The relationship of platelet activating factors and vascular endothelial activity markers to lacunar infarction_West China Medical Journal

Authors：

 LI Wei ¹ , ZHANG Mijuan ² , WANG Yan ² , WANG Tao ¹ , MA Minjiang ² , TIAN Chun’e ² , YANG Qian ¹ , CHEN Ruili ¹

1. Department of Neurology, Shaanxi People’s Hospital, Xi’an, Shaanxi 710068, P. R. China;
2. Graduate School, Xi’an Medical College, Xi’an, Shaanxi 710068, P. R. China;

Corresponding author：

LI Wei, Email: liwei.996@163.com

Keywords：

Platelet activating factor; Vascular endothelial activity markers; Lacunar infarction

DOI：

10.7507/1002-0179.201908056

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Objective To explore the relationship of platelet-activating factors and vascular endothelial activity markers to lacunar infarction (LI).Methods A total of 100 inpatients diagnosed with LI in Shaanxi Provincial People’s Hospital between March 2018 and February 2019 were included, and 100 matched healthy controls were collected. Basic information, clinical baseline data, laboratory examinations, cerebral MRI and treatment data were collected after admission. The platelet-activating factors (platelet membrane glycoprotein Ⅱb/Ⅲa receptor and P-selectin) and vascular endothelial activity markers [von Willebrand factor (vWF), homocysteine (HCY), and high-sensitivity C-reactive protein (hsCRP)] levels of patients with LI were detected one month and three months after onset, and those of the control group were decteted when they were selected. SPSS 25.0 software was used for statistical analysis.Results At one month after onset, there was no statistically significant difference in the levels of platelet activating factors between the LI group and the control group [platelet membrane glycoprotein Ⅱb/Ⅲa receptor: (2.84±1.00)% vs. (2.59±0.96)%, P=0.065; P-selectin: (3.05±0.63)% vs. (2.98±0.59)%, P=0.419], while the differences in the levels of vascular endothelial activity markers between the two groups were statistically significant [vWF: (141.80±17.60) vs. (124.63±10.65) ng/mL, P<0.001; hsCRP: (5.53±1.37) vs. (2.17±0.55) mg/L, P<0.001; HCY: (18.76±4.07) vs. (15.81±2.63) mmol/L, P<0.001]. At three months after onset, 94 LI patients were followed up. The levels of vWF and hsCRP between the 100 patients one month after onset and the 94 patients three months after onset were statistically different [(vWF: (141.80±17.60) vs. (134.86±13.35) ng/mL, P=0.002; hsCRP: (5.53±1.37) vs. (2.63±0.55) mg/L, P<0.001], but there was no statistically significant difference between the two time points in the levels of HCY or platelet-activating factors (P>0.05).Conclusion Chronic platelet activation may not play a core role in LI pathophysiology, and endothelial dysfunction may be one of the pathological mechanisms of LI.

Citation： LI Wei, ZHANG Mijuan, WANG Yan, WANG Tao, MA Minjiang, TIAN Chun’e, YANG Qian, CHEN Ruili. The relationship of platelet activating factors and vascular endothelial activity markers to lacunar infarction. West China Medical Journal, 2019, 34(10): 1143-1147. doi: 10.7507/1002-0179.201908056 Copy

1.	平萍, 巴春贺, 张鸿霞, 等. 低频重复经颅磁刺激辅助药物治疗老年脑梗死后焦虑抑郁患者的效果. 中国临床保健杂志, 2018, 21(1): 55-58.
2.	Wardlaw JM, Smith C, Dichgans M. Mechanisms underlying sporadic cerebral small vessel disease: insights from neuroimaging. Lancet Neurol, 2013, 12(5): 70060-70067.
3.	Staszewski J, Piusińska-Macoch R1, Brodacki B1, et al. IL-6, PF-4, sCD40 L, and homocysteine are associated with the radiological progression of cerebral small-vessel disease: a 2-year follow-up study. Clin Interv Aging, 2018, 13: 1135-1141.
4.	Lavallée PC, Labreuche J, Faille D, et al. Circulating markers of endothelial dysfunction and platelet activation in patients with severe symptomatic cerebral small vessel disease. Cerebrovasc Dis, 2015, 36(2): 131-138.
5.	Bennett JS. Structure and function of the platelet integrin α_IIbβ₃. J Clin Invest, 2005, 115(12): 3363-3369.
6.	Pawelczyk M, Glabiński A, Kaczorowska B, et al. sP-and sE-selectin in stroke patients with metabolic disorders. Neurol Neurochir Pol, 2018, 52(5): 599-605.
7.	Wardlaw JM, Sandercock PA, Dennis MS, et al. Is breakdown of the blood-brain barrier responsible for lacunar stroke, leukoaraiosis, and dementia?. Stroke, 2003, 34(3): 806-812.
8.	中华医学会神经病学分会, 中华医学会神经病学分会脑血管病学组. 中国脑小血管病诊治共识. 中华神经科杂志, 2015, 48(10): 838-844.
9.	Oksala NK, Heikkinen M, Mikkelsson JA, et al. Smoking and the platelet fibrinogen receptor glycoprotein IIb/IIIA Pl(A1/A2) polymorphism interact in the risk of lacunar stroke and midterm survival. Stroke, 2007, 38(1): 50-55.
10.	Fiodorenko-Dumas Ż, Dumas I, Mastej K, et al. Receptor GP IIb/IIIa as an indicator of risk in vascular events. Clin Appl Thromb Hemost, 2019, 25: 1-8.
11.	许海霞, 李国丽, 王洪权, 等. 血小板活化标记物与脑小血管病相关性研究. 内蒙古医学杂志, 2016, 48(9): 1036-1038.
12.	Petter J, Eriksson-Franzen M, Oweling M, et al. Platelets and inflammatory parameters do not affect long-term survival after acute stroke. J Stroke Cerebrovasc Dis, 2016, 25(8): 1936-1938.
13.	Hein TW, Singh U, Vasquez-Vivar J, et al. Human C-reactive protein induces endothelial dysfunction and uncoupling of eNOS in vivo. Atherosclerosis, 2009, 206(1): 61-68.
14.	Rajeshwar K, Kaul S, Al-Hazzani A, et al. C-Reactive protein and nitric oxide levels in ischemic stroke and its subtypes: correlation with clinical outcome. Inflammation, 2012, 35(3): 978-984.
15.	Woywodt A, Gerdes S, Ahl B, et al. Circulating endothelial cells and stroke: influence of stroke subtypes and changes during the course of disease. J Stroke Cerebrovasc Dis, 2012, 21(6): 452-458.
16.	Fan H, Yang S, Li Y, et al. Assessment of homocysteine as a diagnostic and early prognostic biomarker for patients with acute lacunar infarction. Eur Neurol, 2018, 79(1/2): 54-62.
17.	Lehmann MF, Kallaur AP, Oliveira SR, et al. Inflammatory and metabolic markers and short-time outcome in patients with acute ischemic stroke in relation to TOAST subtypes. Metab Brain Dis, 2015, 30(6): 1417-1428.
18.	Wiseman S, Marlborough F, Doubal F, et al. Blood markers of coagulation, fibrinolysis, endothelial dysfunction and inflammation in lacunar stroke versus non-lacunar stroke and non-stroke: systematic review and meta-analysis. Cerebrovasc Dis, 2014, 37(1): 64-75.

1. 平萍, 巴春贺, 张鸿霞, 等. 低频重复经颅磁刺激辅助药物治疗老年脑梗死后焦虑抑郁患者的效果. 中国临床保健杂志, 2018, 21(1): 55-58.
2. Wardlaw JM, Smith C, Dichgans M. Mechanisms underlying sporadic cerebral small vessel disease: insights from neuroimaging. Lancet Neurol, 2013, 12(5): 70060-70067.
3. Staszewski J, Piusińska-Macoch R1, Brodacki B1, et al. IL-6, PF-4, sCD40 L, and homocysteine are associated with the radiological progression of cerebral small-vessel disease: a 2-year follow-up study. Clin Interv Aging, 2018, 13: 1135-1141.
4. Lavallée PC, Labreuche J, Faille D, et al. Circulating markers of endothelial dysfunction and platelet activation in patients with severe symptomatic cerebral small vessel disease. Cerebrovasc Dis, 2015, 36(2): 131-138.
5. Bennett JS. Structure and function of the platelet integrin α_IIbβ₃. J Clin Invest, 2005, 115(12): 3363-3369.
6. Pawelczyk M, Glabiński A, Kaczorowska B, et al. sP-and sE-selectin in stroke patients with metabolic disorders. Neurol Neurochir Pol, 2018, 52(5): 599-605.
7. Wardlaw JM, Sandercock PA, Dennis MS, et al. Is breakdown of the blood-brain barrier responsible for lacunar stroke, leukoaraiosis, and dementia?. Stroke, 2003, 34(3): 806-812.
8. 中华医学会神经病学分会, 中华医学会神经病学分会脑血管病学组. 中国脑小血管病诊治共识. 中华神经科杂志, 2015, 48(10): 838-844.
9. Oksala NK, Heikkinen M, Mikkelsson JA, et al. Smoking and the platelet fibrinogen receptor glycoprotein IIb/IIIA Pl(A1/A2) polymorphism interact in the risk of lacunar stroke and midterm survival. Stroke, 2007, 38(1): 50-55.
10. Fiodorenko-Dumas Ż, Dumas I, Mastej K, et al. Receptor GP IIb/IIIa as an indicator of risk in vascular events. Clin Appl Thromb Hemost, 2019, 25: 1-8.
11. 许海霞, 李国丽, 王洪权, 等. 血小板活化标记物与脑小血管病相关性研究. 内蒙古医学杂志, 2016, 48(9): 1036-1038.
12. Petter J, Eriksson-Franzen M, Oweling M, et al. Platelets and inflammatory parameters do not affect long-term survival after acute stroke. J Stroke Cerebrovasc Dis, 2016, 25(8): 1936-1938.
13. Hein TW, Singh U, Vasquez-Vivar J, et al. Human C-reactive protein induces endothelial dysfunction and uncoupling of eNOS in vivo. Atherosclerosis, 2009, 206(1): 61-68.
14. Rajeshwar K, Kaul S, Al-Hazzani A, et al. C-Reactive protein and nitric oxide levels in ischemic stroke and its subtypes: correlation with clinical outcome. Inflammation, 2012, 35(3): 978-984.
15. Woywodt A, Gerdes S, Ahl B, et al. Circulating endothelial cells and stroke: influence of stroke subtypes and changes during the course of disease. J Stroke Cerebrovasc Dis, 2012, 21(6): 452-458.
16. Fan H, Yang S, Li Y, et al. Assessment of homocysteine as a diagnostic and early prognostic biomarker for patients with acute lacunar infarction. Eur Neurol, 2018, 79(1/2): 54-62.
17. Lehmann MF, Kallaur AP, Oliveira SR, et al. Inflammatory and metabolic markers and short-time outcome in patients with acute ischemic stroke in relation to TOAST subtypes. Metab Brain Dis, 2015, 30(6): 1417-1428.
18. Wiseman S, Marlborough F, Doubal F, et al. Blood markers of coagulation, fibrinolysis, endothelial dysfunction and inflammation in lacunar stroke versus non-lacunar stroke and non-stroke: systematic review and meta-analysis. Cerebrovasc Dis, 2014, 37(1): 64-75.

West China Medical Journal

The relationship of platelet activating factors and vascular endothelial activity markers to lacunar infarction

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