Schnaubelt Sebastian, Jakobljevich Anna, Brock Roman, Oppenauer Julia, Kornfehl Andrea, Eibensteiner Felix, Veigl Christoph, Perkmann Thomas, Haslacher Helmuth, Strassl Robert, Reindl-Schwaighofer Roman, Schlager Oliver, Sulzgruber Patrick
Department of Emergency Medicine, Medical University of Vienna, 1090 Vienna, Austria.
Emergency Medical Service Vienna, 1030 Vienna, Austria.
J Clin Med. 2025 Mar 25;14(7):2233. doi: 10.3390/jcm14072233.
: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing coronavirus disease 2019 (COVID-19) can damage the endothelium and increase arterial stiffness, potentially leading to adverse cardiovascular events. In parallel, systemic inflammation in COVID-19 also impacts endothelial function. Angiotensin-converting enzyme 2 (ACE2) promotes vasodilation and anti-inflammatory effects, but also facilitates SARS-CoV-2 entry into human cells. Thus, concerns have been raised about the use of RAAS inhibitors (RAASi) in COVID-19 patients due to potential ACE2 upregulation. However, the clinical significance of increased plasma ACE2 (sACE2) in RAASi-treated COVID-19 patients remains unclear. : This prospective, single-centre study evaluated RAASi, sACE2, and vascular function in acutely ill patients with COVID-19 in comparison with acutely ill patients without COVID-19. Adult emergency department patients with confirmed or suspected COVID-19 were enrolled and underwent pulse wave velocity, ankle brachial index, and sACE2 measurements. : In the 152 included patients (50% female, median age 62 years, 68% COVID-19 positive), the sACE2 values were slightly higher in the COVID-19 (0.485 [0.364-1.329]) than in the non-COVID-19 subgroup (0.458 [0.356-1.138]; = 0.70). No significant differences in sACE2 were observed between patients with and without RAASi, regardless of COVID-19 status. Pulse wave velocity values differed significantly between groups ( = 0.015). : In emergency department patients, sACE2 was upregulated in COVID-19 patients, probably due to oxidative stress and inflammation. RAASi did not increase sACE2, but may have protective effects against inflammation. Elevated sACE2 appeared to have a beneficial effect on arterial stiffness in all patients. These findings support continued RAASi therapy in COVID-19 patients to protect against chronic inflammation and apoptosis.
导致2019冠状病毒病（COVID-19）的严重急性呼吸综合征冠状病毒2（SARS-CoV-2）可损害内皮细胞并增加动脉僵硬度，可能导致不良心血管事件。与此同时，COVID-19中的全身炎症也会影响内皮功能。血管紧张素转换酶2（ACE2）可促进血管舒张和抗炎作用，但也有助于SARS-CoV-2进入人体细胞。因此，由于可能导致ACE2上调，人们对在COVID-19患者中使用肾素-血管紧张素-醛固酮系统抑制剂（RAASi）产生了担忧。然而，在接受RAASi治疗的COVID-19患者中，血浆ACE2（sACE2）升高的临床意义仍不清楚。 ：这项前瞻性单中心研究评估了急性病COVID-19患者与无COVID-19的急性病患者的RAASi、sACE2和血管功能。纳入确诊或疑似COVID-19的成人急诊科患者，并进行脉搏波速度、踝臂指数和sACE2测量。 ：在纳入的152例患者中（50%为女性，中位年龄62岁，68%为COVID-19阳性），COVID-19患者的sACE2值（0.485[0.364-1.329]）略高于非COVID-19亚组（0.458[0.356-1.138]；P=0.70）。无论COVID-19状态如何，使用和未使用RAASi的患者之间sACE2均无显著差异。脉搏波速度值在各组之间存在显著差异（P=0.015）。 ：在急诊科患者中，COVID-19患者的sACE2上调，可能是由于氧化应激和炎症。RAASi不会增加sACE2，但可能对炎症有保护作用。sACE2升高似乎对所有患者的动脉僵硬度都有有益影响。这些发现支持在COVID-19患者中继续使用RAASi治疗，以预防慢性炎症和细胞凋亡。
