中西医结合治疗慢性充血性心力衰竭的疗效观察

目的观察中西医结合治疗慢性充血性心力衰竭的疗效。方法选择100例CHF患者随机分成治疗组和对照组,2组均采用西医常规治疗,治疗组在对照组的基础上加用中药治疗,观察2组的治疗效果。结果治疗组总有效率93.33%,对照组总有效率85.005%,P<0.05。结论中西医结合治疗充血性心力衰竭疗效优于单纯西医常规治疗。     

中西医结合治疗充血性心力衰竭67例临床观察

目的观察中西医结合治疗充血性心力衰竭的疗效。方法135例充血性心力衰竭患者随机分成两组:中西医结合治疗组67例,西医治疗组68例,西医治疗组根据病情选用利尿剂、血管紧张素转换酶抑制剂、醛固酮拮抗剂、血管扩张剂及洋地黄类药物等;中西医结合治疗组在西医组治疗基础上加服中药辨证施治,应用苓桂术甘汤合五皮饮加减。治疗2周后分别观察两组心功能改善情况。结果中西医结合组和西医组的显效率分别为43.3%和29.4%,总有效率分别为89.6%和75.0%,两组对比有显著性差异(P<0.05)。结论在西医治疗基础上加用中药辨证施治可提高充血性心力衰竭的疗效。     

美卡素治疗充血性心力衰竭68例疗效观察

目的观察美卡素(替米沙坦)治疗充血性心力衰竭(CHF)的疗效。方法将136例CHF患者分为2组:(1)替米沙坦组:常规治疗的基础上加服替米沙坦。(2)对照组:仅给予除ACEI以外的常规治疗。观察2组患者的心功能改善情况。结果治疗组疗效明显优于对照组,未发现明显不良反应。结论 CHF患者在常规治疗基础上加服替米沙坦可以显着改善心功能。     

依那普利联合倍他乐克治疗充血性心力衰竭的疗效观察

目的观察依那普利联合倍他乐克治疗慢性心力衰竭(CHF)的临床疗效和安全性。方法将50例CHF患者随机分成A组和B组各25例,2组均予常规抗心衰治疗,A组加依那普利10mgqd,B组加依那普利10mgqd及倍他乐克6.25mgBid,若能耐受6d后增加剂量1倍,剂量为12.5～100mg/d,疗程12周。全组病例治疗前后观察临床疗效、血压、心率、左室射血分数(EF)的变化。结果A组显效20%,有效率80%;B组显效36%,有效率92%。2组间比较收缩压(SBP)、舒张压(DBP)、EF及心率B组优于A租。结论依那普利联合倍他乐克治疗CHF疗效优于单用依那普利。     

卡托普利联合美托洛尔治疗慢性充血性心力衰竭54例临床疗效分析

目的探讨卡托普利联合美托洛尔治疗慢性充血性心力衰竭临床治疗效果。方法选择我院2007年5月至2009年5月慢性充血性心力衰竭患者104例,随机分为2组,治疗组和对照组。对照组给予常规治疗,治疗组在常规治疗基础上给以美托洛尔和卡托普利治疗。治疗后评价2组临床治疗效果。结果治疗组总有效率为90.7%,对照组为70.0%,2组患者治疗后总有效率比较,差异有统计学意义,P<0.05。结论卡托普利联合美托洛尔治疗慢性充血性心力衰竭临床效果显著,值得临床借鉴。     

心室再同步化治疗慢性充血性心力衰竭的护理

目的观察CRT治疗技术对慢性充血性心力衰竭患者的治疗效果,进一步探讨CRT技术的有效应用以及病患的治疗。方法对3例心力衰竭患者进行CRT治疗。结果效果较好,未有1例发生意外。结论耐心的心理护理、术前准备以及术后观察和指导,是取得满意效果的重要保证。     

乌司他丁辅助治疗顽固性充血性心力衰竭的临床疗效观察

目的观察乌司他丁辅助治疗顽固性充血性心力衰竭的临床效果。方法选取我院自2009年3月至2010年4月收治的136例顽固性充血性心力衰竭患者随机分为观察组(乌司他丁辅助治疗组)和对照组(常规治疗组)各68例,比较2组患者的治疗效果。结果观察组显效27例,有效31例,总有效率为85.3%;对照组显效11例,有效26例,总有效率为54.4%;2组患者治疗后超声心动图指标均有所改善,但观察组改善较对照组明显(P<0.01),具有统计学意义。结论乌司他丁辅助治疗顽固性充血性心力衰竭可以提高临床治疗效果,值得了临床推广应用。     

联合用药治疗慢性充血性心力衰竭的临床研究

目的探讨联合用药在治疗慢性充血性心力衰竭(CHF)上的临床效果。方法将2009年5月至2010年11月来我院治疗的120例慢性CHF患者随机分为观察组和对照组,每组60例,分别行常规方法与美托洛尔联合治疗和常规治病,疗程15周,对比分析治疗前后的超声心动图及6min步行距离。结果观察组的心功能改善明显、左心室射血分数和6min步行距离增加明显。结论美托洛尔联合常规治疗可极大改善慢性CHF患者的心脏功能,安全有效,可在临床上广泛应用。     

不同剂量比索洛尔治疗慢性充血性心力衰竭的疗效及耐受性比较观察

目的 探讨不同剂量比索洛尔对慢性充血性心力衰竭的疗效及耐受性.方法 173例慢性充血性心力衰竭(CHF)患者在常规传统治疗基础上口服比索洛尔,按比索洛尔日用总量分为2组,≥7.5mg/d为高剂量组(n=73),≤5mg/d为低剂量组(n=100),对治疗前、治疗后12周和24周做心功能评估及耐受性比较,并做心脏彩色超声心动图,对各项心功能参数进行比较.结果 低剂量组开始治疗12周后LVEF有改善,但总体状况改善不明显,治疗24周后状况大致同12周.高剂量组治疗12周后各项心功能指标均明显改善.高剂量组耐受性略差于低剂量组,差异具有显著意义(P＜0.05),但均无恶性不良事件发生.结论 高剂量组在改善心功能、改善心肌重构方面优于低剂量组,所以只要患者在耐受范围内应尽可能使比索洛尔达到目标剂量.     

辛伐他汀联用阿司匹林治疗扩张型心肌病的临床分析

目的评价辛伐他汀及联用阿司匹林对扩张型心肌病患者栓塞事件及死亡率的影响。方法将27例扩张型心肌病患者分为辛伐他汀及联用阿司匹林组27例和对照组26例,追踪观察两组的栓塞事件发生率、死亡率及总有效率。结果辛伐他汀及联用阿司匹林组栓塞事件发生率明显低于对照组(P<0.05);两组治疗总有效率及死亡率相比差异无统计学意义(P>0.05)。治疗前、后未发现皮肤黏膜淤斑及内脏出血情况、过敏反应等不良反应。结论扩张型心肌病患者应用应用辛伐他汀及联用阿司匹林抗血小板治疗,可降低患者的栓塞事件发生,但并不增加患者治疗总有效率及减少死亡率。     

缬沙坦联合卡维地洛治疗慢性心力衰竭的临床疗效观察

目的探讨缬沙坦联合卡维地洛治疗慢性心力衰竭的临床疗效。方法选择我院2007年5月至2009年9月慢性心力衰竭患者112例,随机分为2组,观察组和对照组。对照组患者采用常规治疗,如低盐饮食、给予洋地黄强心、利尿剂等,患者有心绞痛的给予硝酸酯类药物,观察组在对照组用药基础上,给予缬沙坦和卡维地洛。2组患者疗程为2个月。结果 2组患者治疗后,总有效率比较,差异有统计学意义,P<0.05。结论缬沙坦联合卡维地洛治疗慢性心力衰竭临床治疗效果显著,值得借鉴。     

慢性心力衰竭患者QT离散度和心率变异性分析

目的 探讨慢性心力衰竭患者QT离散度和心率变异性变化特点及关系.方法 56例心力衰竭患者和54例健康对照者为观察对象,全部入选者作静息状态下12导心电图和24h动态心电图,分析心衰组及健康对照组QT离散度及心率变异性.结果 心衰组QT离散度为(48.4±17.45)ms,对照组为(27.87±10.74)ms,有显著性差异(P＜0.001).心衰组IIRV各项指标较对照组明显减低(P＜0.05～0.01).结论 心衰时,由于自主神经受损,导致QT离散度及HRV异常;QT离散度和HRV改变与心衰程度明显相关.     

Pathophysiology and Treatment of Diabetic Cardiomyopathy and Heart Failure in Patients with Diabetes Mellitus

There is a close relationship between diabetes mellitus and heart failure, and diabetes is an independent risk factor for heart failure. Diabetes and heart failure are linked by not only the complication of ischemic heart disease, but also by metabolic disorders such as glucose toxicity and lipotoxicity based on insulin resistance. Cardiac dysfunction in the absence of coronary artery disease, hypertension, and valvular disease is called diabetic cardiomyopathy. Diabetes-induced hyperglycemia and hyperinsulinemia lead to capillary damage, myocardial fibrosis, and myocardial hypertrophy with mitochondrial dysfunction. Lipotoxicity with extensive fat deposits or lipid droplets is observed on cardiomyocytes. Furthermore, increased oxidative stress and inflammation cause cardiac fibrosis and hypertrophy. Treatment with a sodium glucose cotransporter 2 (SGLT2) inhibitor is currently one of the most effective treatments for heart failure associated with diabetes. However, an effective treatment for lipotoxicity of the myocardium has not yet been established, and the establishment of an effective treatment is needed in the future. This review provides an overview of heart failure in diabetic patients for the clinical practice of clinicians.     

The Multi-Biomarker Approach for Heart Failure in Patients with Hypertension

We assessed the predictive ability of selected biomarkers using N-terminal pro-brain natriuretic peptide (NT-proBNP) as the benchmark and tried to establish a multi-biomarker approach to heart failure (HF) in hypertensive patients. In 120 hypertensive patients with or without overt heart failure, the incremental predictive value of the following biomarkers was investigated: Collagen III N-terminal propeptide (PIIINP), cystatin C (CysC), lipocalin-2/NGAL, syndecan-4, tumor necrosis factor-α (TNF-α), interleukin 1 receptor type I (IL1R1), galectin-3, cardiotrophin-1 (CT-1), transforming growth factor β (TGF-β) and N-terminal pro-brain natriuretic peptide (NT-proBNP). The highest discriminative value for HF was observed for NT-proBNP (area under the receiver operating characteristic curve (AUC) = 0.873) and TGF-β (AUC = 0.878). On the basis of ROC curve analysis we found that CT-1 > 152 pg/mL, TGF-β < 7.7 ng/mL, syndecan > 2.3 ng/mL, NT-proBNP > 332.5 pg/mL, CysC > 1 mg/L and NGAL > 39.9 ng/mL were significant predictors of overt HF. There was only a small improvement in predictive ability of the multi-biomarker panel including the four biomarkers with the best performance in the detection of HF—NT-proBNP, TGF-β, CT-1, CysC—compared to the panel with NT-proBNP, TGF-β and CT-1 only. Biomarkers with different pathophysiological backgrounds (NT-proBNP, TGF-β, CT-1, CysC) give additive prognostic value for incident HF in hypertensive patients compared to NT-proBNP alone.     

Urine Aquaporin-2: A Promising Marker of Response to the Arginine Vasopressin Type-2 Antagonist,Tolvaptan in Patients with Congestive Heart Failure

Aquaporin-2, a member of the aquaporin family, is an arginine vasopressin-regulated water channel expressed in the renal collecting duct, and a promising marker of the concentrating and diluting ability of the kidney. The arginine vasopressin type-2 antagonist, tolvaptan, is a new-generation diuretic; it is especially indicated in patients with decompensated heart failure refractory to conventional diuretics. However, the ideal responders to tolvaptan have not yet been identified, and non-responders experience worse clinical courses despite treatment with tolvaptan. Urine aquaporin-2 has recently been demonstrated as a promising predictor of response to tolvaptan. We here validated aquaporin-2-guided tolvaptan therapy in patients with decompensated heart failure. Long-term efficacy of tolvaptan treatment in the responders defined by aquaporin-2 needs to be validated in the future prospective study.     

Cardiac Arrhythmias and Sleep-Disordered Breathing in Patients with Heart Failure

The relationship between heart failure (HF), sleep-disordered breathing and cardiac arrhythmias is complex and poorly understood. Whereas the frequency of predominantly obstructive sleep apnea in HF patients is low and similar or moderately higher to that observed in the general population, central sleep apnea (CSA) has been observed in approximately 50% of HF patients, depending on the methods used to detect CSA and patient selection. Despite this high prevalence, it is still unclear whether CSA is merely a marker or an independent risk factor for an adverse prognosis in HF patients and whether CSA is associated with an increased risk for supraventricular as well as ventricular arrhythmias in HF patients. The current review focuses on the relationship between CSA and atrial fibrillation as the most common atrial arrhythmia in HF patients, and on the relationship between CSA and ventricular tachycardia and ventricular fibrillation as the most frequent cause of sudden cardiac death in HF patients.     

慢性心力衰竭患者血浆脂联素与脑钠肽及左室重量指数的相关性

目的探讨慢性心力衰竭(Chronic heart failure,CHF)患者血浆脂联素(Adiponectin,APN)水平的变化及其与脑钠肽(Brain natriuretic peptide,BNP)及左室重量指数(Left ventricular mass index,LVMI)的相关性,评价APN水平在预测心衰进程及预后中的价值。方法分别选取90例男性CHF患者及90名男性健康查体者(对照组),应用ELISA法测定血浆APN和BNP水平,通过超声心动图测定左室舒张末期室间隔厚度、左室后壁厚度、左室舒张末期内径、左室舒张末期容积和收缩末期容积,计算LVMI,比较CHF患者和对照组的APN、BNP和LVMI水平;不同病因所致CHF患者血浆APN和LVMI的水平;不同心功能患者血浆APN和BNP的水平;并进行APN与BNP及LVMI的相关性分析。结果 CHF患者血浆APN和BNP水平及LV-MI均明显高于对照组(P均<0.05);不同病因所致CHF患者的APN水平差异无统计学意义(P>0.05);NYHAⅣ患者血浆APN和BNP水平明显高于NYHAⅢ及NYHAⅡ患者(P均<0.05);APN与BNP和LVMI均呈正相关(r=0.528,P<0.001;r=0.269,P<0.05)。结论 CHF患者血浆APN水平随心功能的恶化而增高,并可能参与心肌重塑的病理生理过程,测定CHF患者血浆APN水平有可能作为预测CHF进程及评价预后的重要指标。     

安体舒通联合卡托普利治疗慢性心衰50例临床观察

目的探讨卡托普利与安体舒通联合治疗慢性心力衰竭的疗效观察。方法选择我院100例慢性心力衰竭患者,随机分为治疗组和对照组。2组均积极治疗原发病,对照组使用洋地黄及速尿。治疗组在对照组治疗方法的基础上加用卡托普利和安体舒通,3～4周为1个疗程,观察治疗后2组疗效。结果2组患者治疗前、后收缩压(SBP),舒张压(DBP)、心率、6min步行距离间差异均有显著性意义,2组患者治疗前、后左室射血分数(EF),每搏输出量(SV),每分输出量(CO)均有显著性意义,治疗组总有效率显著高于对照组。结论联合使用小剂量的安体舒通和卡托普利治疗CHF,能够有效的抑制RASS系统,拮抗醛固酮,从而改善左室血流动力学,长期使用安全有效。     

Epigenetics and Heart Failure

Epigenetics refers to changes in phenotypes without changes in genotypes. These changes take place in a number of ways, including via genomic DNA methylation, DNA interacting proteins, and microRNAs. The epigenome is the second dimension of the genome and it contains key information that is specific to every type of cell. Epigenetics is essential for many fundamental processes in biology, but its importance in the development and progression of heart failure, which is one of the major causes of morbidity and mortality worldwide, remains unclear. Our understanding of the underlying molecular mechanisms is incomplete. While epigenetics is one of the most innovative research areas in modern biology and medicine, compounds that directly target the epigenome, such as epidrugs, have not been well translated into therapies. This paper focuses on epigenetics in terms of genomic DNA methylation, such as 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) modifications. These appear to be more dynamic than previously anticipated and may underlie a wide variety of conditions, including heart failure. We also outline possible new strategies for the development of novel therapies.