促红细胞生成素治疗慢性心衰合并贫血的临床观察

目的:观察在慢性充血性心力衰竭合并贫血时标准治疗基础上加用促红细胞生成素(EPO)的临床疗效。方法:入选的57例伴有贫血的慢性充血性心力衰竭患者随机分为治疗组(30例)和对照组(27例)。对照组给予心衰的标准治疗,治疗组给予标准治疗同时给予EPO和铁剂,观察并比较两组治疗6个月前后Hb、心功能分级、LVEF及BNP。结果:治疗组Hb、心功能分级和LVEF较治疗前有显著改善(P<0.05);两组治疗后血浆BNP水平均下降,两组治疗后血浆BNP比较有差异(P<0.05)。结论:EPO治疗慢性充血性心力衰竭合并贫血患者有效,能改善心功能指标。     

心脏康复综合治疗对PCI术后患者临床预后的影响分析

目的研究分析心脏康复综合治疗对PCI术后患者预后的临床影响。方法选择2016年9月至2017年12月我院心内科住院性PCI手术患者120例,随机分组每组60例,对照组患者进行常规内科药物治疗,观察组患者进行心脏康复综合治疗,内容包括:药物治疗、心理治疗、营养指导、戒烟指导、运动治疗等。比较患者治疗前后左心室射血分数、左心室后壁厚度、左心室舒张末期内径进行测量。结果在治疗前观察组和对照组患者的心功能指标差异无统计学意义(P> 0.05),治疗后患者心功能指标与治疗前比较有改善,并且对照组患者心功能指标改善程度低于对照组,差异有统计学意义(P <0.05)。结论 PCI术后患者运用心脏康复综合治疗可有效改善患者预后情况,对患者心功能改善有明显作用,利于患者提高生活质量可在临床广泛推广应用。     

螺内酯对急性心肌梗死患者近期左心室重构及心功能的近期影响研究

目的 探讨螺内酯对急性心肌梗死(AMI)患者左心室重构及心功能的近期影响,为临床治疗提供参考依据.方法 选择2012年1月至2014年12月收治的70例AMI患者做为研究对象,根据随机数字表法分为观察组和对照组,每组35例,对照组给予常规药物治疗,观察组在对照组治疗的基础上加用螺内酯治疗.治疗6个月后,比较2组患者的心功能、左心室血流动力学、心脏重构等指标变化及心脏事件发生情况.结果 治疗后,观察组LA、LVEDD、LVMI、LVESV、LVEDV显著低于对照组,IVST、LVPWT显著高于对照组,差异有统计学意义(P<0.05);观察组BNP、Tei指数、Vp、Vop显著低于对照组,LVEF显著高于对照组,差异有统计学意义(P<0.05);观察组心律失常发生率为14.29%,显著低于对照组的34.29%(P<0.05).结论 在常规治疗的基础上加用螺内酯,显著改善了AMI患者近期心功能和左心室重构,且减少了心脏事件的发生,值得临床重视.     

阿托伐他汀联合辅酶Q10治疗冠心病早期心功能减退效果观察

目的观察阿托伐他汀联合辅酶Q10治疗冠心病早期心功能减退的临床效果。方法选取2017年10月-2019年7月东莞市清溪医院收治的冠心病早期心功能减退患者74例,按照随机表法分为观察组和对照组,每组37例。对照组给予阿托伐他汀治疗,观察组在对照组基础上联合辅酶Q10治疗。比较2组治疗前后心功能分级、收缩压、舒张压、心率、超声心动图检查指标及不良反应发生率。结果治疗后,2组心功能分级、收缩压、舒张压、心率均低于治疗前,且观察组优于对照组(P<0.05);治疗后,2组左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)、心脏指数(CI)均低于治疗前,左心室射血分数(LVEF)高于治疗前,且观察组优于对照组(P<0.01);2组不良反应发生率比较差异不显著(P>0.05)。结论阿托伐他汀联合辅酶Q10治疗冠心病早期心功能减退的临床效果显著,可有效改善患者心率、血压和心功能,且不良反应少,治疗安全性高。     

早期心脏康复对冠心病患者经皮冠状动脉介入术后心功能及生存质量的随访研究

目的探讨经皮冠状动脉介入术(PCI)后早期心脏康复对冠心病(CHD)患者心功能及生存质量的影响。方法 2015年1月至2017年1月间成功行PCI的62例CHD患者随机分为心脏康复组(31例)和对照组(31例)。对照组给予常规PCI术后治疗和护理,心脏康复组在此基础上给予院内、院外心脏康复干预、危险因素控制、心理干预及随访。比较2组之间心功能、生存质量变化及主要终点事件的发生情况。结果康复6个月,心脏康复组左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)、左心室射血分数(LVEF)各心功能指标均较康复前显著改善,且明显优于对照组(P<0.05)。与康复前比较,康复3、6个月后2组WHOQOL-BREF量表各维度评分明显升高(P<0.05),且生理、心理、社会关系3个维度评分心脏康复组高于对照组(P<0.05)。康复期间,心脏康复组终点事件的总发生率为6.5%,显著低于对照组25.8%(P<0.05)。结论早期心脏康复可改善PCI术后患者心功能,减少术后不良终点事件,提高患者生活质量。     

辛伐他汀联合曲美他嗪对慢性充血性心力衰竭患者左心室重构的影响

目的 探讨辛伐他汀联合曲美他嗪治疗慢性充血性心力衰竭的临床疗效及其对慢性充血性心力衰竭患者左心室重构的影响.方法 将276例慢性充血性心力衰竭患者完全随机分为常规治疗组、辛伐他汀治疗组、曲美他嗪治疗组、辛伐他汀联合曲美他嗪治疗组,每组69例.4组均给予常规纠正心功能不全及针对原发病的药物治疗,其中3组按分组分别加用辛伐他汀、曲美他嗪或二药联用,疗程12个月.分别于治疗前后评价患者的心功能分级及心脏的形态学参数,比较其变化.结果 辛伐他汀联合曲美他嗪治疗组与其他3组比较,心功能分级及形态学参数差异均有统计学意义[左心室射血分数:(0.51±0.12)%比(0.47±0.20)%、(0.48±0.17)%、(0.43±0.20)%;左心室收缩末期内径:(40.1±0.7)mm比(42.3±0.5)mm、(42.2±0.7)mm、(44.2±0.6)mm;均P<0.05).结论 对慢性充血性心力衰竭患者,在常规抗心力衰竭治疗基础上加用辛伐他汀和曲美他嗪可提高疗效,改善左心室重构,明显改善心功能.     

血液透析病人应用促红细胞生成素体会

贫血是慢性肾功能不全(尿毒症期)严重并发症,发生率几乎为100%,原因为肾脏分泌促红细胞生成素不足.以往输血是常用的手段,但即使反复输血,由于输入尿毒症患者循环中的红细胞寿命缩短,故不能满意改善症状,又增加了输血相关疾病的发生。从2000年1月开始我院应用人类重组红细胞生成素(EPO)纠正肾性贫血,使90%尿毒症患者贫血得到改善,弥补了以往输血的不足,也深刻认识到贫血对于尿毒症患者生活质量影响程度以及贫血与存活率,脏器功能、特别是左心室肥厚、心脏缺血耐受的关系。现将我院近5年我们应用EPO纠正血液透析病人贫血情况报道如下。1 资料与方法     

促红细胞生成素对慢性肾脏疾病患者的肾保护作用研究

目的:研究患贫血的慢性肾脏疾病(CKD)患者,确定促红细胞生成素(EPO)是否影响肾血管和氧化应激生物标志物。方法:30例患有贫血的CKD患者采用重组人EPO治疗,每2周皮下注射1次12000U的EPO,治疗前和治疗后6个月测定各种参数。结果:6个月后,血清血红蛋白(Hbg)显著增加(P<0.05),尿蛋白水平、尿中肝型脂肪酸结合蛋白(L-FABP)、尿中8-羟基脱氧鸟苷(8-OHdG)、颈动脉内膜中层厚度(IMT)、臂踝脉搏波速度(baPWV)、血浆脑钠肽(BNP)和血清非对称二甲基精氨酸(ADMA)水平显著下降(P<0.05);血清肌酐、肾小球滤过率(eGFR)、左心室射血分数(LVEF)、心胸比(CTR)和下腔静脉尺寸(IVCD)差异不大。结论:重组人EPO可改善肾功能损伤、氧化应激和动脉粥样硬化进展,还可改善CKD患者贫血。     

左卡尼汀对促红细胞生成素治疗血液透析患者贫血的疗效影响

目的观察左卡尼汀对促红细胞生成素(EPO)治疗维持性血液透析(MHD)患者贫血疗效的影响。方法随机选取我院血液净化中心行MHD的慢性肾衰合并贫血患者共50例,分为对照组及试验组。对照组25例,单用EPO治疗,试验组25例,在EPO治疗的同时加用左卡尼汀,试验周期为12周。治疗期末观察各组贫血指标的变化。结果①与治疗前相比,两组的贫血状况均明显改善。②两组之间对比,试验组的血红蛋白(Hb)及红细胞压积(Hct)水平明显高于对照组(P<0.01)。结论 EPO治疗可以改善MHD患者的贫血状况,左卡尼汀可明显提高EPO治疗MHD患者贫血的疗效。     

阿托伐他汀、辅酶Q_(10)联合应用治疗冠心病早期心功能减退的效果分析

目的探讨阿托伐他汀、辅酶Q_(10)联合应用治疗冠心病早期心功能减退的效果。方法选取我院2015年1月至2017年1月收治的120例冠心病早期心功能减退患者作为研究对象,根据治疗方案分为两组,各60例。对照组采取阿托伐他汀治疗,观察组在其基础上加用辅酶Q_(10)治疗,比较两组的治疗效果。结果观察组治疗有效率显著优于对照组(P <0.05)。治疗后观察组左心室射血分数(LVEF)、左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)等指标显著优于对照组(P <0.05)。结论采取阿托伐他汀联合辅酶Q_(10)治疗冠心病早期心功能减退,疗效显著,可明显改善患者心功能,值得在临床进一步探讨和推广。     

Hb对心力衰竭患者BNP、心肌重构影响的研究

目的研究Hb水平对心力衰竭（CHF）患者BNP、LVMI、MWS及心功能的影响。方法研究对象分为CHF贫血组、CHF非贫血组和对照组,每组30例,测定每个研究对象的Hb、BNP,LVEF,计算LVMWS和LVMI。结果CHF贫血组BNP水平、LVMWS和LVMI与CHF非贫血组对比,有统计学意义（P〈0．01）,而LVEF低于CHF非贫血组（P〈0．01）;CHF患者的Hb水平与BNP、LVMWS和LVMI呈负相关（P〈0．01）。结论CHF患者Hb水平参与心室重构,Hb水平越低心室重构程度越重。     

冬虫夏草对肾性高血压大鼠血管重构的影响

目的 :观察冬虫夏草对肾性高血压大鼠心肌肥厚、血管重构的影响。方法 :体重为 160～ 180 g健康雄性 Wistar大鼠随机分为对照组、高血压组及治疗组 ,于术后第 10天大鼠灌胃 (ig)冬虫夏草煎剂 2 ml,每日两次 (bid) ,连续 2 0天 ,观察冬虫夏草对心肌肥厚、血管重构的影响。结果 :冬虫夏草明显改善高血压大鼠血压、心肌肥厚及血管重构。结论 :冬虫夏草对肾性高血压有治疗作用。     

Comparative effects of torasemide and furosemide in rats with heart failure

It has been reported that torasemide but not furosemide, may block the renin-angiotensin-aldosterone system and therefore it might attenuate myocardial remodeling accompanied by left ventricular (LV) dysfunction. We therefore compared the therapeutic effects of torasemide, a long-acting loop diuretic, and furosemide, a short-acting one, on the progression of LV remodeling in a rat model of chronic heart failure (CHF) after experimental autoimmune myocarditis (EAM). CHF was elicited in Lewis rats by immunization with porcine cardiac myosin. Twenty-eight days after immunization, rats were treated for 28 days with torasemide, furosemide, or vehicle. We investigated the effects on metabolic and neurohumoral parameters, cardiac fibrosis and remodeling in EAM rats. Diuresis was increased dose dependently by both torasemide and furosemide, showed an equipotent natriuretic effect. The urinary potassium excretion was significantly increased with furosemide in comparison to torasemide. Myocardial functional parameters were significantly improved by torasemide. Conversely, these parameters did not change in rats receiving furosemide. Torasemide suppressed LV fibrosis, myocardial protein levels of transforming growth factor-beta1, collagen III, and aldosterone synthase and improved survival rate to the control level, but furosemide did not. Moreover, both pharmacological interventions significantly elevated plasma angiotensin II and decreased atrial natriuretic peptide in a dose-dependent manner. Our results demonstrate that compared with furosemide, torasemide treatment significantly improved survival rate, LV function and ameliorated the progression of cardiac remodeling in rats with CHF after EAM.     

Torasemide, a long-acting loop diuretic, reduces the progression of myocarditis to dilated cardiomyopathy

Torasemide is a long-acting loop diuretic that combines the effects of both furosemide and spironolactone. It has been reported that torasemide may block the renin-angiotensin-aldosterone system and therefore it might attenuate myocardial remodeling accompanied by left ventricular dysfunction. However, nothing is known about the effect of torasemide on myocardial remodeling in a rat model in which myosin-induced experimental autoimmune myocarditis might develop into dilated cardiomyopathy. Experimental autoimmune myocarditis was elicited in Lewis rats by immunization with porcine cardiac myosin. Twenty-eight days after immunization, we investigated the effects of torasemide on metabolic and neurohumoral parameters, cardiac fibrosis and remodeling in experimental autoimmune myocarditis rats. Diuresis was increased dose-dependently by torasemide; the urinary potassium and sodium excretion was significantly decreased and increased, respectively. Myocardial functional parameters measured by hemodynamic and echocardiographic studies were significantly improved by torasemide treatment in a dose-dependent manner. The area of fibrosis, myocyte size and the myocardial protein levels of transforming growth factor-beta1, collagen III, and aldosterone synthase were significantly decreased, and the sarcoplasmic reticulum Ca2+ ATPase2 protein level was significantly increased by torasemide treatment. Moreover, the plasma levels of angiotensin II and aldosterone were increased and atrial natriuretic peptide was decreased in a dose-dependent manner. Our results indicate that torasemide treatment significantly improved left ventricular function and ameliorated the progression of cardiac remodeling beyond its renal effects in rats with chronic heart failure after experimental autoimmune myocarditis.     

Erythropoietin in heart failure and other cardiovascular diseases: hematopoietic and pleiotropic effects

Erythropoietin is a hypoxia-induced hormone that is a major regulator of normal erythropoiesis. Over the last decade, the production of recombinant human erythropoietin has revolutionized the treatment of anemia associated with chronic renal failure, and has led to a greater understanding of anemia pathophysiology and to the elucidation of the interactions of erythropoietin, iron, and erythropoiesis. Anemia has been shown to be independently associated with increased mortality and disease progression. Potential survival benefits associated with correction of anemia have expanded considerably the indications of erythropoietin use in various patient populations and are leading to consideration of earlier, more aggressive treatment of mild to moderate anemia. The results of such treatment are promising in a variety of new clinical settings, including anemia associated with congestive heart failure. Furthermore, the erythropoietin receptor is widely distributed in the cardiovascular system, including endothelial cells, smooth muscle cells and cardiomyocytes and preclinical studies have established erythropoietin to be a pleiotropic cytokine with anti-apoptotic activity and tissue-protective actions in the cardiovascular system, beyond correction of hemoglobin levels. Despite some potential adverse effects, such as hypertension, and the occurrence of erythropoietin resistance, early studies in heart failure patients with anemia suggest that erythropoietin therapy is safe and effective in reducing left ventricular hypertrophy, enhancing exercise performance and increasing ejection fraction. Anemia is found in about one-third of all cases of congestive heart failure (CHF). The most likely common cause is chronic renal insufficiency, which is present in about half of all CHF cases. However, anemia can occur in CHF without renal insufficiency and is likely to be due to excessive cytokine production. The anemia itself can worsen cardiac function, both because it causes cardiac stress through tachycardia and increased stroke volume, and because it can cause a reduced renal blood flow and fluid retention, adding further stress to the heart. Long-standing anemia of any cause can cause left ventricular hypertrophy, which can lead to cardiac cell death through apoptosis and worsen CHF. Therefore, a vicious circle, cardio-renal anemia syndrome, is set up wherein CHF causes anemia, and the anemia causes more CHF and both damage the kidneys worsening the anemia and the CHF further and increasing mortality. There is now evidence that early correction of the CHF anemia with subcutaneous erythropoietin and intravenous iron improves shortness of breath and fatigue, cardiac function, renal function and exercise capacity, reducing the need for hospitalization and improving quality of life. In the present review we discuss the data on current clinical use of erythropoietin in cardiovascular disease, with the main focus on the treatment of congestive heart failure, and summarize the advances and progress made in the understanding of the hematopoietic and pleiotropic effects of erythropoietin in the cardiovascular system.     

沙库巴曲缬沙坦抑制心脏重构的研究进展

心脏重构是心血管疾病发生、发展的重要病理生理基础，与患者预后关系密切。沙库巴曲缬沙坦（LCZ696）是一种血管紧张素受体脑啡肽酶抑制剂，可同时作用于肾素-血管紧张素-醛固酮系统（RAAS）和利钠肽系统，主要用于治疗射血分数降低的心力衰竭。在不同类型的心血管疾病中，与肾素-血管紧张素系统抑制剂（RASI）比较，LCZ696能够显著抑制心脏重构，改善心功能及心血管病预后。本文就LCZ696对心脏重构抑制作用的机制及研究现状作一综述。     

Inhibition of Rho-kinase ameliorates myocardial remodeling and fibrosis in pressure overload and myocardial infarction: role of TGF-β1-TAK1

Inhibition of Rho-kinase displays vasodilation property although its effect on cardiac remodeling in heart against pressure overload and ischemia has not been fully elucidated. The present study was designed to examine the effect of fasudil, a Rho-kinase (ROCK) inhibitor, on myocardial remodeling and underlying mechanisms in pressure overload and myocardial infarction (MI) mice. Pressure overload was produced by constriction of the transverse aorta (TAC) for 3 weeks. Left ventricular (LV) geometry, cardiac hypertrophy, fibrosis, and remodeling were evaluated by transthoracic echocardiography and cardiac histology. Expressions of the hypertrophic and profibrotic markers were analyzed in TAC and MI mice with or without fasudil treatment. LV cavity dilatation and dysfunction evaluated by echocardiography were significantly suppressed in the fasudil-treated MI group compared with the MI group (P<0.05); however, there were no significant difference between the TAC group and the fasudil-treated TAC group. Inhibition of ROCK exhibited reduced interstitial fibrosis, which was observed both in TAC and MI mice (P<0.05). The beneficial effects of fasudil were closely associated with the change of the specific profibrotic gene expression and TGF-β1-TAK1 pathway. Taken together, these results indicate that Rho-kinase is substantially involved in the myocardial remodeling after TAC and MI associated with upregulation of profibrotic gene expression and TGF-β1-TAK1 pathway; further suggest the protective effect of fasudil on heart against pathological stimuli by inhibiting reactive fibrosis.     

黄芪多糖抑制TGF-β1和Nox4/Akt/mTOR信号通路保护心肌重构的作用研究

目的 研究黄芪多糖（Astragalus polysaccharide,APS）对心肌重构的保护作用及机制。方法 通过主动脉弓缩窄（transverse aortic constriction,TAC）构建心肌重构小鼠模型并使用APS进行干预。利用心脏超声成像系统,心肌组织麦胚凝集素染色、天狼星红染色及Real-time PCR评价APS对心肌重构小鼠模型的保护作用。Western blotting检测心肌组织中Nox4、TGF-β1、mTOR及Akt的表达水平,探讨APS保护心肌重构的机制。结果 TAC手术4周后,TAC组小鼠左心室舒张末期后壁厚度（left ventricular end-diastolic posterior wall dimension,LVPWd）较空白对照组显著增加（P<0.01）,左心室收缩功能显著下降,而APS+TAC组小鼠LVPWd较TAC组显著降低（P<0.05）,左心室收缩功能明显改善。APS对TAC诱导的小鼠心体比和心胫比增加具有显著的保护作用（P<0.001）。心肌组织病理染色结果显示,TAC组小鼠心肌细胞肥大水平和心肌纤维化水平较空白对照组小鼠显著增加（P<0.01）,而APS对TAC诱导的心肌细胞肥大和纤维化具有显著的保护作用（P<0.01或P<0.05）。与空白对照组比较,TAC组小鼠心肌组织中心钠素和脑钠肽的表达水平显著升高（P<0.001）,而APS对此有显著的抑制作用（P<0.01或P<0.05）。进一步研究发现,APS干预对TAC诱导的Nox4、TGF-β1、mTOR及p-Akt在心肌组织中的表达具有显著的抑制作用。结论 APS能够通过抑制TGF-β1和Nox4/Akt/mTOR信号通路发挥对心肌重构小鼠模型的保护作用。     

试论心室重构及其药物逆转

重构（remodeling）由Baumbach等在1989年首次提出。高血压左室重构是心脏事件的重要独立危险因素,与心率失常,猝死,心力衰竭等密切相关。现已证明,在高血压情况下,心血管系统会发生相应的结构和功能的变化,这与高血压的预后密切相关。高血压时心脏的前后负荷增加,血流动力学改变伴随神经—内分泌异常,左心室肥厚以及心腔扩大,此过程即为左心室重构。本文就心室重构的机制及其药物逆转做一综述。     

永久心脏起搏器植入对心脏重塑影响的临床观察(附48例分析)

目的分析植入永久心脏起搏器对心脏重塑的影响。方法本研究入组病例48例,其中植入双腔起搏双腔感知P波/R波抑制型(DDD)起搏器25例,心室起搏心室感知R波抑制型(VVI)起搏器23例。采用PHILIPS7500型二维超声心动图诊断系统,分别测定患者安置永久性心脏起搏器前、安置>半年后心脏各房室大小,并进行数据间的比较分析。结果除植入DDD型起搏器组右心房发生重塑改变(P<0.05)外,DDD型起搏器植入者植入前后二维超声心动图的其余指标对比和VVI型起搏器植入者植入前后二维超声心动图的各项指标对比均未见有统计学意义改变(P>0.05)。结论植入DDD型永久心脏起搏器早期就可对右心房的重塑有影响,植入各型永久性心脏起搏器对心脏重塑的远期影响还有待于进一步的长期临床观察和扩大样本数。