Abstract
Background
There are no effective therapies to prevent the occurrence and progression of vertebrobasilar dolichoectasia (VBD). In this study, we investigated the relationship between serum levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) and the occurrence and progression of VBD.
Methods
Sixty (60) cases without VBD and ischemia stroke were considered as Group A, 100 cases with VBD were further divided into Group B (VBD without ischemic stroke, n = 54) and Group C (VBD with first ever acute posterior circulation ischemic stroke, n = 46). Demographic data (such as gender and age) and past medical history (such as hypertension, diabetes, and smoking history) were collected. The levels of serum low-density lipoprotein cholesterol (LDL-C), hypersensitivity C reactive protein (hs-CRP), glycosylated hemoglobin (HbAlc), homocysteine (HCY), uric acid (UA), fibrinogen (Fib), and Lp-PLA2, etc. were measured. Logistic regression analysis was used to assess the related factors of VBD and ischemic stroke secondary to VBD.
Results
Logistic multivariate regression analysis showed that only age and the level of serum Lp-PLA2 were significantly higher in group B than those in group A (P < 0.012, P < 0.001, respectively), however, only the level of serum Lp-PLA2 was significantly higher in group C than those in group B (P < 0.001).
Conclusions
The serum marker Lp-PLA2 is an independent risk factor for the occurrence of VBD and the progression of VBD to posterior circulation ischemic stroke. Whether intervening on atherosclerosis could prevent the occurrence and development of VBD needs to be further studied.
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This project was supported by the College Students Innovative Training Planning Project of Guangdong Province, Education Department (No. 201410560092) and this work was also supported by Sanming Project of Medicine in Shenzhen (SZSM201801014).
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Liu, Y., Zhu, J., Deng, X. et al. Serum level of lipoprotein-associated phospholipase A2 is a potential biomarker of vertebrobasilar dolichoectasia and its progression to cerebral infarction. Neurol Sci 42, 599–605 (2021). https://doi.org/10.1007/s10072-020-04563-7
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DOI: https://doi.org/10.1007/s10072-020-04563-7