MHR、LMR与急性缺血性脑卒中患者颈动脉内膜增厚及早期神经功能恶化的关系

Correlation of MHR,LMR with carotid intima-media thickening and early neurological deterioration in patients with acute ischemic stroke

目的研究单核细胞计数和高密度脂蛋白胆固醇的比值(MHR)、淋巴细胞计数和单核细胞计数的比值(LMR)与急性缺血性脑卒中患者颈动脉内膜增厚及早期神经功能恶化(END)的关系。方法450例急性缺血性脑卒中患者,根据颈部血管超声测量结果分为内膜正常组(120例)和内膜增厚组(330例);根据美国国立卫生研究院卒中量表(NIHSS)评分变化情况分为END组(72例)和非END组(378例)。收集所有患者的临床资料,比较内膜正常组和内膜增厚组、END组和非END组的临床资料,并采用多因素Logistic回归分析急性缺血性脑卒中患者发生颈动脉内膜增厚和END的影响因素。结果内膜增厚组糖尿病史占比48.48%(160/330)、尿酸(UA)(359.62±103.31)μmol/L、MHR(0.41±0.25)高于内膜正常组的20.83%(25/120)、(331.72±105.00)μmol/L、(0.34±0.23),LMR(3.50±1.12)低于内膜正常组的(3.90±1.06),差异均具有统计学意义(P<0.05)。多因素Logistic回归分析显示,UA、MHR水平高是急性缺血性脑卒中患者发生颈动脉内膜增厚的独立危险因素(OR=1.003、3.323,P<0.05)。END组糖尿病史占比69.44%(50/72)、初次血糖(10.47±5.68)mmol/L、总胆固醇(TC)(4.55±0.17)mmol/L、低密度脂蛋白胆固醇(LDL-C)(2.57±0.11)mmol/L、LMR(3.91±0.80)高于非END组35.71%(135/378)、(8.52±4.31)mmol/L、(4.51±0.12)mmol/L、(2.53±0.14)mmol/L、(3.55±0.70),双抗治疗占比40.28%(29/72)、MHR(0.31±0.18)低于非END组的52.91%(200/378)、(0.41±0.25),差异均具有统计学意义(P<0.05)。多因素Logistic回归分析显示,有糖尿病史是急性缺血性脑卒中患者发生END的独立危险因素(OR=1.945,P<0.05),双抗治疗是急性缺血性脑卒中患者预防END的保护因素(OR=0.566,P<0.05)。结论MHR、UA可能与急性缺血性脑卒中患者发生颈动脉内膜增厚有关,推测血清中MHR和UA水平越高,颈动脉粥样硬化程度越严重。既往血糖异常为急性缺血性脑卒中患者发生END的独立危险因素,双抗治疗为缺血性脑卒中患者预防END的独立保护因素。

Objective To study the correlation of monocyte count to high-density lipoprotein cholesterol ratio(MHR)and lymphocyte-to-monocyte ratio(LMR)with carotid intima-media thickening and early neurological deterioration(END)in patients with acute ischemic stroke.Methods 450 patients with acute ischemic stroke were divided into normal group(120 cases)and intima-media thickening group(330 cases)based on cervical vascular ultrasound measurements;they were divided into END group(72 cases)and non-END group(378 cases)according to National Institutes of Health Stroke Scale(NIHSS)score.The clinical data of the two groups were collected,and the clinical data of the normal and the intima-media thickening group,the END group and the non-END group were compared.Multivariate Logistic regression was used to analyze the influencing factors of intima-media thickening and END in patients with acute ischemic stroke.Results In the intima-media thickening group,the proportion of history of diabetes mellitus was 48.48%(160/330),uric acid(UA)was(359.62±103.31)μmol/L,and MHR was(0.41±0.25),which were higher than those of 20.83%(25/120),(331.72±105.00)μmol/L,and(0.34±0.23)in the normal group;LMR of(3.50±1.12)in the intima-media thickening group was lower than that of(3.90±1.06)in the normal group;all differences were statistically significant(P<0.05).Multivariate Logistic regression analysis showed that high levels of UA and MHR were independent risk factors for carotid intima-media thickening in patients with acute ischemic stroke(OR=1.003,3.323;P<0.05).In END group,the proportion of history of diabetes mellitus was 69.44%(50/72),the initial blood glucose was(10.47±5.68)mmol/L,the total cholesterol(TC)was(4.55±1.07)mmol/L,the low density lipoprotein cholesterol(LDL-C)was(2.57±0.11)mmol/L,and LMR was(3.91±0.80),which were higher than those of 35.71%(135/378),(8.52±4.31)mmol/L,(4.51±0.12)mmol/L,(2.53±0.14)mmol/L,and(3.55±0.70)in the non-END group;the proportion of dual antibody therapy of 40.28%(29/72)and MHR of(0.31±0.18)in END group were lower than those of 52.91%(200/378)and(0.41±0.25)in non-END group;the differences were statistically significant(P<0.05).Multivariate Logistic regression analysis showed that a history of diabetes mellitus was an independent risk factor for END in patients with acute ischemic stroke(OR=1.945,P<0.05),and dual antibody therapy was a protective factor for preventing END in patients with acute ischemic stroke(OR=0.566,P<0.05).Conclusion MHR and UA may be related to the occurrence of carotid intima-media thickening in patients with acute ischemic stroke,and it is hypothesized that the higher the serum levels of MHR and UA,the more severe the degree of carotid atherosclerosis.Previous abnormal blood glucose is an independent risk factor for the occurrence of END in patients with acute ischemic stroke,and dual-antibody therapy is an independent protective factor for the prevention of END in patients with ischemic stroke.