心衰和急性冠状动脉综合征患者的炎症生物标志物和内皮改变

Andreea-Luciana Buicu, Răzvan-Andrei Licu, Emil Blîndu, D. Opincariu, R. Hodaș, Alexandra Ștefania Polexa, T. Benedek
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引用次数: 0

摘要

摘要简介:全身性炎症在急性冠脉综合征(ACS)的病理生理中起关键作用,直接促进易损冠脉斑块的进展和破裂。本研究的目的是研究确诊心力衰竭患者的炎症生物标志物与ACS类型(st段抬高型心肌梗死- STEMI、非st段抬高型心肌梗死- NSTEMI或不稳定型心绞痛- UA)之间的关系。材料与方法:本研究共纳入2017年1月1日至2020年12月31日期间在鲁格·穆列斯特县急诊临床医院临床心内科-心脏重症监护病房(CICU)收治的266例不同类型ACS (UA、NSTEMI或STEMI)患者,这些患者根据临床和临床旁数据确定心力衰竭的诊断。在患者总数中,36例因UA住院,230例因MI住院,其中165例为STEMI, 65例为NSTEMI。结果:心肌梗死患者只有hs-CRP和IL-6明显高于UA。UA患者的hs-CRP平均值为4.9±4.5 mg/mL,而MI患者为20.4±42.2 mg/mL (p = 0.001), UA患者的IL-6平均值为7.2±13.8 pg/mL, MI患者为31.6±129.2 pg/mL (p <0.0001)。在心力衰竭患者中,ICAM似乎在STEMI和其他类型ACS之间具有更大的区分力,在STEMI患者中具有两倍以上的值(216.1±149.6 ng/mL vs. 448.2±754.4 ng/mL, p <0.0001)。结论:在心力衰竭患者中,炎症生物标志物(如hs-CRP)的增加与急性心肌梗死的发展有关,但与其类型无关。与其他类型的ACS相比,STEMI患者的粘附分子,特别是ICAM升高,表明内皮改变在ACS发展中的潜在作用,当它增加与心力衰竭相关的全身性炎症时。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inflammatory Biomarkers and Endothelial Alteration in Patients with Heart Failure and Acute Coronary Syndromes
Abstract Introduction: Systemic inflammation plays a key role in the pathophysiology of acute coronary syndrome (ACS), having a direct effect in promoting the progression and rupture of vulnerable coronary plaques. The aim of this study was to investigate the association between inflammatory biomarkers and the type of ACS (ST-elevation myocardial infarction – STEMI, non-ST-elevation myocardial infarction – NSTEMI, or unstable angina – UA) in patients with confirmed heart failure. Material and Methods: This study included a total of 266 patients admitted to the Clinical Department of Cardiology of the County Emergency Clinical Hospital of Târgu Mureș – Cardiac Intensive Care Unit (CICU) for ACS of various types (UA, NSTEMI or STEMI) between January 1, 2017 and December 31, 2020, in whom the diagnosis of heart failure was established based on clinical and paraclinical data. From the total number of patients, 36 were hospitalized for UA and 230 for MI, of which 165 were STEMI and 65 were NSTEMI. Results: Only hs-CRP and IL-6 were significantly higher in MI compared to UA. Mean hs-CRP was 4.9 ± 4.5 mg/mL in patients with UA vs. 20.4 ± 42.2 mg/mL in patients with MI (p = 0.001), and mean IL-6 was 7.2 ± 13.8 pg/mL in UA vs. 31.6 ± 129.2 pg/mL in MI (p <0.0001). ICAM seems to have had a greater discriminating power between STEMI and other types of ACS in those with heart failure, having a value more than double in those with STEMI (216.1 ± 149.6 ng/mL vs. 448.2 ± 754.4 ng/mL, p <0.0001). Conclusions: In patients with heart failure, the increase of inflammatory biomarkers such as hs-CRP is associated with the development of an acute myocardial infarction but not with its type. Adhesion molecules, especially ICAM, are elevated in patients with STEMI compared to other types of ACS, indicating a potential role of endothelial alteration in the development of an ACS when it adds to systemic inflammation linked to heart failure.
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