曲美他嗪治疗冠心病伴慢性心力衰竭的临床疗效

目的观察曲美他嗪治疗冠心病伴慢性心力衰竭的临床疗效。方法120例冠心病合并慢性心力衰竭的患者,随机分为对照组(常规治疗)和曲美他嗪组各60例(常规治疗加曲美他嗪20mg,3次/d),观察3个月。结果曲美他嗪组的心衰缓解情况、超声心动图的心功能指标均显著优于对照组(P<0.05)。结论常规药物联合曲美他嗪治疗冠心病伴慢性心力衰竭是一种疗效确切,安全简便的方法,值得临床推广使用。     

盐酸曲美他嗪治疗稳定型心绞痛临床疗效观察

目的观察盐酸曲美他嗪（万爽力）治疗稳定型心绞痛的临床效果。方法将50例稳定型劳力型心绞痛患者随机分为两组。观察组25例,予口服万爽力20mg,3次/d、联合倍他乐克（美托洛克）、伯基（肠道阿司匹林）、长效的硝酸脂类、辛伐他汀等治疗;对照组25例,予口服倍他乐克、伯基、长效的硝酸脂类、辛伐他汀等治疗,12周为1个疗程。观察两组用药前后心绞痛发作情况、运动耐受改善情况、心功能及血压、心率、心电图的变化。结果观察组与对照组均能减少心绞痛发作,运动耐受及心电图均得到改善,但两组比较差异有统计学意义（P〈0.05）。结论万爽力联合其他药物对稳定型心绞痛患者疗效显著。     

曲美他嗪联合培哚普利治疗慢性充血性心力衰竭疗效观察

目的观察曲美他嗪（TMZ）联合培哚普利治疗慢性充血性心力衰竭（CHF）患者的临床疗效。方法72例CHF患者随机分为研究组和对照组，均给予内科常规抗心衰治疗。对照组加服培哚普利，初始剂量2mg，每日1次，逐渐加至靶剂量4mg，每日1次；研究组在对照组的基础上接受曲美他嗪20mg／次，3次/d。治疗12周。结果治疗12周，两组心功能较治疗前有明显改善，治疗组临床总有效率为93．4％，较对照组（80．6％）显著提高（P〈0．05）；超声心动图LVEF均较治疗前有明显改善（P〈0．01或P〈0．051．但治疗组较对照组改善更为显著（P〈0．05）。治疗组LVEDD、LVESD、LADD均较治疗前改善，差异有显著性（P〈0．01或P〈0．05），而对照组无改善；两组均未发现有明显的不良反应。结论TMZ联合培哚普利治疗CHF是一种安全有效的方法。     

卡维地洛联合曲美他嗪辅助治疗慢性充血性心力衰竭疗效观察

目的观察卡维地洛联合曲美他嗪治疗慢性充血性心力衰竭（CHF）的临床疗效。方法选择慢性CHF患者60例，随机分为两组：对照组30例，给予洋地黄制剂、利尿剂、血管扩张剂、血管紧张素转换酶抑制剂（ACEI）等常规药物治疗；治疗组30例，在常规药物治疗基础上加用卡维地洛（2次／d，25mg／次，疗程60d）和曲美他嗪（3次/d，20mg／次，疗程60d）。结果治疗组心功能改善有效率为90．0％，明显高于对照组的60、0％（P〈0．01）。治疗前后相比，治疗组心率、血压、左室射血分数、左室舒张末期容积、左室收缩末期容积均有显著改善（P〈0．01或P〈0．05），治疗组与对照组比较差异有统计学意义（P〈0、01或P〈0．05）。结论用卡维地洛和曲美他嗪辅助治疗慢性CHF是一种安全有效的方法。     

曲美他嗪对冠心病舒张性心力衰竭的疗效观察

目的观察曲美他嗪对冠心病舒张性心力衰竭(Diastolic heart failure,DHF)的临床疗效。方法入选冠心病伴DHF病人86例,随机分为曲美他嗪组44例和对照组42例。对照组采用常规治疗,曲美他嗪组加用曲美他嗪,60mg/d,疗程6个月。在治疗前后检测6分钟步行试验及心脏超声。结果治疗后曲美他嗪组6分钟步行距离(561±63)m,较治疗前(310±49)m改善;与对照组(417±58)m比较差异有显著性。两组治疗后左心室舒张功能超声指标优于治疗前,且曲美他嗪组优于对照组。结论曲美他嗪治疗冠心病DHF病人可改善心脏舒张功能,提高活动耐量。     

Trimetazidine modulates AMPA/kainate receptors in rat vestibular ganglion neurons

Trimetazidine (1[2,3,4-trimethoxy-benzyl] piperazine, 2 HCl) is an anti-ischemic agent frequently administered as a prophylactic treatment for episodes of angina pectoris and chorioretinal disturbances. It is also employed as a symptomatic treatment of vertigo but its mechanism of action is yet to be defined. Using Fura-2 fluorescence photometry and whole-cell patch-clamp recordings we investigated the effect of trimetazidine on the [Ca(2+)](i) and current responses induced by the application of non-N-methyl-D-aspartate (NMDA) receptor agonists on low density vestibular ganglion neuronal cultures explanted from 3 day s postnatal rats. Trimetazidine blocked the [Ca(2+)](i) and current responses induced by 100 microM applications of both kainate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA). These responses were dependent on external Ca(2+) and were blocked by the voltage-dependent Ca(2+) channel blockers Ni(2+) and Cd(2+) . Trimetazidine only acts on the AMPA/kainate receptors and had no effect on K(+)-induced depolarizations. Dose-dependent curves were obtained for the inhibition by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and trimetazidine (IC(50) 7 microM and 0.7 microM) of kainate stimulations. After AMPA stimulation, dose-response inhibition curves showed an IC(50) of 3 microM for CNQX and 25 microM for trimetazidine. These results indicate that trimetazidine could be a potent antagonist of AMPA/kainate receptors in vestibular ganglion neurons. This may explain the protective role of trimetazidine in the inner ear suggesting an anti-excitotoxic activity.     

曲美他嗪与低分子肝素治疗不稳定型心绞痛临床观察

目的:观察低分子肝素与曲美他嗪治疗不稳定型心绞痛(UAP)的疗效。方法:172例UAP患者随机分为2组,其中对照组88例;两组均常规给予硝酸酯类、β-受体阻滞剂及阿司匹林等;治疗给予低分子肝素钠4000 IU,2次/d,皮下注射,连用5~7d,加用曲美他嗪20?,每日3次及心电图改变情况。结果:治疗组临床总有效率为90.91%,对照组总有效率为69.05%,治疗组明显优于对照组(P<0.01)。治疗后治疗组ST段下降导联数(NST)ST段下降的数值总和(ΣST)及心肌缺血总负荷均较治疗前显著改善(P<0.01)。治疗组有5例皮下瘀斑,2例进展为AM I;而对照组有8例进展为AM I。结论:低分子肝素联用曲美他嗪,治疗UAP安全有效。     

The acute effect of trimetazidine on the high frequency fatigue in the isolated Rat diaphragm muscle

The objective of this study was to determine the acute effect of trimetazidine (TMZ) on the pre-fatigue, fatigue and post-fatigue contractile characteristics and tension-frequency relationships of isolated rat diaphragm muscle. Muscle strips were taken from the ventral-costal aspects of the diaphragm muscle of rats killed by decapitation. The muscle strips were suspended in organ baths containing Krebs solution, with a gas mixture of 95% O2 and 5% CO2 at 37 degrees C and pH 7.35-7.45. After determining the thermoregulation and optimum muscle length the muscles were subjected to direct supramaximal stimulation with 0.05 Hz frequency square pulses for periods of 0.5 msec to obtain control values. After adding 5 x 10(-6) and 5 x 10(-5) M trimetazidine solution to the respective bath media, the contractile parameters of the muscles were recorded. The contractile parameters were also recorded for both the trimetazidine and trimetazidine-free media after application of the high frequency fatigue protocols. Later, the tension-frequency relationship was determined by applying stimulating pulses of 10, 20, 50 and 100 Hz to the muscle strips. Whilst the twitch tension obtained from the 5 x 10(-6) and 5 x 10(-5) M trimetazidine media showed numerical increases compared to that of the controls, these were not statistically significant (p>0.05). The contraction time exhibited a dose dependent increase (p<0.001), whilst the contraction and relaxation rates did not differ significantly. The isometric contraction forces obtained with the different stimulating frequencies showed a significant increase in the tetanic contraction only at 100 Hz (p<0.05). A comparison of the pre- and post-fatigue twitch tensions in the trimetazidine media showed the post- fatigue twitch tensions to be significantly higher than those of the pre-fatigue contraction forces (p<0.05). In the 5 x 10(-6) and 5 x 10(-5) M trimetazidine media the increases in the post-fatigue contraction force were 22 and 30%, respectively. These results demonstrated that in isolated rat diaphragm muscle, TMZ significantly limited the mechanical performance decrease during fatigue. It is our opinion that trimetazidine contributed to the observed fatigue tolerance by eliminating the factors of fatigue, due to preservation of intracellular calcium homeostasis, provision of the ATP energy levels needed by ATPase dependent pumps and especially by keeping the intracellular pH within certain limits.     

曲美他嗪治疗老年冠心病心力衰竭的疗效及其对患者 炎症因子的影响

目的 探讨美托洛尔联合曲美他嗪治疗老年冠心病心力衰竭的疗效。方法 收集我院自2016年8月~2018年9月收治的76例冠心病心力衰竭患者,按随机数字表法分为观察组和对照组,各38例。两组均给予标准化心力衰竭治疗方案治疗,对照组加服酒石酸美托洛尔片治疗,观察组在对照组基础上联合曲美他嗪片治疗,比较两组治疗前后超敏C反应蛋白（hs-CRP）、白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）水平及临床疗效。结果 治疗后,两组hs-CRP、IL-6、TNF-α水平均下降,且观察组低于对照组,差异有统计学意义（P＜0.05）,观察组总有效率为92.11%,高于对照组的73.68%,差异有统计学意义（P＜0.05）。结论 美托洛尔联合曲美他嗪能够有效提高老年冠心病心力衰竭患者心功能,减轻机体炎症反应。     

Trimetazidine Limits the Effects of Myocardial Ischaemia During Percutaneous Coronary Angioplasty

Summary

This open-label, randomised, controlled study is aimed at assessing the effect of pre-treatment with the metabolic agent trimetazidine on the degree of ischaemia during percutaneous transluminal coronary angioplasty (PTCA).

Overall 44 patients with one-vessel coronary artery stenosis (>70%) in the medial part of the left anterior descending artery were included. One group (n?=?22) was pre-treated with oral trimetazidine. The other group (n?=?22) was the control. All patients (n?=?44) were administered aspirin and conventional treatment.

All patients underwent PTCA; stents were implanted in 11 trimetazidine patients and in seven control patients.

The mean ST-segment elevation during all balloon inflations was significantly lower in the trimetazidine group than in the control group (?1.66?±?1.50?mm vs. 3.29?±?1.59?mm, p?=?0.001). Maximal ST-segment elevations and

mean ST elevation values during sequential balloon inflations were also significantly lower with trimetazidine (p?=?0.018). The mean amplitude of the T-wave alterations during all balloon inflations was significantly lower with trimetazidine (3.09?±?2.39?mm vs. 6.83?±?4.31?mm; p?=?0.001). Similarly, the maximal amplitude of the T-wave alterations was 4.50?±?2.90?mm with trimetazidine vs. 9.25?±?4.97?mm in control patients (p?=?0.0005). Angina and rhythm disturbances were more frequent in the control group. Time from balloon inflation to onset of angina was 50?±?26.2s with trimetazidine vs. 32?±?15.0s, for control group (p?=?0.03). The time to pain relief after deflation was 19.3?±?11.4s with trimetazidine vs. 28.2?±?16.8s (p?=?0.001).

Trimetazidine administered a few days before PTCA appears to be a cardioprotective agent for the prevention of myocardial ischaemia.