左西孟旦与多巴酚丁胺治疗急性失代偿性心力衰竭疗效和血液学指标比较

目的比较左西孟旦与多巴酚丁胺治疗急性失代偿性心力衰竭的临床效果及对血液学指标的影响。方法选取2018年1月-2019年6月厦门大学附属福州第二医院收治的急性失代偿性心力衰竭患者60例为研究对象,按照随机数字表法分为观察组和对照组各30例。观察组给予左西孟旦治疗,对照组给予多巴酚丁胺治疗。比较2组患者临床疗效及治疗前后血液学指标。结果观察组患者总有效率为90.0%,高于对照组的66.7%(χ2=4.812,P=0.028)。治疗后,2组患者脑钠肽(BNP)、血管内皮生长因子(VEGF)、基质金属蛋白酶-9(MMP-9)水平均低于治疗前,且观察组优于对照组(P<0.01或P<0.05)。结论左西孟旦治疗急性失代偿性心力衰竭效果好,能显著降低BNP、VEGF、MMP-9水平,且不良反应发生率低,值得临床推广。     

重组人脑利钠肽在不同利钠肽水平的急性失代偿性心力衰竭的疗效观察

目的:探讨重组人脑利钠肽在不同利钠肽(BNP)水平的急性失代偿性心力衰竭的疗效。方法:将160例左室射血分数<40%的急性失代偿性心力衰竭患者依据不同的BNP水平分成普通增高组(BNP≤5 000 pg/m L)和极度增高组(BNP>5 000 pg/m L),两组再分成对照组和重组人脑利钠肽亚组(以下称rh BNP组)。在普通增高组患者中,对照组和rh BNP组各40例患者,在极度增高组患者中,对照组和rh BNP组各40例患者。结果:在普通增高组中,rh BNP组治疗后有效率高于对照组,尿量明显多于对照组(P<0.05),治疗后彩超情况也明显优于对照组(P<0.05);在极度增高组中,rh BNP组治疗后并没有体现出较大优势,尿量与对照组比较差异无统计学意义(P<0.05);其治疗后彩超情况与对照组比较差异无统计学意义(P>0.05)。结论:短期重组人脑利钠肽对于BNP≤5 000 pg/m L的患者急性失代偿性心力衰竭的患者具有良好的疗效,但对于BNP>5 000 pg/m L的患者,与对照组相比并没有明显的优势。     

重组人钠脲肽联合左西孟旦对急性失代偿心力衰竭患者LVEF和BNP水平的影响

目的:探讨重组人钠脲肽联合左西孟旦对急性失代偿心力衰竭患者左室射血分数(LVEF)及脑尿钠肽(BNP)水平的影响。方法:将68例急性失代偿心力衰竭患者分为两组,每组34例。对照组采用左西孟旦治疗,研究组在对照组基础上给予重组人钠脲肽治疗;对比两组治疗后心功能改善情况。结果:两组患者治疗后BNP、醛固酮、肾上腺素、血管紧张素Ⅱ水平显著降低(P<0.05),LVEF、每搏输出量(SV)水平显著提高(P<0.05);研究组治疗后BNP、醛固酮、肾上腺素、血管紧张素Ⅱ水平显著优于对照组,差异有统计学意义(t=2.133、6.212、4.055、2.969、2.284、5.999,P<0.05);研究组治疗后LVEF、SV水平显著高于对照组,差异有统计学意义(t=3.705、3.217,P<0.05);两组患者在治疗过程中均无明显不良反应发生,肝肾功能指标均未出现明显异常,无死亡病例出现。结论:重组人钠脲肽联合左西孟旦治疗急性失代偿心力衰竭,能显著提高患者的LVEF,降低BNP水平,改善心功能。     

急性失代偿性心力衰竭患者采用左西孟旦治疗的临床疗效观察

目的探讨急性失代偿性心力衰竭采用左西孟旦治疗的临床效果。方法选取我院收治的86例急性失代偿性心力衰竭患者作为研究对象,按照患者就诊顺序将其随机分为对照组与研究组,每组43例,研究组患者行左西孟旦治疗,对照组行多巴酚丁胺药物治疗,观察两组患者病症改善情况,统计两组治疗的不良反应发生率。结果研究组治疗总有效率为79.1%,对照组总有效率为58.2%,组间比较差异明显(P<0.05);两组治疗后患者每搏心排血量与左心室射血分数均有提升,且相比于对照组,研究组每搏心排血量改善效果更加明显(P<0.05);研究组不良反应发生率明显低于对照组,组间比较差异有统计学意义(P<0.05)。结论应用左西孟旦治疗急性失代偿性心力衰竭能够有效改善患者心功能,疗效显著且无严重的不良反应,可以进行推广应用。     

连续性静脉血液超滤治疗急性失代偿性心力衰竭的疗效及对脑钠肽的影响

目的 探讨连续性静脉血液超滤治疗急性失代偿性心力衰竭的疗效及对脑钠肽的影响.方法 选取在本院进行治疗的急性失代偿性心力衰竭患者94例,随机分为两组,每组47例.对照组实施利尿扩血管和强心治疗,观察组在此基础上采用连续性静脉血液超滤治疗,比较两组患者相关指标及呼吸困难情况.结果 治疗后,观察组心率及脑钠肽(BNP)水平较对照组明显降低,差异有统计学意义(P＜0.05);观察组呼吸困难改善情况较对照组明显提高,差异有统计学意义(P＜0.05).结论 对急性失代偿性心力衰竭患者实施连续性静脉血液超滤治疗效果较为显著,可有效改善患者呼吸困难情况,促进心功能恢复.     

左西孟旦治疗老年缺血性心肌病所致急性失代偿性心力衰竭100例

目的:探究左西孟旦治疗老年缺血性心肌病所致急性失代偿性心力衰竭的效果。方法:将某院2016年1月~2017年1月老年缺血性心肌病所致急性失代偿性心力衰竭患者100例根据方法不同分对照组、研究组各50例。对照组采用基础治疗方法,研究组在对照组基础上辅以左西孟旦治疗,比较两组患者临床治疗效果、心衰纠正时间、心电图恢复正常时间、副作用发生率、治疗前后心功能。结果:研究组患者临床治疗效果比对照组高,P0.05;研究组心衰纠正时间、心电图恢复正常时间比对照组短,P0.05;两组均无严重副作用,P0.05。两组治疗前心功能无显著差异,P0.05;研究组治疗后心功能指标优于对照组,P0.05。结论:左西孟旦治疗老年缺血性心肌病所致急性失代偿性心力衰竭效果确切,可有效改善患者病情,纠正心衰,改善心电图和心功能,对患者预后有益,值得推广。     

重组人脑利钠肽用于治疗失代偿性心力衰竭患者的疗效及其护理对策

目的:评价冻干重组人脑利钠肽对失代偿性心力衰竭患者的临床疗效用其护理对策。方法:选取2014年1月—2015年12月间收治的失代偿性心力衰竭患者74例作为研究对象,根据治疗方法的不同将其分为对照组(n=37)和观察组(n=37);对照组患者均给予冻干重组人脑利钠肽和常规护理方法治疗,观察组患者均给予冻干重组人脑利钠肽和综合护理方法治疗,评价两组患者治疗后的总有效率和护理措施对心动图的变化情况。结果:观察组患者治疗后的总有效率为94.59%高于对照组为81.80%(P<0.05);两组患者治疗后LVD、LVEF均有所改善;观察组患者治疗1周后LVEF分值高于对照组(P<0.05)。结论:采用冻干重组人脑利钠肽治疗失代偿性心力衰竭患者并配予综合护理干预,能提高患者的临床疗效和心动图的改善。     

连续性血液净化技术在失代偿性心力衰竭合并急性肾损伤治疗中的临床研究

目的探讨连续性血液净化技术在失代偿性心力衰竭合并急性肾损伤治疗的临床研究。方法回顾性分析2015年5月~2016年12月于本院收治失代偿性心力衰竭合并急性肾损伤患者60例根据治疗措施不同将其分为试验组及对照组,每组各30例,对照组给予标准治疗+利尿剂强化治疗,试验组给予标准治疗+连续性血液净化治疗,统计分析两组患者治疗前后心率、平均动脉压、血氧饱和度、APACHEⅡ得分、肌酐、尿素氮、葡萄糖及钾的水平情况。结果试验组患者治疗后心率、APACHEⅡ得分均低于对照组,而平均动脉压及血氧饱和度试验组高于对照组,差异均有统计学意义(P<0.05);试验组患者干预后6、24、72h血清肌酐、尿素氮及钾水平均低于对照组,差异有统计学意义(P<0.05),而干预后6、24、72h血清葡萄糖水平两组患者无明显差异(P>0.05)。结论连续性血液净化技术能有效改善失代偿性心力衰竭合并急性肾损伤患者肾功能,同时能改善患者血流动力学,提高临床治疗效果。     

不同类型急性失代偿心力衰竭患者运用冻干重组人脑利钠肽治疗的临床研究

目的探讨冻干重组人脑利钠肽对不同类型心力衰竭患者的治疗效果。方法将本院2008年6月～2011年6月收治的190例患者按心力衰竭类型分组,各心力衰竭类型组患者随机平均分为观察组和对照组。观察组患者给予常规治疗;对照组患者在常规治疗的基础上辅以冻干重组人脑利钠肽药物治疗。分析各组患者的临床疗效。结果急性失代偿性右心力衰竭观察组患者治疗前、后的临床疗效与对照组患者比较,差异存在统计学意义（P〈0.05）;急性失代偿性左心力衰竭观察组患者治疗前、后的临床疗效与对照组患者比较,差异无统计学意义（P〉0.05）;急性失代偿性全心力衰竭观察组患者治疗前、后的临床疗效与对照组患者比较,差异存在统计学意义（P〈0.05）。结论冻干重组人脑利钠肽联合常规治疗对不同程度心力衰竭患者的疗效良好,值得临床关注。     

重组人脑钠肽治疗慢性心力衰竭急性发作失代偿期的临床疗效观察

目的对慢性心力衰竭患者在急性发作失代偿期应用重组人脑钠肽(rh BNP)进行治疗的临床效果进行分析研究。方法将我院收治的急性发作期的慢性心力衰竭患者随机分为两组,一组接受常规抗心力衰竭治疗,一组在常规治疗上加用rh BNP进行治疗,比较两组患者临床治疗效果。结果接受rh BNP治疗的患者组,其临床治疗有效率明显高于接受常规治疗的患者组,P<0.05。结论 rh BNP在慢性心力衰竭患者急性发作期治疗上具有突出效果,能够有效纠正心力衰竭症状,减少不良反应的发生。     

Congestive Heart Failure

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ß-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: (i) maximal tolerated dosages of ACE inhibitors; (ii) ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema; (iii) adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; (iv) relatively low dosages of digoxin (serum concentrations of ≤ 1.0 ng/dl) if not contraindicated; and (v) diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.     

Chronic Heart Failure

Heart failure (HF) is a complex syndrome characterized by the inability of the heart to maintain a normal cardiac output without elevated intracardiac filling pressures, resulting in signs of pulmonary and peripheral edema and symptoms of dyspnea and fatigue. Central to the management of HF is a multifaceted pharmacological intervention to abate the harmful counter-regulatory effects of neurohormonal activation and avid salt and water retention. Whereas up to 40 years ago HF was managed with diuretics and leaf of digitalis, the cornerstones of therapy for HF patients with systolic dysfunction now include ACE inhibitors or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers), β-adrenoceptor antagonists (β-blockers), and aldosterone antagonists, which have significantly improved survival. However, with the increasing number of beneficial therapies, there are challenges to implementing all of them. Specific cardiomyopathies also merit specific considerations with respect to treatment, and — unfortunately — there is no therapy for HF with preserved left ventricular ejection fraction that has been shown to improve survival. Although mortality has improved in HF, the biggest challenge to treatment lies in addressing the morbidity of this disease, which is now the most common reason for hospital admission in our aged population. As such, there are many therapies that may serve to improve the quality of life of HF patients. Future HF treatment regimens may include direct cellular therapy via hormone and cytokine signaling or cardiac regeneration through growth factors or cell therapy.     

Apoptosis and Heart Failure

A large volume of experimental data supports the presence of apoptosis in failing hearts. Apoptosis in many types of cells results from exposure to cytotoxic cytokines or damaging agents. Cytotoxic cytokines such as tumor necrosis factor (TNF)-α; or Fas ligand (FasL) bind to their receptors to activate caspase-8, while damaging agents can cause mitochondrial release of cytochrome c, which can initiate activation of caspase-9. Caspase-8 or -9 can activate a cascade of caspases. The p53 protein is often required for damaging agent-induced apoptosis. An imbalance of proapoptotic factors versus prosurvival factors in the bcl-2 family precedes the activation of caspases. Given these typical changes of apoptosis found in many cell types, the apoptotic pathway in cardiomyocytes is somewhat unconventional since in vivo experimental data reveal that apoptosis does not appear to be controlled by TNF-α;, FasL, p53 or decrease of bcl-2. In vitro and in vivo studies suggest the importance of mitochondria and activation of caspases in cell death occurring in failing hearts. Oxidants, excessive nitric oxide, angiotensin II and catecholamines have been shown to trigger apoptotic death of cardiomyocytes. Eliminating these inducers reduces apoptosis and reverses the loss of contractile function in many cases, indicating the feasibility of the pharmacological application of antioxidants, nitric oxide synthetase inhibitors, ACE inhibitors, angiotensin II receptor antagonists and adrenergic receptor antagonists. Most inducers of apoptosis initiate a cascade of signaling events, including activation of the p38 mitogen-activated protein kinase. Small molecule inhibitors of p38 have been shown to be capable of preventing apoptosis and loss of contractile function associated with ischemia and reperfusion. Although further experimental work is needed, several studies have already indicated the beneficial effect of caspase inhibitors against cell loss and features of heart failure in vitro and in vivo. These studies indicate the importance of inhibiting apoptosis in therapeutic interventions against heart failure.     

慢性心衰的药物治疗

心衰内科治疗近10年有重大进展。轻中度心衰2级OPT治疗(Optimal Medical Therapy)应用ACE抑制剂与β受体阻滞剂可降低死亡率40％以上，如果再加CRT-D治疗可进一步降低死亡率超出60％。     

Device Therapy for Heart Failure

Surgical approaches to heart failure (HF) management have become a necessary strategy in response to a waiting list that is expanding in the face of a limited supply of organ donors. Multiple studies have supported the safety and efficacy of device-based therapy. Among the device-based therapy options, ventricular assist devices (VADs) represent an alternative to heart transplantation with the capability to function as short-term support, bridge-to-transplantation or recovery and as long-term support. VAD support may be considered in those with refractory cardiogenic shock or those with decompensated chronic HF that is unresponsive to maximized medical therapy. Composite scoring scales may be used to risk-stratify patients using clinical and laboratory values to allow more systematic patient selection. As the pursuit for a perfect device continues, so does the search for the best objective index to guide referral. Technologic advances will enhance device performance and extend VAD use into community practice. This discussion aims to highlight criteria for candidate selection and referral for VAD implantation.     

Immunosuppressive Therapy for Heart Failure

Therapy with β-adrenoceptor antagonists, ACE inhibitors and most recently, Spironolactone was established for reducing all-cause mortality in patients with congestive heart failure (CHF), improving patient clinical status and inhibiting the disease progression. Unfortunately, despite optimal therapy for CHF in some patients, the disease progresses and, as yet, no conclusive mechanism has been identified for deterioration of cardiac function in patients with heart failure. Defining the cause of CHF in patients with dilated cardiomyopathy may have prognostic and therapeutic implications. Clinical and experimental evidence suggests that long-term inflammation may play a key part in the development of heart failure in patients with cardiomyopathy due to ischemic heart disease and those with cardiomyopathy due to non-ischemic cases. Because chronic immune myocardial injury, found in patients with CHF is myocardial restricted, endomyocardial biopsy with immunohistological markers of immune-mediated injury may offer us new guidelines to patient selection for immunomodulatory therapies. Few randomized placebo controlled studies addressing the effectiveness of suppression and modulation of the immune system in patients with heart failure gave unequivocal results. Moreover, none of the abovementioned randomized studies has shown decreased mortality in the immunosuppressively treated patients compared with conventionally treated patients. In the US Myocarditis Treatment Trial, for example, mortality was 20% overall at 1 year and 56% at 4.3 years of follow-up. In addition, spontaneous improvement of left ventricular systolic function has been reported in 30–40% of conventionally treated patients with CHF due to dilated cardiomyopathy. Given the high proportion of patients who improve spontaneously, selection of patients for immunosuppressive therapy should be preceded by treating heart failure with the individualized conventional therapy (ACE inhibitors, β-adrenoceptor antagonists, Spironolactone) for at least 6 months. Final decision to use immunomodulatory therapies should be based on comprehensive clinical measures of disease progression.     

ACE Inhibitors in Heart Failure

ACE inhibitors have significantly decreased cardiovascular mortality, myocardial infarction (MI), and hospitalizations for heart failure (HF) in patients with asymptomatic or symptomatic left ventricular (LV) systolic dysfunction. Furthermore, the extended 12-year study of the SOLVD (Studies Of Left Ventricular Dysfunction) Prevention and Treatment trials (X-SOLVD) demonstrated a significant benefit with a reduction of cumulative all-cause death compared with placebo (50.9% vs 56.4%) [hazard ratio (HR) 0.86; 95% CI 0.79, 0.93; p < 0.001]. The survival benefits and significant reductions in cardiovascular morbidity related to treatment with ACE inhibitors are likely achieved by titrating the dose of ACE inhibitors to the target dose achieved in clinical trials. Although the ATLAS (Assessment of Treatment with Lisinopril And Survival) study, which randomly allocated HF patients to low- or high-dose lisinopril, showed no significant difference between groups for the primary outcome of all-cause mortality (HR 0.92; 95% CI 0.82, 1.03), the predetermined secondary combined outcome of all-cause mortality and HF hospitalization was reduced by 15% for the patients receiving high-dose lisinopril compared with low-dose (p < 0.001) with a 24% reduction in HF hospitalization (p = 0.002). Despite the use of ACE inhibitors, blockade of the renin angiotensin aldosterone system (RAAS) remains incomplete, with evidence of continued production of angiotensin II by non-ACE-dependent pathways. The safety and potential benefits of angiotensin receptor antagonists (angiotensin receptor blockers [ARBs]) in patients with impaired systolic function have been assessed in moderate to large clinical trials. In patients with impaired LV systolic function and HF, combination therapy with ARBs with recommended HF therapy including ACE inhibitors in patients who remain symptomatic may be considered for its morbidity benefit. Based on the CHARM (Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity)-Added data, candesartan cilexetil in addition to standard HF therapy results in a further reduction of cardiovascular mortality. Close monitoring of renal function and serum potassium levels is needed in this setting. The VALIANT (VALsartan In Acute myocardial iNfarction Trial) results suggest that valsartan is as effective as captopril in patients following an acute MI with HF and/or LV systolic dysfunction and may be used as an alternative treatment in ACE inhibitor-intolerant patients. There was no survival benefit with valsartan-captopril combination compared with captopril alone in this trial. Despite these results, ACE inhibitors remain the first-choice therapeutic agent in post-MI patients, and ARBs can be used in patients with clear intolerance. Although the use of ACE inhibitors may be appealing in patients with HF and preserved LV systolic function, there is currently no evidence from large clinical trials to support this.     

心力衰竭合并心律失常的治疗

心力衰竭是一种复杂的临床综合征,具有很高的致残和致死率。心力衰竭患者死亡的主要原因为泵衰竭或心源性猝死（SCD）,而后者最主要的原因就是恶性心律失常。随着循证医学证据的增加和心力衰竭机制研究的进展,并通过肾素一血管紧张素系统抑制药（RAS抑制药）和β受体阻滞药等药物的广泛应用,心力衰竭患者的死亡率显著降低,患者的生命得到了延长,生活质量也有很大的改善。但在心力衰竭患者中复杂性恶性心律失常仍有很高的发病率,且伴有此类心律失常者年死亡率可高达50％,其中相当的比例死于心律失常导致的猝死。因此要提高心力衰竭患者的生存率,除了有效的抗心力衰竭治疗外,还应正确、合理地抗心律失常治疗。