通心络胶囊治疗冠心病(附90例疗效观察)

目的　观察通心络胶囊治疗冠心病的临床疗效。方法　对 180例住院的冠心病患者 ,随机分成 2组。对照组 90例在应用极化液及消心痛等常规治疗的基础上加通心络胶囊 ,3次 /d ,3片 /次 ,疗程均为 1个月。结果　临床疗效 :治疗组总有效率 87 78% ,对照组 70 0 0 % (P <0 0 5 ) ;心电图疗效 :总有效率治疗组84 4 4% ,对照组 72 2 2 % (P <0 0 5 ) ;血流变及血脂疗效 :治疗后两组各指标差异显著 (P <0 0 5 ,P <0 0 1) ,治疗组治疗前后比较 ,全血黏度与纤维蛋白差异显著 (P <0 0 1) ,其余各项观察指标差异显著 (P <0 0 5 )。结论　通心络胶囊具有降脂、抗凝、增强纤溶活性 ,改善血管内皮细胞功能 ,缓解冠心病缺血程度 ,促进受损心肌修复     

通心络胶囊对不同载脂蛋白E基因冠状动脉粥样硬化性心脏病的影响

目的应用基因测序技术观察通心络胶囊对不同载脂蛋白E(ApoE)基因冠状动脉粥样硬化性心脏病(CHD)的治疗效果,并探究ApoE基因多态性与治疗前后CHD中医证型证候积分、血脂水平的相关性,为中医辨证施治CHD提供分子生物学依据。方法将118例CHD患者采用随机、对照、盲法试验设计,分为2组,对照组予单硝酸异山梨酯缓释片40mg,每日1次口服;酒石酸美托洛尔片25mg,每日2次口服;阿司匹林肠溶片25mg,每日1次口服;治疗组在对照组基础上同时予通心络胶囊3粒,每日3次口服。分别检测不同中医证型的ApoE基因多态性和治疗前后血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C),统计证候积分,比较通心络胶囊对不同ApoE等位基因、不同ApoE基因表型、不同证型CHD的中医证候积分和血脂水平的差异及疗效。结果 2组中医证候总积分治疗前后比较差异有统计学意义(P0.05),治疗后中医证候总积分组间比较差异有统计学意义(P0.05)。2组ε2、ε3、ε4各等位基因治疗前后自身比较,气阴两虚证、痰阻心脉证、心血瘀阻证均有统计学意义(P0.05);治疗组ε4与ε2、ε3比较,痰阻心脉证积分降低改善率最高(P0.05),其他各基因表型间的气阴两虚证及心血瘀阻证改善率比较差异无统计学意义(P0.05),治疗组ε4型改善率痰阻心脉证疗效最好,优于ε2、ε3型;对照组各等位基因对于气阴两虚证、痰阻心脉证、心血瘀阻证积分改善率比较差异无统计学意义(P0.05)。2组组内各不同基因表型调脂疗效比较,TC、LDL-C降低和HDL-C升高的改善率比较差异有统计学意义(P0.05),TG降低的改善率比较差异无统计学意义(P0.05),2组组间各相同基因表型间治疗前后改善率比较差异无统计学意义(P0.05)。结论通心络胶囊干预CHD疗效显著,对不同ApoE基因CHD的不同中医证型的疗效均具有影响,但对气阴两虚证、痰阻心脉证、心血瘀阻证具有明显疗效,尤以痰阻心脉证疗效最为显著;可有效降低TC、LDL-C和升高HDL-C。     

通心络胶囊联合瑞舒伐他汀钙片治疗冠心病不稳定型心绞痛的临床效果及对血脂、血清炎症因子水平的影响

目的探讨通心络胶囊联合瑞舒伐他汀钙片治疗冠心病不稳定型心绞痛的临床效果及对血脂、血清炎症因子水平的影响。方法选择我院2018年6月至2019年6月收治的80例冠心病不稳定型心绞痛患者作为研究对象,采用随机数字表法将其分为对照组(40例,基础治疗+瑞舒伐他汀钙片)和观察组(40例,基础治疗+瑞舒伐他汀钙片+通心络胶囊)。比较两组患者的临床疗效、血脂和血清炎症因子水平。结果观察组的治疗总有效率明显高于对照组(P<0.05)。治疗后,两组的TC、TG、LDL-C水平均降低,HDL-C水平均升高,且观察组明显优于对照组(P<0.05)。治疗后,两组的hs-CRP、TNF-α、IL-6水平均降低,且观察组明显低于对照组(P<0.05)。结论通心络胶囊联合瑞舒伐他汀钙片治疗冠心病不稳定型心绞痛的临床效果显著,可改善患者的血脂水平,减轻组织炎性反应程度,值得在临床上推广和应用。     

通心络胶囊联合β-受体阻滞剂及其他抗心衰药物对老年高血压合并慢性心力衰竭患者心功能的影响

目的探究通心络胶囊联合β-受体阻滞剂及其他抗心衰药物对老年高血压合并慢性心力衰竭患者心功能的影响。方法纳入2017年1月至2018年3月来本院就诊的高血压伴慢性心力衰竭老年患者共计90例,随机将其分为对照组和观察组,各45例。对照组患者给予硝苯地平+美托洛尔+贝那普利治疗,观察组患者在对照组基础上联合通心络胶囊治疗。比较两组患者的治疗效果、心脏功能及不良反应发生情况。结果观察组的治疗总有效率高于对照组(P<0.05)。治疗后,两组LVESD、LVEDD、BNP水平均降低,LVEF和6MWT均升高,且观察组优于对照组(P<0.05)。两组的恶心呕吐、头晕、皮疹及肝、肾功损害发生率比较,差异无统计学意义(P>0.05)。结论通心络胶囊联合β-受体阻滞剂及其他抗心衰药物应用于老年高血压伴慢性心力衰竭患者中,有利于提高治疗效果,改善心脏功能,值得临床推广和应用。     

Inhibiting leukocyte-endothelial cell interactions by Chinese medicine Tongxinluo capsule alleviates no-reflow after arterial recanalization in ischemic stroke

Aims

Despite successful vascular recanalization in stroke, one-fourth of patients have an unfavorable outcome due to no-reflow. The pathogenesis of no-reflow is fully unclear, and therapeutic strategies are lacking. Upon traditional Chinese medicine, Tongxinluo capsule (TXL) is a potential therapeutic agent for no-reflow. Thus, this study is aimed to investigate the pathogenesis of no-reflow in stroke, and whether TXL could alleviate no-reflow as well as its potential mechanisms of action.

Methods

Mice were orally administered with TXL (3.0 g/kg/d) after transient middle cerebral artery occlusion. We examined the following parameters: neurological function, no-reflow, leukocyte-endothelial cell interactions, HE staining, leukocyte subtypes, adhesion molecules, and chemokines.

Results

Our results showed stroke caused neurological deficits, neuron death, and no-reflow. Adherent and aggregated leukocytes obstructed microvessels as well as leukocyte infiltration in ischemic brain. Leukocyte subtypes changed after stroke mainly including neutrophils, lymphocytes, regulatory T cells, suppressor T cells, helper T type 1 (Th1) cells, Th2 cells, B cells, macrophages, natural killer cells, and dendritic cells. Stroke resulted in upregulated expression of adhesion molecules (P-selectin, E-selectin, and ICAM-1) and chemokines (CC-chemokine ligand (CCL)-2, CCL-3, CCL-4, CCL-5, and chemokine C-X-C ligand 1 (CXCL-1)). Notably, TXL improved neurological deficits, protected neurons, alleviated no-reflow and leukocyte-endothelial cell interactions, regulated multiple leukocyte subtypes, and inhibited the expression of various inflammatory mediators.

Conclusion

Leukocyte-endothelial cell interactions mediated by multiple inflammatory factors are an important cause of no-reflow in stroke. Accordingly, TXL could alleviate no-reflow via suppressing the interactions through modulating various leukocyte subtypes and inhibiting the expression of multiple inflammatory mediators.