Tsalamandris Sotirios, Koliastasis Leonidas, Miliou Antigoni, Oikonomou Evangelos, Papageorgiou Nikos, Antonopoulos Alexis, Hatzis George, Mourouzis Konstantinos, Vogiatzi Georgia, Siasos Gerasimos, Xaplanteris Panagiotis, Tousoulis Dimitris
1st Department of Cardiology, School of Medicine, 'Hippokration' General Hospital, National and Kapodistrian University of Athens, 11527 Athens, Greece.
3rd Department of Cardiology, "Sotiria" Chest Disease Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Diagnostics (Basel). 2025 Apr 18;15(8):1033. doi: 10.3390/diagnostics15081033.
Endothelial dysfunction and inflammation are associated with the progression of coronary artery disease (CAD) and the pathophysiology of acute coronary syndrome (ACS). We examined the prognostic role of endothelial function and pro-inflammatory cytokines in patients admitted with ACS. The study population consisted of 864 subjects. From 663 subjects who presented with chest pain, ACS was diagnosed in 460. We additionally recruited 201 consecutive patients with stable CAD. Endothelial function was assessed using flow-mediated dilatation (FMD). Tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels were measured via ELISA. Subjects with ACS were followed up for major adverse cardiovascular events (MACE), defined as cardiovascular death, cardiac arrest, myocardial infarction, stroke, nonfatal stroke, other arterial thrombotic events, and hospitalization due to cardiovascular conditions. There was a stepwise impairment in FMD, logTNF-α, and logIL-6 in patients with chest pain of non-epicardial CAD etiology compared to patients with stable CAD and those with ACS ( < 0.001 for all). Moreover, patients who presented with chest pain had increased odds of ACS in accordance with the increasing levels of TNF-α, IL-6, and impaired FMD ( < 0.05 for all). Interestingly, from all these markers, in patients with ACS, we found that only TNF-α levels above 5.19 pg/mL had a 2.5-times-increased risk of MACE compared to patients with TNF-α levels below 5.19 pg/mL, independently of other confounders. In the current study, we found that patients who presented with ACS had impaired endothelial function and increased levels of IL-6 and TNF-α.
内皮功能障碍和炎症与冠状动脉疾病（CAD）的进展及急性冠状动脉综合征（ACS）的病理生理学相关。我们研究了内皮功能和促炎细胞因子在因ACS入院患者中的预后作用。研究人群包括864名受试者。在663名出现胸痛的受试者中，460例被诊断为ACS。我们还连续招募了201例稳定型CAD患者。使用血流介导的血管舒张（FMD）评估内皮功能。通过酶联免疫吸附测定（ELISA）测量肿瘤坏死因子α（TNF-α）和白细胞介素-6（IL-6）水平。对ACS患者进行主要不良心血管事件（MACE）随访，MACE定义为心血管死亡、心脏骤停、心肌梗死、中风、非致命性中风、其他动脉血栓形成事件以及因心血管疾病住院。与稳定型CAD患者和ACS患者相比，非心外膜CAD病因胸痛患者的FMD、logTNF-α和logIL-6存在逐步损害（所有P均<0.001）。此外，出现胸痛的患者发生ACS的几率随着TNF-α、IL-6水平升高及FMD受损而增加（所有P<0.05）。有趣的是，在所有这些标志物中，我们发现，在ACS患者中，与TNF-α水平低于5.19 pg/mL的患者相比，仅TNF-α水平高于5.19 pg/mL的患者发生MACE的风险增加2.5倍，且独立于其他混杂因素。在本研究中，我们发现出现ACS的患者存在内皮功能受损以及IL-6和TNF-α水平升高。
