叶酸、维生素B6、维生素B12对冠心病的二级预防作用

目的探讨服用叶酸、维生素B6、维生素B12对中国人群冠心病的二级预防效果。方法随机双盲法将100例心肌梗死后3个月至5年的冠心病患者分为叶酸治疗组及对照组,叶酸治疗组中再分为高同型半胱氨酸(Hcy)组及Hcy正常组。观察3～5年Hcy变化、临床理化指标及临床终点事件包括总死亡、冠心病死亡、非致死性心肌梗死、非心梗性冠心病心绞痛恶化住院,对经皮穿刺腔内冠状动脉成形术(PTCA)及冠状动脉旁路移植术(CABG)需求。结果叶酸治疗组Hcy水平均有显著下降(P<0.001),但临床终点事件却未能有明显改善。结论叶酸、维生素B6、维生素B12长期治疗不具有冠心病二级预防效益。     

叶酸、B族维生素对高同型半胱氨酸血症脑梗死患者血管内皮细胞功能的影响

将120例高同型半胱氨酸(Hcy)血症的脑梗死患者随机分为治疗组和对照组,治疗组口服叶酸、维生素B6、维生素B12,对照组不服用上述药物.治疗前和治疗4周后分别测定血浆Hcy水平及内皮素(ET)、一氧化氮(NO)水平.发现治疗组治疗4周后,血浆Hcy、ET水平明显降低,NO水平明显升高.提示叶酸、B族维生素干预治疗能降低血浆Hcy水平,对高Hcy血症脑梗死患者血管内皮细胞功能损害有一定的改善作用.     

血浆同型半胱氨酸水平与帕金森病相关研究

目的探讨血浆同型半胱氨酸（homocysteine,Hcy）水平与帕金森病（Parkinson＇s disease,PD）之间的相关性,观察B族维生素、恩他卡朋治疗左旋多巴诱导的高同型半胱氨酸血症的疗效。方法选择年龄及性别基本匹配的PD病例90例（未治疗的病例15例、非左旋多巴治疗的病例21例、左旋多巴治疗的病例54例）。体检健康老年人90例。检测PD患者、健康老年人的血浆同型半胱氨酸、维生素B12和叶酸水平。将左旋多巴治疗的PD病例采用随机数字表法随机分为3组,分别给予口服安慰剂、B族维生素（维生素B12 1 mg/d、叶酸500 ug/d）和恩他卡朋200 mg/d,检测三组用药前后的血浆Hcy水平。结果各组血浆Hcy水平差异有统计学意义（F=25.580,P=0.001）。PD患者血浆Hcy水平高于健康老年人组（P〈0.05）。左旋多巴治疗PD组血浆Hcy水平高于未治疗PD组和非左旋多巴胺治疗PD组（P〈0.05）。PD组叶酸水平低于健康老年人组（P〈0.05）。维生素B12、叶酸和恩他卡朋均能使左旋多巴治疗的PD患者血浆Hcy水平下降（P〈0.05）。相关分析显示,PD患者血浆Hcy水平与叶酸水平呈负相关（r=-0.425,P=0.000）。结论高同型半胱氨酸血症可能是帕金森病的危险因素之一,并与缺乏B族维生素和使用左旋多巴治疗有一定的联系。B族维生素、恩他卡朋可能降低左旋多巴引起的高同型半胱氨酸血症。     

维生素干预治疗对阿尔茨海默病病人血浆同型半胱氨酸水平的影响

目的探讨阿尔茨海默病(AD)病人血浆同型半胱氨酸(Hcy)水平的变化及维生素干预治疗对AD病人血浆Hcy水平的影响。方法选取75例AD病人为病例组,71例同龄非痴呆老人为对照组,测定两组血浆Hcy、叶酸、维生素B12水平,并随机选取15例AD病人接受口服叶酸5mg及维生素B12500μg,每日晨服1次,干预治疗4周。结果AD病人血浆Hcy水平显著高于对照组(P<0.001),血浆叶酸水平、维生素B12显著低于对照组(P<0.001),接受维生素干预治疗的15例AD病人,4周后血浆Hcy水平下降(P<0.001),叶酸及维生素B12水平均升高(P<0.001)。结论AD病人存在血浆高Hcy水平;AD血浆Hcy水平升高与饮食中摄入维生素不足关系密切,维生素干预治疗能够有效地降低AD病人血浆Hcy水平。     

冠心病患者同型半胱氨酸水平及叶酸、维生素B6和B12的干预效果

目的观察冠心病患者同型半胱氨酸（Hcy）水平与血浆叶酸、维生素B12浓度之间的关系,以及高同型半胱氨酸血症联合补充叶酸、维生素B6和维生素B12对Hcy水平的影响。方法冠心病患者332例,正常对照组194例。采用高压液相色谱法测定空腹血浆Hcy水平,应用放免分析法测定基础血浆叶酸及维生素B12浓度。Hcy水平高于15μmol/L者为高同型半胱氨酸血症,随机分为治疗组（55例）和对照组（43例）,均为冠心病患者,治疗组予以每日补充叶酸5mg,维生素B620mg,每日3次,维生素B120.5mg,,每日1次,4周后复查血浆Hcy水平。结果冠心病患者血浆Hcy水平高于正常组,基础叶酸浓度明显低于正常组,直线相关分析结果显示冠心病组血浆Hcy水平与基础叶酸浓度呈明显负相关（r=-0.149,P<0.05）,治疗组4周后Hcy水平平均降低了37.7%,治疗前后Hcy水平有显著差异（P<0.01）,结论冠心病患者Hcy水平较正常对照组显著升高,联合补充叶酸、维生素B6和维生素B12可明显降低冠心病患者高同型半胱氨酸血症者的血浆Hcy水平。     

对原发性高血压伴缺血性脑卒中患者血浆同型半胱氨酸水平的临床观察

目的 :探讨叶酸、维生素B6、腺苷辅酶维生素B12 对原发性高血压伴缺血性脑卒中患者血浆同型半胱氨酸 (Hcy)水平的影响。方法 :血浆Hcy水平增高的缺血性脑卒中住院患者 70例分为干预组 (n =3 5 )和对照组 (n =3 5 )。干预组口服叶酸10mg/d ,维生素B610mg/d ,腺苷辅酶维生素B12 5 0 0 μg/d 4周。对照组未服用上述药物。入院时及 4周后采用高压液相色谱法 (HPLC)测定血浆Hcy含量。结果 :干预组在实施叶酸、维生素B6、腺苷辅酶维生素B12 干预 4周后 ,血浆Hcy水平下降 ,与对照组相比有显著性差异 (P <0 0 5 )。两组患者 4周前后血浆Hcy水平的变化差值具有极显著性差异 (P <0 0 0 1)。结论 :口服叶酸、维生素B6、腺苷辅酶维生素B12 可使原发性高血压伴缺血性脑卒中患者血浆Hcy水平下降     

叶酸和维生素B12、B6对阿尔茨海默症患者血浆Hcy、血脂水平的影响

目的观察叶酸和维生素B12、B6对阿尔茨海默症患者血浆同型半胱氨酸(Hcy)、血脂水平的影响。方法选择阿尔茨海默症患者42例,随机分为干预组和对照组,各21例。两组常规治疗相同,干预组同时服用叶酸和维生素B12、B6,均治疗30 d。治疗前后检测两组血浆Hcy、D-二聚体(D-D)、纤维蛋白原(FIB)和血脂,并进行长谷川痴呆量表(HDS)评分。结果干预组治疗后血浆Hcy、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、极低密度脂蛋白胆固醇(LDL-V)、D-D、FIB下降水平高于对照组(P均<0.05),HDS评分高于对照组(P<0.05)。结论补充叶酸和维生素B12、B6可降低阿尔茨海默症患者血浆Hcy和血脂水平。     

同型半胱氨酸水平在急性脑梗死再发中的作用

目的 探讨血清同型半胱氨酸（homocysteine,Hcy）水平对脑梗死再发的影响.方法 选择急性脑梗死患者105例,健康对照组90例,比较两者的血清Hcy、叶酸及维生素B12水平;脑梗死组再随机分为A组和B组,A组给予抗血小板、他汀类及活血化瘀等药物,同时口服叶酸和甲钴胺;B组仅给予抗血小板、他汀类及活血化瘀等药物,随访12 m复查血清Hcy水平;观察治疗1年内脑梗死的再发情况.结果 （1）治疗前脑梗死组的Hcy水平显著高于健康对照组,其叶酸和维生素B12水平显著低于对照组（P＜0.001）;且脑梗死组的Hcy水平与叶酸、维生素B12水平呈负相关（P＜0.001）.（2）治疗前A、B两组Hcy水平无显著差异（P＞0.05）,治疗后两者Hcy水平有显著差异（P＜0.001）;A组治疗后Hcy水平显著低于治疗前（P＜0.001）;B组治疗前后Hcy水平无显著差异（P＞0.05）;（3）A组1年内脑梗死再发率为15.01％,B组为21.15％,两组比较差异无统计学意义（P＞0.05）.结论 高同型半胱氨酸血症是脑梗死的危险因素,给予叶酸和维生素B12治疗可有效降低脑梗死患者Hcy水平,但对脑梗死再发影响不大.     

急性脑梗死患者血浆Hcy水平及相关因素分析

目的探讨血浆同型半胱氨酸(Hcy)在急性脑梗死发生发展中的作用,并分析其相关因素。方法取30例急性脑梗死患者为观察组,同期30例健康体检者为对照组。采用化学发光法检测两组血浆Hcy、维生素B12及叶酸水平。两组均行颈动脉彩超检查,测定颈动脉内膜中层厚度(IMT),观察有无动脉粥样硬化。结果观察组血浆Hcy水平明显高于对照组(P<0.05);高Hcy血症(Hcy>15μmol/l)发生率明显高于对照组P<0.05;血浆维生素B12及叶酸水平均明显低于对照组、P均<0.05。观察组23例高Hcy血症患者中,血浆维生素B12下降15例,叶酸下降12例,两者同时下降7例。血浆Hcy水平与维生素B12及叶酸水平呈显著负相关(r分别为-0.624、-0.719,P均<0.01)。观察组IMT明显高于对照组,颈动脉粥样硬化发生率明显高于对照组,P均<0.05。直线相关分析表明,血浆Hcy水平与颈动脉IMT呈正相关(r=0.489,P<0.001)。结论急性脑梗死患者血浆Hcy水平升高,其与维生素B12及叶酸水平呈负相关,与颈动脉粥样硬化程度呈正相关。     

血浆同型半胱氨酸水平与脑梗死复发率的关系

目的研究血浆同型半胱氨酸水平与3年内脑梗死复发率的关系。方法 220例脑梗死患者,根据血浆同型半胱氨酸水平分为82例正常同型半胱氨酸组(A组)和138例高同型半胱氨酸组(未干预为B组,干预为C组),其中69例高同型半胱氨酸患者予以口服维生素B6、叶酸等控制同型半胱氨酸水平,追踪观察3年,观察3组脑梗死复发率。结果随访期间,正常同型半胱氨酸组3年内脑梗死复发率为6.6%,高同型半胱氨酸未干预组复发率为14.5%,高同型半胱氨酸干预组复发率为7.6%,B组复发率远高于A组,差异有统计学意义(P<0.05),C组发病率略高于A组,但差异无统计学意义(P>0.05)。结论血浆同型半胱氨酸水平与脑梗死复发有相关性,控制同型半胱氨酸水平可降低脑梗死复发率。     

Reduction of homocysteine levels in coronary artery disease by low-dose folic acid combined with vitamins B6 and B12

An increased plasma homocysteine concentration is a risk factor for atherosclerosis. Folic acid lowers homocysteine but the optimal dose in patients with coronary artery disease (CAD) is unclear. This placebo-controlled, single-blind, dose-ranging study evaluates the effect of low-dose folic acid on homocysteine levels in 95 patients aged 61 +/- 11 years (mean +/- SD) with documented CAD. Patients in each group were given either placebo or 1 of 3 daily supplements of folic acid (400 microg, 1 mg, or 5 mg) for 3 months. Each active treatment arm also received 500 microg vitamin B12 and 12.5 mg vitamin B6. Total plasma homocysteine levels were measured after 30 and 90 days. Folic acid 400 microg reduced homocysteine levels from 13.8 +/- 8.8 to 9.6 +/- 2.0 micromol/L at 90 days (p = 0.001). On 1- and 5-mg folic acid, levels decreased from 13.0 +/- 6.4 to 9.8 +/- 4.0 micromol/L (p = 0.001) and from 14.8 +/- 6.9 to 9.7 +/- 3.3 micromol/L (p < 0.001), respectively. The decrease was similar in all treatment groups. There was no significant change with placebo. Although the sample size is small, these findings suggest that daily administration of 400 microg/day folic acid combined with vitamin B12 and vitamin B6 may be equivalent to higher doses in reducing homocysteine levels in patients with CAD.     

叶酸、VitB_(12)和VitB_6在冠心病防治中的作用

本文对近年来国内外有关叶酸、Vit B6 、Vit B1 2 在冠心病防治中的作用进行综述 ,其机制主要是通过降低血清同型半胱氨酸的浓度 ,改善了冠心病患者血管内皮功能 ,调节血小板聚集 ,血管张力和血栓形成 ,从而支持了补充 B族维生素能降低心血管疾病危险性的观点     

Randomized trial of folic acid supplementation and serum homocysteine levels

BACKGROUND: Lowering serum homocysteine levels with folic acid is expected to reduce mortality from ischemic heart disease. Homocysteine reduction is known to be maximal at a folic acid dosage of 1 mg/d, but the effect of lower doses (relevant to food fortification) is unclear. METHODS: We randomized 151 patients with ischemic heart disease to 1 of 5 dosages of folic acid (0.2, 0.4, 0.6, 0.8, and 1.0 mg/d) or placebo. Fasting blood samples for serum homocysteine and serum folate analysis were taken initially, after 3 months of supplementation, and 3 months after folic acid use was discontinued. RESULTS: Median serum homocysteine level decreased with increasing folic acid dosage, to a maximum at 0.8 mg of folic acid per day, when the homocysteine reduction (placebo adjusted) was 2.7 micromol/L (23%), similar to the known effect of folic acid dosages of 1 mg/d and above. The higher a person's initial serum homocysteine level, the greater was the response to folic acid, but there were statistically significant reductions regardless of the initial level. Serum folate level increased approximately linearly (5.5 nmol/L for every 0.1 mg of folic acid). Within-person fluctuations over time in serum homocysteine levels, measured in the placebo group, were large compared with the effect of folic acid, indicating that monitoring of the reduction in an individual is impractical. CONCLUSIONS: A dosage of folic acid of 0.8 mg/d appears necessary to achieve the maximum reduction in serum homocysteine level across the range of homocysteine levels in the population. Current US food fortification levels will achieve only a small proportion of the achievable homocysteine reduction.     

MTHFR C677T基因多态性对稳定性冠心病患者叶酸降低同型半胱氨酸治疗的影响

目的探讨MTHFR C677T基因多态性对河南中部汉族稳定性冠状动脉粥样硬化性心脏病(冠心病)患者叶酸降低同型半胱氨酸(Hcy)治疗的影响。方法连续入选2018年4月至2018年9月于许昌市中心医院心血管内科住院的冠心病患者362例,依据MTHFR C677T基因检测结果分为A(CC型)、B(CT型)、C(TT型)三组,三组患者均在冠心病二级预防治疗的基础之上给予叶酸片降低Hcy治疗。记录患者应用叶酸治疗前、治疗后1个月、3个月血浆Hcy的变化,计算三组治疗3个月时降低Hcy治疗有效率,并对影响降低Hcy治疗的因素进行二元logistic回归分析。结果A、B、C三组分别有81例(22.4%)、169例(46.7%)和112例(30.9%)患者,三组治疗前血浆Hcy水平差异无统计学意义(P>0.05);三组治疗1个月和3个月血浆Hcy水平均低于治疗前,且A组治疗1个月时血浆Hcy水平低于B组和C组,差异均有统计学意义(P<0.05)。A组治疗有效率高于B组和C组,差异有统计学意义(P<0.05)。二元logistic回归分析显示,CC型患者降低Hcy治疗有效的可能是TT型患者的2.626倍,有熬夜史患者降低Hcy治疗有效的可能是无熬夜史患者的44.3%。结论MTHFR C677T基因多态性对稳定性冠心病患者叶酸降低Hcy治疗有影响,患者在降低Hcy治疗时应改变熬夜习惯。     

同型半胱氨酸与叶酸、维生素B12及维生素B6的关系

目的　探讨正常人群血同型半胱氨酸 (Hcy)水平分布及Hcy与年龄和性别的关系 ,Hcy水平与叶酸 ,维生素B1 2 及维生素B6之间的关系。方法　应用高效液相色谱 (HPLC)荧光检测法测定6 88例正常人血浆Hcy水平 ,用放射免疫方法测定叶酸及维生素B1 2 水平 ,用 96孔板微生物学法测定血清维生素B6水平。结果　相关分析结果显示 :血浆Hcy水平在正常人中呈非正态分布 ,随年龄增长血浆Hcy水平增加 ,男性比女性高。血浆Hcy水平与维生素B6、维生素B1 2 及叶酸水平呈负相关 (r分别为 - 0 35 4 8,- 0 2 91 6 ,- 0 32 76 ,P值均 <0 0 1 )。高Hcy血症者较非高Hcy血症者其血维生素B6、维生素B1 2 及叶酸水平均明显降低 (P值均 <0 0 1 )。结论　正常人中增高的血浆Hcy浓度与体内的维生素水平低下有关。     

伴高同型半胱氨酸的老年女性高血压急症患者叶酸治疗的5年预后

目的研究伴高同型半胱氨酸(Hcy)老年女性高血压急症患者叶酸治疗的5年预后。方法入选伴高Hcy(>10μmol/L)血症的老年女性高血压急症患者319例,随机分低剂量组(叶酸0.4mg/d)159例和高剂量组(叶酸0.8mg/d)160例。嘱患者规律服药降压治疗,补充叶酸。出院后通过复诊或电话随访5年,记录相关事件,并进行分析。结果随访5年结束时,高剂量组缺血性脑卒中入院发生率明显低于低剂量组(41.0%vs 54.4%,P=0.02)。高剂量组直立性低血压发生率明显低于低剂量组(45.8%vs 68.4%,P=0.00)。高剂量组较低剂量组降低23.5%的缺血性脑卒中再住院发生率(P=0.021)。结论在稳定降压、限钠、补充维生素B12的基础上,补充叶酸0.8mg/d可更好的预防老年女性高血压急症患者的心脑血管事件。     

Secondary prevention with folic acid: effects on clinical outcomes

OBJECTIVES: We sought to conduct a randomized trial with folic acid 0.5 mg/day in a patient population with stable coronary artery disease (CAD). BACKGROUND: Folic acid has favorable effects on vascular endothelium and lowers plasma homocysteine levels. In addition, homocysteine appears to be an independent risk factor for atherosclerotic disease. However, the value of folic acid in secondary prevention had seldom been tested. METHODS: In this open-label study, 593 patients were included; 300 were randomized to folic acid and 293 served as controls. Mean follow-up time was 24 months. At baseline all patients had been on statin therapy for a mean of 3.2 years. RESULTS: In patients treated with folic acid, plasma homocysteine levels decreased by 18%, from 12.0 +/- 4.8 to 9.4 +/- 3.5 micromol/l, whereas these levels remained unaffected in the control group (p < 0.001 between groups). The primary end point (all-cause mortality and a composite of vascular events) was encountered in 31 (10.3%) patients in the folic acid group and in 28 (9.6%) patients in the control group (relative risk 1.05; 95% confidence interval: 0.63 to 1.75). In a multifactorial survival model with adjustments for clinical factors, the most predictive laboratory parameters were, in order of significance, levels of creatinine clearance, plasma fibrinogen, and homocysteine. CONCLUSIONS: Within two years, folic acid does not seem to reduce clinical end points in patients with stable coronary artery disease (CAD) while on statin treatment. Homocysteine might therefore merely be a modifiable marker of disease. Thus, low-dose folic acid supplementation should be treated with reservation, until more trial outcomes become available.     

Effect of folic acid on endothelial function following acute myocardial infarction

The aim of this study was to test the influence of high-dose folic acid (10 mg/d) on endothelial function in patients referred for coronary intervention after an acute myocardial infarction (AMI) and determine its relation to homocysteine levels. Flow-mediated dilation (FMD) of the brachial artery was performed in 40 patients after AMI (16 with normal homocysteine levels and 24 patients with elevated levels [>11 micromol/L]). Subjects were randomized to receive first folic acid (10 mg/day; group A) or placebo (group B) for 6 weeks in a double-blind crossover trial with a 2-week washout. Plasma folate, total homocysteine and its subtypes (oxidized, reduced, and protein-bound), FMD, and nitroglycerin-mediated dilation were assessed at baseline and at 6 and 14 weeks. In group A, folic acid improved FMD from 3.98 +/- 0.35% to 6.44 +/- 0.56% (p <0.001). This effect persisted after the crossover with placebo (5.42 +/- 0.59, p = 0.13). In group B, placebo did not increase FMD (4.01 +/- 0.34% vs 4.46 +/- 0.38, p = 0.38); however, a significant increase was observed in the second active treatment period (6.49 +/- 0.56%, p = 0.005). In both groups, improved FMD neither correlated with basal levels of homocysteine and its subtypes nor with changes induced during the folate treatment. Nitroglycerin-mediated dilation did not change significantly in either group. Folic acid increased FMD in both normo- and hyperhomocysteinanemic groups (p = 0.006 and p <0.001). In conclusion, 6-week treatment with high-dose folic acid improves endothelial function in post-AMI patients, independent from homocysteine status. Folic acid can be recommended to improve postinfarction endothelial dysfunction in patients with normo- and hyperhomocysteinemia.     

Optimization of folic acid, vitamin B(12), and vitamin B(6) supplements in pediatric patients with sickle cell disease

Using homocysteine as a functional marker, we determined optimal folic acid, vitamin B(12), and vitamin B(6) dosages in 21 pediatric sickle cell disease (SCD) patients (11 HbSS, 10 HbSC; 7-16 years). Daily supplements of folic acid (400, 700, or 1,000 microg), vitamin B(12) (1, 3, or 5 U.S. 1989 RDA), and vitamin B(6) (1 or 3 U.S. 1989 RDA) were gradually increased in an 82-week dose-escalation study. Blood was taken at 9 occasions for measurements of erythrocyte (RBC) and serum folate, plasma vitamin B(12), whole-blood vitamin B(6), and plasma homocysteine. Augmentation of folic acid from 700 to 1,000 microg and vitamin B(12) from 3 to 5 RDA did not further decrease homocysteine. Percentages of patients exhibiting significant individual homocysteine decreases amounted to 43% (folic acid from 0 to 400 microg, vitamins B(12) and B(6) from 0 to 1 RDA), 14% (folic acid from 400 to 700 microg), 24% (vitamin B(12) from 1 to 3 RDA), and 18% (vitamin B(6) from 1 to 3 RDA ). The lowest plasma homocysteine at 82 weeks was 5.9 +/- 2.2 micromol/L. Patients with HbSS had higher RBC folate than HbSC. The entire group exhibited an inverse relation between RBC folate and hemoglobin. We conclude that RBC folate is less valuable for folate status assessment in SCD patients. Optimal dosages are as follows: 700 microg folic acid (3.5-7 U.S. 1989 RDA), 3 U.S. 1989 RDA vitamin B(12) (4.2-6.0 microg), and 3 U.S. 1989 RDA vitamin B(6) (4.2-6.0 mg). A practical daily combination is 1 mg folic acid (4.3-8.5 U.S. 1998 RDA when taken with meals), 6 microg vitamin B(12) (2.5-5 U.S. 1998 RDA), and 6 mg vitamin B(6) (4.6-10 U.S. 1998 RDA). This combination may by simple and relatively inexpensive means reduce these patients' inherently high risk of endothelial damage.     

Effect of folic acid combined with pravastatin on arteriosclerosis in elderly hypertensive patients with lacunar infarction

This study aimed to assess the effect of folic acid combined with pravastatin on atherosclerosis-related indexes in elderly patients with hypertension complicated with lacunar cerebral infarction.A total of 134 elderly hypertensive patients with lacunar cerebral infarction were randomly divided into 3 groups using the random number table method. Group A, the folic acid group, had 45 cases and received low-dose folic acid (0.8 mg/d) treatment on the basis of antihypertensive treatment. Group B, the pravastatin group, had 45 cases and received pravastatin (20 mg/d) treatment on the basis of antihypertensive treatment. Group C, the folic acid combined with the pravastatin group, had 44 cases. Members of this group received pravastatin (20 mg/d) and low-dose folic acid (0.8 mg/d) based on antihypertensive treatment. Levels of folic acid, homocysteine (Hcy), tumor necrosis factor alpha (TNF-a), matrix metallopeptidase 9 (MMP-9), cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) were measured by ELISA before treatment in all 3 groups. Carotid intima-media thickness (IMT) was measured using ultrasound, and systolic and diastolic blood pressure were measured with a mercury column. After 8 weeks of treatment, the levels of folic acid, Hcy, TNF-a, MMP-9, TC, LDL-C, and systolic and diastolic blood pressure were compared among the 3 groups. IMT levels were measured at 12 weeks of treatment.After 8 weeks of treatment, compared with group B, patients in groups A and C had folic acid levels significantly higher than baseline levels, with significantly lower Hcy levels (both P < .05). Patients in group C presented significantly decreased TNF-a, MMP-9, TC, and LDL-C levels and systolic and diastolic blood pressure after 8 weeks of treatment, compared with those in groups A and B (both P < .05). These patients also showed significantly decreased IMT levels compared with those in the other groups (P < .05).Low-dose folic acid combined with pravastatin in elderly patients with lacunar cerebral infarction can reduce the level of homocysteine, improve the degree of carotid atherosclerosis, protect vascular endothelium, and reduce blood lipids and blood pressure, presenting better benefits than pravastatin alone.