摘要
目的观察瑞舒伐他汀联合替米沙坦治疗持久性心房颤动(房颤)患者的临床疗效并探讨其作用机制。方法选择2015年2月至2018年2月沧州市中心医院收治的120例诊断为持久性房颤患者,按信封法将患者随机分为两组,每组60例。研究组给予瑞舒伐他汀联合替米沙坦治疗,对照组给予替米沙坦治疗,治疗6个月后观察临床疗效。观察两组患者治疗前后静息心率的变化。采用心脏超声检测两组患者左心房内径、左心房左右径、左心房球形指数与左心室收缩期末容积、左心室舒张期末容积、左心室后壁厚度;采用酶联免疫吸附试验(ELISA)检测血清肿瘤坏死因子-a (TNF-a)、白细胞介素-6(IL-6)水平;采用免疫比浊法检测血清超敏C-反应蛋白(hs-CRP)水平;采用免疫发光法检测血浆N末端B型钠尿肽前体(NT-proBNP)水平。结果研究组治疗后静息心率较治疗前明显下降(次/min :76.37±7.25比89.76±8.79, P<0.05),对照组治疗前后静息心率比较差异无统计学意义(次/min : 90.71 ±8.56比87.80±6.26, P>0.05),而研究组治疗后静息心率水平明显低于对照组(次/min :76.37±7.25比87.80±6.26, PV0.05)。两组治疗后左心房内径、左心房左右径、左心房球形指数、左心室舒张期末容积均较治疗前增加,但研究组治疗后上述指标均低于对照组〔左心房内径(mm): 40.68 ±3.86 tt 41.99 ±3.97,左心房左右径(mm): 41.07 ± 2.85 比 42.69 ± 2.90,左心房球形指数:0.77±0.08 比 0.86±0.07,左心室舒张期末容积(mL): 107.48±32.90 比 118.98±35.75,均 PV0.05〕;两组治疗前后左心室收缩期末容积与左心室后壁厚度比较差异均无统计学意义〔研究组:左心室收缩期末容积(mL)为 38.59±12.37 比 39.81 ± 12.03,左心室后壁厚度(mm)为 11.34±2.39 比 12.80±3.27;对照组:左心室收缩期末容积(mL)为39.90± 11.54比40.65±11.50,左心室后壁厚度(mm)为11.90±2.57比12.99±3.16,均P>0.05〕。两组治疗后血清TNF-a、IL-6、hs-CRP水平均较治疗前明显下降,且研究组治疗后上述指标均明显低于对照组〔TNF-a (ng/L):29.76±5.31 比 36.63±5.11, IL-6(ng/L): 14.37±3.36 比 22.65±4.58, hs-CRP(mg/L): 13.68 ±2.75比20.63 ±2.69,均P<0.05〕。对照组治疗后血浆NT-pmBNP水平较治疗前明显升高(咧:431.80±42.54比365.89±39.81, P<0.05),研究组治疗前后血浆NT-proBNP比较差异无统计学意义(ng/L :351.80±38.76比346.89±35.82, P>0.05),故研究组治疗后血浆NT-proBNP水平明显低于对照组(P<0.05)。结论瑞舒伐他汀联合替米沙坦可以防治持久性房颤患者左心房重构,延缓左心室泵功能减退。分析其机制可能与瑞舒伐他汀联合替米沙坦能降低患者血清炎症因子水平有关。
Objective To investigate the clinical efficacy and mechanism of rosuvastatin combined with telmisartan in the treatment of persistent atrial fibrillation. Methods One hundred and twenty patients with persistent atrial fibrillation admitted to Cangzhou Central Hospital from February 2015 to Februaiy 2018 were enrolled and they were divided into study group and control group by random envelope method, with 60 patients in each group. The patients in study group were treated with rosuvastatin combined with telmisartan;and in control group they were treated with telmisartan, and after treatment for 6 weeks the clinical efficacy was observed. Resting heart rates were observed in two groups. The left atrial inner diameter, left atrium left and right diameter, left atrial sphericity index and left ventricular end diastolic volume, left ventricular end systolic volume, left ventricular posterior wall thickness of two groups were detected by ultrasond before and after treatment;the levels of serum tumor necrosis factor- a (TNF- a) and interleukin-6 (IL-6) were tested by enzyme linked immunosorbent assay (ELISA) in two groups before and after treatment;and the level of serum hypersensitive C-reactive protein (hs-CRP) was detected by immunoturbidimetry;the level of plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) was tested by immunoluminometric assay. Results Resting heart rate was significantly decreased in study group after treatment compared with that before treatment (bpm: 76.37 ±7.25 vs. 89.76 ± 8.79, P < 0.05), while in control group, the comparison of resting heart rate before and after treatment was of no statistical significant differences (bpm: 90.71 + 8.56 vs. 87.80 ± 6.26, P > 0.05), resulting that the post-treatment resting heart rate of study group was significantly lower than that of control group (bpm: 76.37 ± 7.25 vs. 87.80 ± 6.26, P < 0.05). After treatment, the left atrial inner diameter, left atrium left and right diameter,left atrial sphericity index and left ventricular end diastolic volume were increased compared with those before treatment in both groups;after treatment, above various index levels in study group were lower than those of control group [left atrial inner diameter (mm): 40.68 ± 3.86 vs. 41.99 ± 3.97, left atrium left and right diameter (mm): 41.07 ± 2.85 vs. 42.69 ± 2.90, left atrial sphericity index: 0.77 ± 0.08 vs. 0.86 ±0.07, left ventricular end diastolic volume (mL): 107.48 ±32.90 vs. 118.98 ± 35.75, all P < 0.05]. There were no statistical significant differences between the two groups in left ventricular end systolic volume and posterior wall thickness of left ventricle after treatment [study group: left ventricular end systolic volume (mL) was 38.59 ± 12.37 vs. 39.81 ± 12.03, posterior wall thickness of left ventricle (mm) was 11.34 ±2.39 vs. 12.80 ± 3.27, control group: left ventricular end systolic volume (mL) was 39.90 ± 11.54 vs. 40.65 ± 11.50, posterior wall thickness of left ventricle (mm) was 11.90 ± 2.57 vs. 12.99 ±3.16, all P > 0.05], Besides, the serum levels of TNF- a , IL-6 and hs-CRP were obviously decreased in two groups after treatment (all P < 0.05), after treatment, above indexes in study group were significantly lower than those in control group [TNF- a (ng/L): 29.76 ±5.31 vs. 36.63 ± 5.11, IL-6 (ng/L): 14.37 ±3.36 vs. 22.65 ±4.5& hs-CRP (mg/L): 13.68 ±2.75 vs. 20.63 ±2.69, all P < 0.05]. Plasma NT-proBNP was increased in control group after treatment compared with that before treatment (|ig/L: 431.80 ±42.54 vs. 365.89 ± 39.81, P < 0.05), whereas there was no significant difference in the study group between pre- and post-treatment (^ig/L: 351.80 ±38.76 vs. 346.89 ±35.82, P > 0.05), resulting in post-treatment plasma NT-proBNP significantly lower in study group (P < 0.05). Conclusions Rosuvastatin combined with telmisartan can prevent left atrial remodeling in patients with persistent atrial fibrillation and delay the dysfunction of left ventricular pump. The therapeutic mechanism was related to the decrease in the levels of serum inflammatory factors in patients treated with such therapy.
作者
李晓红
胡亚民
刘丽娜
张剑波
刘海霞
吴萍
Li Xiaohong;Hu Yamin;Liu Lina;Zhang Jianbo;Liu Haixia;Wu Ping(Department of Cardiology,Cangzhou Central Hospital,Cangzhou 061000,Hebei,China)
出处
《中国中西医结合急救杂志》
CAS
CSCD
北大核心
2019年第2期176-180,共5页
Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
关键词
瑞舒伐他汀
替米沙坦
心房颤动
持久性
炎症反应
心房重构
Rosuvastatin
Telmisartan
Persistent atrial fibrillation
Inflammatory response
Atrial remodeling
