| Background and Purpose: Atherosclerosic stenosis of intracranial and extracranial arteries is the most common cause of ischemic stroke.Moreover chronic inflammation has received increasing attention in recent years as a cause of atherosclerosis and has been proved to play an important role in initiation,progression and loss of stability,even rupture of plaque.Recently lipoprotein-associated phospholipase A2 is a novel specific inflammatory markers associated with vulnerable plaque in serum.At present,the previous research about Lp-PLA2 and atherosclerotic plaque was based on the extracranial carotid or coronary artery plaque,but there are no studies on the associations between Lp-PLA2 and intracranial atherosclerotic plaque.As imaging technology has progressed,high-resolution magnetic resonance imaging(HRMRI)could clearly show vascular wall and morphology and composition of plaque in main intracranial arteries characterized by sensitivity and specifity.This study aims to investigate the association of Lp-PLA2 level and intracranial plaque assessed by HRMRI in patients with moderate or severe intracranial arteries stenosis,including cerebral middle artery or basilar artery,and to explore whether Lp-PLA2 is a biomarker of intracranial unstable plaque to offer effective guidlines.Methods:1 A total of 64 patients with ischemic cerebrovascular diseases(cerebral infarction and transient ischemic attacks)were selected at admission from January 2016 to December 2016 in Neurology 3 department of Cangzhou center hospital.There were 44 patients in case group and 20 subjects in control group.2 All patients underwent computed tomographic angiography(CTA)after admission.Based on the CTA results,44 patients with ≥50% middle cerebralartery(MCA)or basilar artery(BA)stenosis identified by computed tomographic angiography constituted the case group who were diagnosed as ischemic cerebrovascular disease and the control group was composed of 20 patients with normal CTA.3 44 patients after informed consent underwent HRMRI of intracranial plaque in the magnetic resonance imaging department using GE 3.0T MRI machine.Intracranial vunerable plaques:(1)intraplaque hemorrhage(T1WI and T2 WI showed high signals,there were enhancent on T1WI);(2)enhancing plaque(eccentric enhancent on T1WI);(3)mixed plaque:(mixed signals on T1 WI and T2WI).According to the characteristics of plaques signals in HRMRI,the characteristics of intracranial plaques were preliminarily analyzed to classify into stable or unstable plaque.4 Groups4.1 Based on the nature of intracranial plaque,the patients in case group were divided into two groups: unstable plaque group(n=23,52.27%)and stable plaque group(n=21,47.73%).4.2 According to target vessel where plaque originated from whether was responsible for neurological symptoms,the case patients were categorized into2 groups: responsible vascular symptoms(n=18,40.9%)and non-responsible vascular symptoms(n=26,59.1%).The responsible vascular symptom group included 7(39%)patients with transient cerebral ischemic attack and 11(61%)cases of cerebral infarction.4.3 The patients with non-responsible vascular symptoms were divided into 2groups: unstable plaque group(n=10,38.5%)and stable plaque group(n=16,61.55%)according to the nature of plaque.5 All patients were followed up for history and physical examination in detail after admission.And baseline clinical datas were recorded.6 Fasting venous blood samples were taken for subsequent analysis at second days after admission.The levels of Lp-PLA2 in serum were measured using an enzyme-linked immunoassay(ELISA),and high-sensitive C-reactive protein(hs-CRP)was measured using the latex agglutination test.And at thesame time routine biochemical tests were performed,including LDC-C,TC,HDL-C,glycerol three lipids,homocysteine and so on.7 Statistical methods were used to analyze the general baseline data,Lp-PLA2,hs-CRP levels,and other blood biochemical parameters.Results:1 In total,64 patients were enrolled in this study,including 44 cases(61.7±10.0years;52.3% male)and 20 patients with a mean age of 59.6±6.6 years including men(n=9,45.0%)in control group.2 Comparison among groups2.1 The mean Lp-PLA2 was significantly greater in unstable(216.98± 68.59ng/ml vs 127.05±47.77ng/ml,P<0.001)and stable patients(176.33± 49.28ng/ml vs 127.05±47.77ng/ml,P=0.007)than control subjects.2.2 Compared with the control group,the serum hs-CRP levels in the case group was significantly higher(21.8(16.0-28.8)mg/L vs 5.6(2.2-10.2)mg/L,P<0.001;12.9(8.9-22.9)mg/L vs 5.6(2.2-10.15)mg/L,P<0.001).2.3 Lp-PLA2 and hs-CRP were significantly higher in patients with unstable plaque compared with stable plaque(216.98±68.59ng/ml vs 176.33-49.28ng/ml,P=0.020;21.8(16.0-28.8)mg/L vs 12.9(8.9-22.9)mg/L,P=0.014).3 There was significant difference for hs-CRP between responsible vascular symptoms and non-responsible vascular symptoms(23.8(18.7-31.5)mg/L vs12.3(19.6-28.8)mg/L,P<0.001),but not for Lp-PLA2(206.69±60.74ng/ml vs191.26±94.79ng/ml,P=0.430).4 Moreover,Lp-PLA2 and hs-CRP level were not significantly higher between asymptomatic patients with unstable or stable plaque(206.69 ±60.74 ng/ml vs191.26±64.79ng/ml,P=0.430;17.3(11.2-21.2)mg/L vs 10.6(8.5-21.88)mg/L,P=0.246).5 Logistic regression showed that the neurological symptoms(OR9.71(1.05-90.00),P=0.045)and the serum Lp-PLA2 level(OR11.90(1.18-120.05),P=0.036)were independently associated with unstable intracranial plaque assessed by HRMRI.Conclusions:1 This preliminary study demonstrated that the level of Lp-PLA2 in serum was increased in patients with moderate or severe MCA or BA stenosis and unstable plaque based on HRMRI.2 These findings strongly support previous point that role for Lp-PLA2 was a marker for vulnerable plaque.Lp-PLA2 may be a relevant biomarker that could identify vulnerable intracranial stenosis to guide for early intervention and treatment in asymptomatic patients with intracranial artery disease.3 In addition,HRMRI was a current effective adjunct for intracranial plaque.A multi-marker strategy that coupled biology and imaging could improve identification of at-risk asymptomatic atherosclerotic lesions to guide effective therapy. |