培哚普利 螺内酯 美托洛尔联合治疗扩张型心肌病轻中度慢性心力衰竭的疗效观察

目的 探讨培哚普利、螺内酯、美托洛尔联合治疗扩张型心肌病慢性心力衰竭的临床疗效.方法 将138例扩张型心肌病按轻、中度慢性心力衰竭病例随机分为常规治疗组(对照组)和常规+联合治疗组(培哚普利、螺内酯、美托洛尔).比较两组治疗前及治疗4周后心率(HR)、左心室舒张末期内径(LVEDD)和左心室射血分数(LVEF)的变化.结果 (1)治疗前两组HR、LVEDD、LVEF比较差异无统计学意义(P>0.05);(2)治疗4周后,治疗组与对照组三项指标变化比较差异有统计学意义(P＜0.01);(3)治疗组疗效优于对照组(P＜0.05).结论 培哚普利、螺内酯、美托洛尔联合治疗轻、中度扩张型心肌病心力衰竭疗效好,无严重不良反应.     

培哚普利联合螺内酯治疗慢性心力衰竭的临床疗效研究

目的观察血管紧张素转换酶抑制剂培哚普利与醛固酮拮抗剂螺内酯联合治疗慢性心力衰竭(CHF)的疗效。方法将65例CHF患者随机分为试验组和对照组,对照组给予常规治疗,试验组在常规治疗基础上给予培哚普利2～8mg/d,螺内酯20～40mg/d,均治疗8周。结果试验组总有效率为91.0%,对照组总有效率为68.8%,两组疗效比较,差异有统计学意义(P<0.05)。治疗后试验组较对照组,左室射血分数与6min步行试验距离距离增大,左心室舒张末期内径和左心室收缩末期内径减小,差异均有统计学意义(P<0.05)。结论培哚普利联合螺内酯治疗CHF安全有效。     

观察培哚普利、美托洛尔片联合螺内酯治疗慢性心力衰竭的效果分析

目的观察分析培哚普利、美托洛尔片联合螺内酯治疗慢性心力衰竭效果。方法随机选取2016年7月至2018年7月我科收治的慢性心力衰竭患者36例,然后随机分成两组,采用SPSS21.0将入组患者按先后序列号(1-36)随机分为两组:一组培哚普利、美托洛尔片联合螺内酯治疗组(治疗组18例),一组卡托普利、美托洛尔片等常规治疗组(对照组,18例),对两组患者的临床疗效、不良反应发生情况、再住院情况及死亡情况进行统计分析。结果治疗组患者治疗的总有效率88.9%(16/18)显著高于对照组72.2%(13/18)(P0.05),再住院率、死亡率33.3%(6/18)、5.6%(1/18)均显著低于对照组55.6%(10/18)、16.7%(3/18)(P0.05)。结论培哚普利、美托洛尔片联合螺内酯治疗慢性心力衰竭效果较卡托普利、美托洛尔片等常规治疗好。     

螺内酯联合培哚普利治疗老年扩张型心肌病心力衰竭临床观察

目的评价螺内酯联合培哚普利治疗老年扩张型心肌病（DCM）心力衰竭的有效性和安全性。方法以60例老年DCM心力衰竭病人为研究对象,随机分为观察组和对照组,每组各30例。观察组为螺内酯联合培哚普利,加基础用药（地高辛、双氢克尿噻）;对照组为培哚普利加基础用药。治疗10周后复查两组动态心电图、超声心动图及血清钾、镁和肝肾功能。结果治疗后两组左室射血分数（LVEF）均较治疗前显著增加（P〈0.05）,左室收缩末期容积（LVESV）和左室舒张末期容积（LVEDV）、24h室性早搏（VA）数均有减少（P〈0.05或P〈0.01）;观察组与对照组比较,LVEF显著增加（P〈0.05）。两组均未发现高血钾及肝肾功能损害。结论在老年DCM心力衰竭常规用药的基础上,加用螺内酯联合培哚普利治疗较有效、安全。     

螺内酯与培哚普利联合常规疗法治疗心力衰竭的临床效果观察

目的分析螺内酯与培哚普利联合常规疗法治疗心力衰竭临床效果。方法选择2015年8月-2018年8月我院收治的100例慢性心衰患者为实验对象。将其分为两组,每组50例。对照组使用培哚普利联合常规疗法,以此为基础,观察组使用螺内酯,分析结果。结果观察组治疗效果好于对照组,P0.05。和对照组相比,观察组受试者干预后的6min步行结果、左室舒张期内径以及左室射血分数改善情况更好,P0.05。结论对于慢性心衰疾病患者,以常规治疗为基础,联合使用培哚普利以及螺内酯进行治疗,能够取得满意效果。此类方案能够全面延缓心衰疾病进展,安全性强,有效性高,可促进患者疾病转归。因此时都进一步在临床中推广使用。     

培哚普利和坎地沙坦倍增剂量治疗老年退行性心脏瓣膜病心力衰竭疗效观察

目的评估培哚普利和坎地沙坦倍增剂量对老年退行性心脏瓣膜病心力衰竭的疗效。方法 218例老年退行性心脏瓣膜病心力衰竭患者随机分为3组:培哚普利组(4mg/d治疗2周后改用8mg/d)、坎地沙坦组(4mg/d治疗2周后改用8mg/d)、对照组(常规抗心力衰竭治疗,不用血管紧张素转换酶抑制剂),治疗24周,观察患者治疗前后坐位血压、血清高敏C反应蛋白(hsCRP)、脑钠肽、左室质量指数(LVMI)的变化,并记录治疗期间的不良反应。结果培哚普利组治疗后LVMI、血清脑钠肽、hsCRP均明显下降(P0.05);坎地沙坦组血清LVMI、脑钠肽亦出现下降,但无统计学意义,而血清hsCRP则显著降低(P0.05);3组抗心力衰竭治疗的有效率分别为:培哚普利组84.9%,坎地沙坦组69.3%,对照组52.0%,3组间差异有统计学意义(P0.05)。培哚普利组不良反应发生率最高(15.1%),其中咳嗽副反应发生率为6.5%,而双下肢水肿发生率对照组明显高于治疗组(P0.05)。结论培哚普利和坎地沙坦倍增剂量治疗均能减轻左室肥厚,对于老年退行性心脏瓣膜病心力衰竭患者耐受性较好。     

慢性心力衰竭140例治疗体会

目的探讨慢性心力衰竭患者采用不同药物治疗并观察疗效,为临床治疗提供理论依据。方法选择2012年5月~2015年5月我院收治的慢性心力衰竭患者140例作为研究对象,将其平均分成对照组与观察组,各70例。对照组给予地高辛、氢氯噻嗪常规治疗,观察组在对照组的基础上加用美托洛尔联合依那普利、螺内酯治疗,观察两组患者的疗效。结果观察组总有效率为94.3%,显著高于对照组的74.3%,差异有统计学意义(P0.05)。结论慢性心力衰竭患者在临床治疗中,采用地高辛、氢氯噻嗪加用美托洛尔联用依那普利、螺内酯治疗,具有较好的疗效。     

培哚普利和螺内酯对大鼠糖尿病肾病水通道蛋白表达的影响

目的 探讨培哚普利和螺内酯对糖尿病肾病水通道蛋白(AQP)表达的影响.方法 雄性SD大鼠72只,建立由链脲佐菌素(STZ)所诱导的糖尿病肾病大鼠模型.将造模成功的48只随机分为模型组、培哚普利组、螺内酯组、培哚普利联合螺内酯组,每组大鼠12只,正常组大鼠12只.模型组和正常组腹腔注射等剂量生理盐水灌胃;培哚普利组给予2 mg/(kg·d)培哚普利灌胃;螺内酯组给予50 mg/(kg·d)螺内酯灌胃;培哚普利联合螺内酯组给予2 mg/(kg·d)培哚普利+50 mg/(kg·d)螺内酯灌胃.连续8 w.结果 模型组、培哚普利组、螺内酯组和培哚普利联合螺内酯组空腹血糖(FPG)、血肌酐、24 h尿蛋白量、尿液AQP1、AQP2、AQP3、AQP4含量及AQP1、AQP2、AQP3、AQP4表达灰度值明显高于正常组(P<0.05);培哚普利组、螺内酯组和培哚普利联合螺内酯组FPG、血肌酐、24 h尿蛋白量、尿液AQP1、AQP2、AQP3、AQP4含量及AQP1、AQP2、AQP3、AQP4表达灰度值明显低于模型组(P<0.05);培哚普利联合螺内酯组FPG、血肌酐、24 h尿蛋白量、尿液AQP1、AQP2、AQP3、AQP4含量及AQP1、AQP2、AQP3、AQP4表达灰度值明显低于培哚普利组、螺内酯组(P<0.05).结论 培哚普利和螺内酯对糖尿病肾病大鼠肾脏具有一定保护作用,且机制可能与降低尿液AQP水平及抑制肾组织AQP表达有关.     

培哚普利加黄芪注射液治疗难治性心力衰竭疗效观察

目的观察培哚普利(Perindoprol)加黄芪注射液(Milkvetch Injection,MI)治疗充血性心力衰竭(CHF)的疗效。方法器质性心脏病并发CHF心功能IV级(NYHA分级标准)。经2周足量的强心甙、利尿剂、β-受体阻滞剂治疗后心功能无明显改善者64例。随机分成治疗组32例,在常规治疗基础上加培哚普利加MI静脉滴注2周;对照组32例用米力农静脉滴注2周,治疗前后作心肌酶谱、血浆肌钙蛋白I(cTnI)测定,彩色超声心动图测定心功能。结果两组与治疗前比较心功能均有显著改善(P<0.01),两组疗效差异无显著性(P>0.05);治疗后血磷酸肌酸激酶同工酶(CK-MB)及cTnI浓度均有改善,但以治疗组为显著(P<0.01),对照组不明显(P>0.05)。在治疗过程中两组均未见明显不良反应。结论在难治性心力衰竭患者中培哚普利加MI有助于心功能的改善。     

螺内酯治疗冠心病慢性心力衰竭临床观察

目的　观察螺内酯对冠心病慢性心力衰竭的临床疗效。方法　冠心病慢性心力衰竭患者 82例 ,随机分为治疗组 4 2例 ,对照组 4 0例 ,对照组选用利尿剂、ACEI、β_受体阻滞剂、洋地黄制剂为主要治疗药物。治疗组在上述治疗基础上 ,以螺内酯替代保钾利尿剂氨苯喋啶 ,治疗 2 0周后评判疗效。结果　应用螺内酯的治疗组总有效率达 92 8% ,对照组总有效率为 75% ,两组疗效有显著性差异 (P <0 0 5)。结论　醛固酮拮抗剂螺内酯治疗冠心病慢性心力衰竭可明显提高临床效果 ,作为冠心病慢性心力衰竭的常规用药     

Muscle wastage in heart failure: orphan of the heart failure

The patients with heart failure (HF) often exhibit some degree of muscle wasting restricted to the lower limbs. This loss of tissue may become more extensive in some patients, usually when their HF is more advanced, and may affect all body compartments. The underlying metabolic causes are very complex and differ from patient to patient. Three essential contributors are dietary deficiency and loss of nutrients through the digestive tract and metabolic dysfunction. The development of cachexia is an ominous sign and new drugs will be added into our therapeutic armamentarium to fight against cardiac cachexia in the near-future.     

Heart failure in the elderly

Heart failure (HF) is a major disease of the elderly. Since their symptoms of HF are generally light, on admission of the hospitals HF is sometimes in an advanced stage. Therefore, preventive medicine for those with the risk factors of HF is needed as a future strategy of cardiac gerontology. The routine assessment of the HF severity may be performed noninvasively by Nohria's profiles rather than other invasive methods. HF is worsened by the interaction with the co-morbidity factors, such as renal dysfunction and anemia. The interaction between HF and kidney disease (and anemia) is called 'cardiorenal (anemia) syndrome.' Recurrent hospitalization due to HF is common, and the period of hospitalization tends to be long in this syndrome. One of the hopeful therapeutic agents is carperitide, a recombinant human atrial natriuretic peptide. In cardiorenal syndrome, much lower initial doses of carperitide, such as 0.0125 microg/kg/min is recommended for treatment of HF in order to avoid possible worsening of renal dysfunction. In cardiorenal anemia syndrome, supplement of iron, careful blood transfusion in severe cases, administration of recombinant human erythropoietin, should be performed if indicated. However, the possibility of anemia unrelated to HF, such as due to gastrointestinal carcinoma, is also considered in the elderly. In such cases, finding a decrease of serum ferritin preceding that of hemoglobin may contribute to a differential diagnosis of anemia in elderly HF patients. Thus, the therapies considering several features of HF in elderly will contribute to improving quality of life and outcome.     

老年人心力衰竭

心力衰竭（心衰）是老年人常见和主要的疾病。老年人心血管系统及其他脏器结构与功能均呈老龄性变化。心脏储备能力下降,易患高血压、冠心病等多种心血管疾病;同时常又合并多器官疾病。在感染、心肌缺血等多种诱发因素作用下,极易发生心力衰竭。但临床症状较为复杂、多变,且有时又不典型,因此极易误诊或漏诊,故必须及时做出准确的诊断与治疗。老年人心衰必须采用综合治疗措施,并遵循个体化的治疗原则;加强对治疗的指导与管理,缓解症状、提高生活质量、改善预后。     

Heart failure in the elderly

Heart failure (HF) is a clinical syndrome caused by structural and/or functional cardiac abnormalities, resulting in a reduced cardiac output and/or elevated intracardiac filling pressures at rest or during stress. HF is a major public health problem with high prevalence and incidence, involving both high morbidity and mortality, but also high economic costs. The incidence of HF progressively increases with age, reaching around 20% among people over 75 years old. Indeed, HF represents the leading cause of hospitalization in patients older than 65 years in Western countries. Hence, some authors even consider HF a geriatric syndrome, entailing worse prognosis and high residual disability, and often associating some complex comorbidities, common in older population, that may further complicate the course of the disease. On the other hand, however, clinical course and prognosis may be often difficult to predict. In this article, main pathophysiological issues related to the aging heart are addressed, together with key aspects related to both diagnosis and prognosis in elderly patients with HF. Besides, main geriatric conditions, common in the elderly population, are reviewed, highlighting the importance of a comprehensive and multidisciplinary approach.

Heart failure (HF) is a clinical syndrome caused by structural and/or functional cardiac abnormalities, resulting in a reduced cardiac output and/or elevated intracardiac filling pressures at rest or during stress.^[1] HF is a major public health problem with high prevalence and incidence, involving both high morbidity and mortality, but also high economic costs. The incidence of HF progressively increases with age,^[2] reaching around 20% among people over 75 years old.^[3] Indeed, HF represents the leading cause of hospitalization in patients older than 65 years in Western countries.^[4,5]Hence, some authors even consider HF a geriatric syndrome, entailing worse prognosis and high residual disability, often associating some complex comorbidities, common in older population, that may further complicate the course of the disease.^[3,6] However, clinical course and prognosis may be often difficult to predict.^[7,8]In this article, main pathophysiological issues related to the aging heart are addressed, together with key aspects related to both diagnosis and prognosis in elderly patients with HF. Besides, main geriatric conditions, common in the elderly population, are reviewed, highlighting the importance of a comprehensive and multidisciplinary approach.     

Heart failure in the elderly

The aging of the population is, currently, a major phenomenon, drawing the attention of a number of investigators. The significant increase of life expectancies over the past few decades, in addition to social and economic consequences, has lead to a major change in the morbidity and mortality profile of elders. Heart failure (HF) is a condition in which the heart can not pump enough blood to meet the body's needs. HF is predominantly a disorder of the elderly with rates increasing exponentially. The prevalence of HF approximately doubles with each decade of life. As people live longer, the occurrence of HF rises, as well as other conditions that complicate its treatment. Impaired heart function implies a reduced duration of survival. Fortunately, many factors that can prevent HF and improve outcome are known and can be applied at any stage. This review emphasizes the importance of factors inherent in aging itself. Focusing on heart disease, particularly as a disease of aging, can help critically refine management of this acute and chronic disease, as well as foster preventive strategies to reduce the incidence of this common malady.     

Heart failure in the elderly

Invited Editorial