Bianconi Vanessa, Mannarino Massimo R, Ramondino Federica, Fusaro Jessica, Giglioni Francesco, Braca Marco, Ricciutelli Federica, Lombardini Rita, Paltriccia Rita, Greco Alessia, Lega Iliana C, Pirro Matteo
Unit of Internal Medicine, Department of Medicine and Surgery, University of Perugia, 06129 Perugia, Italy.
Women's College Research Institute, Women's College Hospital, Toronto, ON M5G 1N8, Canada.
J Clin Med. 2023 May 18;12(10):3543. doi: 10.3390/jcm12103543.
The prothrombotic and proinflammatory properties of lipoprotein(a) (Lp(a)) have been hypothesized to play a role in the pathogenesis of severe COVID-19; however, the prognostic impact of Lp(a) on the clinical course of COVID-19 remains controversial. This study aimed to investigate whether Lp(a) may be associated with biomarkers of thrombo-inflammation and the occurrence of thrombotic events or adverse clinical outcomes in patients hospitalized for COVID-19. We consecutively enrolled a cohort of patients hospitalized for COVID-19 and collected blood samples for Lp(a) assessment at hospital admission. A prothrombotic state was evaluated through D-dimer levels, whereas a proinflammatory state was evaluated through C-reactive protein (CRP), procalcitonin, and white blood cell (WBC) levels. Thrombotic events were marked by the diagnosis of deep or superficial vein thrombosis (DVT or SVT), pulmonary embolism (PE), stroke, transient ischemic attack (TIA), acute coronary syndrome (ACS), and critical limb ischemia (CLI). The composite clinical end point of intensive care unit (ICU) admission/in-hospital death was used to evaluate adverse clinical outcomes. Among 564 patients (290 (51%) men, mean age of 74 ± 17 years) the median Lp(a) value at hospital admission was 13 (10-27) mg/dL. During hospitalization, 64 (11%) patients were diagnosed with at least one thrombotic event and 83 (15%) patients met the composite clinical end point. Lp(a), as either a continuous or categorical variable, was not associated with D-dimer, CRP, procalcitonin, and WBC levels ( > 0.05 for all correlation analyses). In addition, Lp(a) was not associated with a risk of thrombotic events ( > 0.05 for multi-adjusted odds ratios) nor with a risk of adverse clinical outcomes ( > 0.05 for multi-adjusted hazard ratios). In conclusion, Lp(a) does not influence biomarkers of plasma thrombotic activity and systemic inflammation nor has any impact on thrombotic events and adverse clinical outcomes in patients hospitalized for COVID-19.
脂蛋白(a) [Lp(a)] 的促血栓形成和促炎特性被认为在重症新型冠状病毒肺炎（COVID-19）的发病机制中起作用；然而，Lp(a) 对COVID-19临床病程的预后影响仍存在争议。本研究旨在调查Lp(a) 是否可能与COVID-19住院患者的血栓炎症生物标志物、血栓形成事件的发生或不良临床结局相关。我们连续纳入了一组因COVID-19住院的患者，并在入院时采集血样进行Lp(a) 评估。通过D-二聚体水平评估促血栓形成状态，而通过C反应蛋白（CRP）、降钙素原和白细胞（WBC）水平评估促炎状态。血栓形成事件以深静脉或浅静脉血栓形成（DVT或SVT）、肺栓塞（PE）、中风、短暂性脑缺血发作（TIA）、急性冠状动脉综合征（ACS）和严重肢体缺血（CLI）的诊断为标志。使用重症监护病房（ICU）入院/院内死亡的综合临床终点来评估不良临床结局。在564例患者（290例（51%）男性，平均年龄74±17岁）中，入院时Lp(a) 的中位数为13（10-27）mg/dL。住院期间，64例（11%）患者被诊断至少发生1次血栓形成事件，83例（15%）患者达到综合临床终点。Lp(a) 作为连续或分类变量，与D-二聚体、CRP、降钙素原和WBC水平均无关联（所有相关性分析P>0.05）。此外，Lp(a) 与血栓形成事件风险（多校正比值比P>0.05）和不良临床结局风险（多校正风险比P>0.05）均无关联。总之，Lp(a) 不影响COVID-19住院患者的血浆血栓形成活性和全身炎症生物标志物，对血栓形成事件和不良临床结局也无任何影响。
