| BackgroundThe high morbidity and mortality of cerebrovascular disease has brought great harm to human beings and society.Acute cerebral infarction is the most common cause of disability and death in the elderly.It is a common and frequently occurring disease.A large number of studies have shown that the main pathological basis of it is atherosclerosis.74%of ischemic cerebral infarction is Atherosclerotic cerebral infarction accounts.Carotid atherosclerosis is a manifestation of systemic atherosclerosis.Plaque hemorrhage,plaque rupture,thrombosis,aneurysm formation are secondary changes of carotid plaques.Carotid artery as the upper blood vessel of cerebral blood circulation,the rupture of unstable plaque in the carotid artery is the independent risk factor of ischemic.cerebral infarction.As a new marker of inflammatory response,lipoprotein-associated phospholipase A2 has received more and more attention.Recent studies have suggested that atherosclerosis is caused by chronic inflammation of blood vessels.Lp-PLA2 is involved in the occurrence and development of atherosclerosis.Neovascularization in carotid plaques is an important factor for plaque instability.Studies have shown that it is associated with chronic inflammation of the blood vessels.Contrast enhanced ultrasound(CEUS)has become an important auxiliary technique for ultrasound examination,which can clearly show the carotid artery adventitia nutrient vessels and plaque neovascularization.Since the neovascularization and Lp-PLA2 plaques are associated with vascular inflammation,what is the connection between the two?What roles do they play in the occurrence of acute ischemic cerebral infarction?In this study,the development of new blood vessels in the plaque was analyzed by ultrasonography.We analyzed the relationship among carotid plaque stability,plasma Lp-PLA2 level and ACI from the perspective of neovascularization.ObjectiveTo detect the diagnostic value of plasma lipoprotein-associated phospholipase A2(Lp-PLA2)and the CEU degree of neovascularization of carotid artery plaque in diagnosis of acute cerebral infarction(ACI),and the relationship between them.Methods1.Research objectThe subjects were divided into two groups:ACI group and non ACI group.ACI group was 44 patients with acute anterior circulation cerebral infarction in our hospital from July 2015 to September 2016.There were 41 cases of unstable plaque in non ACI group in the same period.2.Carotid ultrasonography and contrast-enhanced ultrasonography.We used VividE9 ultrasound diagnostic apparatus,9L probe(frequency of 6MHz)for carotid ultrasound contrast examination.The carotid artery was continuously swept and the target plate was selected.Sound of Italy Braceo company(SonoVue)contrast agent was selected.Contrast agent was injected into the median cubital vein.Real time contrast enhanced ultrasound contrast agent was used to observe the contrast-enhanced ultrasound images until 5 min.Then the image was saved and saved it for later analysis.According to the literature data,the development of neovascularization in plaque was classified:No enhanced neovascularization signal(grade ?);The signals of blood vessels in and around the plaques were in a punctate distribution(grade ?);The new blood vessels in the plaques showed scattered punctate and linear distribution(grade?);In the plaques,the blood vessels were diffuse or multiple linear(grade IV).3.Plasma Lp-PLA2 determinationIn the morning,ACI group and non ACI group of elbow vein was taken 4 mL fasting blood.The blood samples with sodium citrate were collected for 30 min,and centrifuged 15min(3000 r/min)at the temperature of 2 to 8?,then the plasma was separated and stored under-20? for preservation.The plasma levels of Lp-PLA2 were detected by double antibody sandwich immunochromatography assay.Results1.Comparison of development and classification of neovascularization in carotid plaques in ACI group and non ACI group:In ACI group,there were 3 cases of contrast agent development intensity of ? grade,accounting for 6.82%;8 cases of contrast agent development intensity of ? grade,accounting for 18.18%;23 cases of contrast agent development intensity of ? grade,accounting for 52.27%;10 cases of contrast agent development intensity of ? grade,accounting for 22.73%.In non-ACI group,there were 19 cases of contrast agent development intensity of ? grade,accounting for 46.34%;15 cases of contrast agent development intensity of ? grade,accounting for 36.59%;5 cases of contrast agent development intensity of ? grade,accounting for 12.20%;2 cases of contrast agent development intensity of ? grade,accounting for 4.88%.The classification of new blood vessels in carotid plaque was significantly higher than that in non ACI group,the difference between the two groups was statistically significant(Z =-5.29,P = 0.00).The grade of neovascularization in ACI group was mostly III and IV(median ?),accounting for 75.0%.Those of non-ACI group was mostly I and II(median ?),accounting for 82.9%.2.Comparison of plasma Lp-PLA2 levels between ACI group and non ACI group:The plasma Lp-PLA2 level of group ACI was 247.37 ± 58.30?g/L,the plasma Lp-PLA2 level of non ACI group was 156.88 ±66.78?g/L,the ACI group was significantly higher than that of non ACI group,the difference was statistically significant(t = 6.64,P = 0.00).Analysis of diagnostic performance of plasma Lp-PLA2 on ACI by ROC curve analysis,to determine the optimal maximum Youden index critical value,the cutoff value was 199.76?g/L,the sensitivity was 84.10%,specificity was 68.30%,the area under the curve was 0.84,diagnostic accuracy was 84.10%.3.The higher the grade of neovascularization of carotid plaque,the higher the levels of plasma Lp-PLA2(rs,0.60,P<0.001),and there was a positive correlation between them.Conclusion1.The CEU degree of neovascularization of carotid artery plaque and the evel of plasma lipoprotein-associated phospholipase A2 of ACI group was higher than that of ACI group.Both of them might be a risk factor for ACI.2.There was a positive correlation between the CEU degree of neovascularization of carotid artery plaque and the evel of plasma lipoprotein-associated phospholipase A2. |
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