Abstract
Background: Symptomatic intracranial atherosclerotic Disease (sICAD) is associated with the risk of recurrence of cerebral ischemic events in 4-19% of stroke patients annually. Previous studies indicate elevated high-sensitivity C-Reactive Protein (hs-CRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) to be associated with risk of recurrence.
Objective: This prospective, observational study investigated serum levels of hs-CRP and the activity of Lp-PLA2 in patients with sICAD in predicting the risk of long-term stroke recurrence.
Methods: We enrolled 48 patients with sICAD at 3 months from onset. The demographics, clinical, and imaging characteristics were recorded. Serum hs-CRP and Lp-PLA2 activity were assessed using automated high-sensitivity C-reactive protein assay and photometric technique, respectively. Patients were followed up at 6 months and 1 year and the presence of new vascular events was recorded.
Results: The mean age of our study population was 59.5 ± 10.3 years and 91.7% were men. Four patients developed recurrent strokes during follow-up. The mean Hs-CRP was elevated in patients with events than in patients without events (5.9 ± 10.4 mg/L vs. 1.7 ± 2.4 mg/L, P=0.03). However, there was no significant association of mean Lp-PLA2 activity (118.3±42.9 nmol/min/ml vs. 111.9 ± 34.2 nmol/min/ml, P=0.73) with recurrence. Elevation of hs-CRP (3.02 ± 4.8 mg/L vs. 0.95 ± 0.57mg/L, P=0.02) and Lp-PLA2 activity (120.1±40.3 nmol/min/ml vs. 103.3 ± 23.9 nmol/min/ml, P=0.04) was correlated with high-grade stenosis in these patients.
Conclusion: Our study suggests serum levels of hs-CRP may serve as a predictor of long-term stroke recurrence risk in sICAD and elevation of hs-CRP and Lp-PLA2 correlated with the severity of stenosis in symptomatic intracranial atherosclerotic disease.
Keywords: Biomarker, intracranial atherosclerosis, high sensitivity C-reactive protein, lipoprotein-associated phospholipase A2, stroke recurrence, plaque.
Graphical Abstract
[http://dx.doi.org/10.1056/NEJMoa1105335] [PMID: 21899409]
[http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2013.08.002] [PMID: 24119624]
[http://dx.doi.org/10.1212/01.wnl.0000208404.94585.b2] [PMID: 16636236]
[http://dx.doi.org/10.3174/ajnr.A3209] [PMID: 22859280]
[http://dx.doi.org/10.1016/j.atherosclerosis.2012.04.013] [PMID: 22727191]
[http://dx.doi.org/10.1161/STROKEAHA.112.661702] [PMID: 22798326]
[http://dx.doi.org/10.1212/01.WNL.0000132637.30287.B4] [PMID: 15249606]
[http://dx.doi.org/10.1016/j.atherosclerosis.2010.07.007] [PMID: 20691971]
[http://dx.doi.org/10.1212/01.wnl.0000263186.20988.9f] [PMID: 17536050]
[http://dx.doi.org/10.1016/j.atherosclerosis.2007.05.013] [PMID: 17604035]
[http://dx.doi.org/10.1111/j.1600-0404.2006.00715.x] [PMID: 17156267]
[http://dx.doi.org/10.1016/j.atherosclerosis.2011.04.031] [PMID: 21620406]
[http://dx.doi.org/10.1161/01.STR.0000089920.93927.A7] [PMID: 14500938]
[http://dx.doi.org/10.1155/2013/850714] [PMID: 24023414]
[http://dx.doi.org/10.1161/01.STR.32.4.917] [PMID: 11283392]
[http://dx.doi.org/10.1373/clinchem.2006.070672] [PMID: 16873290]
[http://dx.doi.org/10.1161/01.CIR.0000116763.91992.F1] [PMID: 14757686]
[http://dx.doi.org/10.1159/000172633] [PMID: 19018137]
[http://dx.doi.org/10.1016/j.amjcard.2008.04.015] [PMID: 18549868]
[http://dx.doi.org/10.1371/journal.pone.0130473] [PMID: 26098634]
[http://dx.doi.org/10.1111/jcmm.13803] [PMID: 30094934]
[http://dx.doi.org/10.1016/j.clinbiochem.2017.08.019] [PMID: 28899631]
[http://dx.doi.org/10.1097/WNR.0000000000000765] [PMID: 28272264]
[http://dx.doi.org/10.1016/S0735-1097(01)01554-6] [PMID: 11691499]
[http://dx.doi.org/10.1016/j.atherosclerosis.2005.05.006] [PMID: 15982658]
[http://dx.doi.org/10.1212/WNL.0000000000001938] [PMID: 26311748]
[http://dx.doi.org/10.1161/STROKEAHA.117.018700] [PMID: 29167386]
[http://dx.doi.org/10.4103/aian.AIAN_86_18] [PMID: 30258264]