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目的:观察非瓣膜性心房颤动(NVAF)患者经阿司匹林和(或)阿托伐他汀干预后血浆溶血磷脂类分子(LPA/AP)含量的变化。方法:测定169例NVAF患者血浆溶血磷脂酸(LPA)及其相似总磷脂(AP)含量,并与124例正常对照者进行比较。169例NVAF患者随机分为NVAF对照组(n=52)、阿司匹林组(n=61)和阿司匹林+阿托伐他汀组(n=56),NVAF对照组不予任何处理,阿司匹林组予阿司匹林(100mg/d),阿司匹林加阿托伐他汀组予阿司匹林(100mg/d)和阿托伐他汀(10mg/d)。检测三组患者治疗前和治疗后3个月和1年时的血浆LPA/AP含量,观察3个月和1年时各组卒中发生情况。结果:NVAF患者血浆LPA及AP含量分别为(3.56±0.42)μmol/L和(6.12±0.57)U,显著高于正常对照者的(2.65±0.44)μmol/L和(4.68±0.45)U(P均<0.01)。治疗前、治疗后3个月和1年时,NVAF对照组血浆LPA含量分别为(3.61±0.49)、(3.52±0.51)和(3.66±0.59)μmol/L,AP分别为(6.23±0.59)、(6.47±0.61)和(6.36±0.79)U,无显著差异;阿司匹林组LPA分别为(3.53±0.46)、(3.12±0.62)和(2.94±0.60)μmol/L,AP分别为(6.37±0.66)、(5.64±0.52)和(5.33±0.61)U,治疗后LPA和AP均较治疗前显著下降(P<0.01);阿司匹林+阿托伐他汀组LPA分别为(3.59±0.33)、(2.58±0.50)和(2.46±0.48)μmol/L,AP分别为(6.19±0.53)、(4.98±0.50)和(4.64±0.58)U,治疗后LPA和AP均较治疗前显著下降(P<0.01),且较阿司匹林组下降更显著(P<0.01)。NVAF对照组、阿司匹林治疗组和阿司匹林+阿托伐他汀组3个月卒中发病例数分别为7、6和3例,1年时分别为16、11和6例,阿司匹林组和阿司匹林+阿托伐他汀组显著少于NVAF对照组(P<0.01),阿司匹林+阿托伐他汀组显著少于阿司匹林组(P<0.05)。结论:NVAF患者血浆LPA/AP含量显著升高,提示其体内血小板处于活化状态,NVAF患者存在缺血性膜损伤。阿司匹林或阿司匹林与阿托伐他汀联合应用均可显著降低NVAF相关性卒中的发生。NVAF患者在实施抗栓治疗时可考虑加用他汀类药物。
Objective: To observe the changes of plasma lysophospholipid molecules (LPA / AP) after aspirin and / or atorvastatin intervention in patients with nonvalvular atrial fibrillation (NVAF). Methods: Plasma lysophosphatidic acid (LPA) and its similar total phospholipid (AP) were measured in 169 patients with NVAF and compared with 124 normal controls. A total of 169 patients with NVAF were randomly divided into NVAF control group (n = 52), aspirin group (n = 61) and aspirin + atorvastatin group (n = 56) 100 mg / d), aspirin plus atorvastatin (aspirin 100 mg / d) and atorvastatin (10 mg / d). Plasma LPA / AP levels were measured before treatment, 3 months and 1 year after treatment, and the incidence of stroke at 3 months and 1 year was observed. Results: The levels of plasma LPA and AP in patients with NVAF were (3.56 ± 0.42) μmol / L and (6.12 ± 0.57) U, respectively, which were significantly higher than those in the normal controls (2.65 ± 0.44 μmol / L and 4.68 ± 0.45 U P <0.01). The levels of LPA in the NVAF control group were (3.61 ± 0.49), (3.52 ± 0.51) and (3.66 ± 0.59) μmol / L before treatment, 3 months and 1 year after treatment, respectively, and were 6.23 ± 0.59 , (6.47 ± 0.61) and (6.36 ± 0.79) U, respectively. The aspirin group had (LP) 3.53 ± 0.46, 3.12 ± 0.62 and 2.94 ± 0.60 μmol / L, (P <0.01); LPA in aspirin + atorvastatin group was (3.59 ± 0.33), ( 2.58 ± 0.50) and (2.46 ± 0.48) μmol / L, respectively. The AP was 6.19 ± 0.53, 4.98 ± 0.50 and 4.64 ± 0.58 U, respectively. 0.01), and more significantly than the aspirin group (P <0.01). The incidence of stroke at three months in NVAF control group, aspirin treatment group and aspirin + atorvastatin group were 7, 6 and 3 respectively, with 16, 11 and 6 cases at 1 year, aspirin group and aspirin + The statin group was significantly less than the NVAF control group (P <0.01), aspirin + atorvastatin group was significantly less than the aspirin group (P <0.05). Conclusions: Plasma LPA / AP levels in patients with NVAF are significantly increased, suggesting that platelets in vivo are activated and that NVAF patients have ischemic membrane damage. Aspirin or aspirin combined with atorvastatin can significantly reduce the incidence of NVAF-related stroke. NVAF patients in the implementation of antithrombotic therapy may consider adding statins.