性研究中，我们进行了乙酰胆碱离子导入结合激光多普勒技术，以研究新型冠状病毒肺炎（COVID-19）患者与非COVID-19细菌性肺炎（NCBP）患者相比的微血管内皮反应性。
在连续三个月的时间里，纳入了32例COVID-19患者和11例患有急性呼吸衰竭的对照NCBP患者。COVID-19组和NCBP组的中位年龄分别为59[50-68]岁和69[57-75]岁（P=0.11）。两组之间的合并症或用药情况没有显著差异，但COVID-19患者的体重指数较高。与COVID-19患者相比，NCBP患者的序贯器官衰竭评估（SOFA）评分更高（P<0.0001），但两组之间的SOFA评分没有差异（P=0.51）。两组之间的整体血流动力学和外周组织灌注参数没有差异。COVID-19患者的皮肤微血管基础血流明显低于NCBP患者（P=0.02）。此外，COVID-19患者的内皮依赖性微血管反应性比NCBP患者低三倍（P=0.008）。
与NCBP患者相比，重症COVID-19患者的基线皮肤微血管血流和皮肤内皮依赖性微血管反应性均受损，尽管疾病严重程度评分较低，这支持了SARS-CoV-2对内皮细胞具有特定致病作用。
