Munteanu Andreea Mara, Lighezan Daniel Florin, Nicoras Violeta Ariana, Dumitrescu Patrick, Bodea Olivia-Maria, Velimirovici Dana Emilia, Otiman Gabriela, Banciu Christian, Nisulescu Daniel-Dumitru
Department V, Internal Medicine I-Discipline of Internal Medicine IV, Center of Advanced Research in Cardiology and Hemostasology, "Victor Babes" University of Medicine and Pharmacy, Eftimie Murgu Sq. No. 2, 300041 Timisoara, Romania.
Department V, Internal Medicine I-Discipline of Medical Semiology I, Center of Advanced Research in Cardiology and Hemostasology, "Victor Babes" University of Medicine and Pharmacy, Eftimie Murgu Sq. No. 2, 300041 Timisoara, Romania.
Viruses. 2025 Feb 23;17(3):305. doi: 10.3390/v17030305.
Most studies analyzing data from patients who experienced at least one episode of acute COVID-19 infection have attributed the cascade of immediate and late complications to disruption of the inflammatory system and neutrophil activity in particular. Among the various functions of neutrophils is the release of pro-inflammatory mediators, including interleukin-6 (IL-6). Oxidative stress induced by pro-inflammatory mediators secreted by neutrophils leads to vascular endothelial dysfunction. Neutrophil counts and the neutrophil-to-lymphocyte ratio (NLR) are directly associated with COVID-19 patient survival, with higher values correlating with increased mortality. To assess endothelial dysfunction secondary to COVID-19 infection, we conducted a retrospective study involving two patient cohorts, each comprising 99 participants: one group with a history of COVID-19 infection and another without. The study aimed to demonstrate the presence of endothelial dysfunction in patients with moderate COVID-19 infection using flow-mediated dilatation (FMD) of the brachial artery and to evaluate its correlation with key inflammatory markers (erythrocyte sedimentation rate-ESR, fibrinogen, NLR, IL-6). FMD values were significantly reduced ( < 0.0001) in post-COVID-19 patients compared to those without prior infection. ESR ( < 0.0001), fibrinogen ( < 0.0001), C-reactive protein (CRP) ( < 0.0001), leukocyte count ( < 0.0001), and granulocyte count ( < 0.0001) were inversely correlated with FMD values. Among post-COVID-19 patients, all analyzed parameters demonstrated a statistically significant impact on FMD, with ESR showing the strongest effect, accounting for nearly 63% of the dependency. ANOVA testing confirmed an inverse association between NLR quartiles and FMD, as well as between IL-6 levels and FMD. In conclusion, this study highlights the presence of endothelial dysfunction in post-COVID-19 patients, as assessed by FMD, and demonstrates statistically significant inverse correlations between FMD values, IL-6 levels, and the neutrophil-to-lymphocyte ratio.
大多数分析至少经历过一次急性新冠病毒感染患者数据的研究，都将一系列即时和晚期并发症归因于炎症系统的破坏，尤其是中性粒细胞活性的破坏。中性粒细胞的各种功能之一是释放促炎介质，包括白细胞介素-6（IL-6）。中性粒细胞分泌的促炎介质诱导的氧化应激会导致血管内皮功能障碍。中性粒细胞计数和中性粒细胞与淋巴细胞比率（NLR）与新冠病毒感染患者的生存率直接相关，数值越高，死亡率越高。为了评估新冠病毒感染继发的内皮功能障碍，我们进行了一项回顾性研究，涉及两个患者队列，每个队列由99名参与者组成：一组有新冠病毒感染史，另一组没有。该研究旨在通过肱动脉的血流介导的扩张（FMD）来证明中度新冠病毒感染患者存在内皮功能障碍，并评估其与关键炎症标志物（红细胞沉降率-ESR、纤维蛋白原、NLR、IL-6）的相关性。与未感染过的患者相比，新冠病毒感染后的患者FMD值显著降低（<0.0001）。ESR（<0.0001）、纤维蛋白原（<0.0001）、C反应蛋白（CRP）（<0.0001）、白细胞计数（<0.0001）和粒细胞计数（<0.0001）与FMD值呈负相关。在新冠病毒感染后的患者中，所有分析参数对FMD均显示出统计学上的显著影响，其中ESR的影响最强，占近63%的相关性。方差分析测试证实了NLR四分位数与FMD之间以及IL-6水平与FMD之间存在负相关。总之，本研究强调了通过FMD评估的新冠病毒感染后患者存在内皮功能障碍，并证明了FMD值、IL-6水平和中性粒细胞与淋巴细胞比率之间存在统计学上的显著负相关。
