舒张性心力衰竭临床诊治分析

目的探讨舒张性心力衰竭的临床特征及治疗方法。方法回顾性分析我院2006年1月至2009年1月收治的98例舒张性心力衰竭患者的临床资料。结果本组98例中,12例治疗无效死亡,其他患者均康复出院。结论舒张性心力衰竭治疗以缓解症状,改善生活质量,阻止或延缓心室重塑,降低病死率为主。改善DHF的症状主要采用：减少回心血量（利尿剂）,改善左室的松弛（钙离子拮抗剂、血管紧张素转换酶抑制剂）,逆转左室肥厚（血管紧张素转换酶抑制剂、血管紧张素II受体拮抗剂、螺内酯）,维持心房的收缩功能,控制过快的心率（β受体阻滞剂及抗心律失常药）。DHF时因其LVEF基本正常,故洋地黄类正性肌力药物一般不用,若有左心力衰竭导致肺水肿时,可短期谨慎应用,合并快速心室率的房颤时则可少量使用。     

老年舒张性心力衰竭193例临床分析

舒张性心力衰竭（diastolic heart failure,DHF）是指一组以具有心力衰竭的症状和体征、左心室射血分数正常而以心室肌舒张功能障碍、顺应性减退、僵硬度增高为特点的临床综合征。有报道30％-40％的心力衰竭患者为单纯舒张性心力衰竭,有研究认为老年即是DHF的危险因素之一皿。。本文旨在对2005年7月-2009年2月我院193例老年DHF患者临床情况分析,报道如下。     

110例舒张性心力衰竭临床分析

目的 分析舒张性心力衰竭的临床特征及治疗方法.方法 回顾我院2005年2月至2009年12月收治110例舒张性心力衰竭(DHF)患者的临床资料进行汇总结分析.结果 本组110例均诊断为DHF,一般心力衰竭程度较轻,可有充血性心力衰竭表现多为肺淤血表现,心脏超声检查,左心室不大,左心室壁大多增厚,左房增大,LVEF正常,舒张功能异常.110例DHF患者经治疗后,显效64例(58.18%),有效39例(35.45%),无效7例(6.37%),总有效率为93.63%.结论 应及早正确诊断DHF,病因预防及抗心室重构治疗对DHF的防治尤其重要;联合治疗DHF减轻心室重构并积极改善心功能;洋地黄类药物治疗DHF不敏感应慎用.     

舒张性心力衰竭的心肌自身机制

舒张性心力衰竭（DHF）是一组以具有心力衰竭的症状和体征,射血分数正常而舒张功能（心肌松弛性和顺应性）异常为特征的临床综合症.且往往发生于收缩性心力衰竭之前,成为临床独立的疾病,约占心力衰竭患者的1/3.舒张性心衰的发生与患者的年龄有关.     

舒张性心力衰竭临床诊治分析

目的探讨舒张性心力衰竭（DHF）的临床特点及诊治情况。方法回顾性分析我院2006年5月至2009年12月住院治疗的66例DHF患者的临床资料。在积极治疗原发病的基础上,以缓解心力衰竭症状为主,同时针对心力衰竭演变过程中的潜在机制采取治疗措施。结果本组66例DHF患者经积极治疗后,症状完全消失、心功能I级以上56例（84.84%）;心功能I或Ⅱ级8例（12.12%）;有效64例（96.97%）。2例（3.03%）临床症状改善不明显自动出院,无死亡病例。结论本组存在心力衰竭的症状和体征,心脏超声示DHF;DHF的治疗在针对基础疾病采取对症治疗措施基础上,以β受体阻滞剂、血管紧张素转换酶抑制（ACEI）、血管紧张素Ⅱ受体阻滞剂（ARB）以及为主。     

舒张性心力衰竭115例临床分析

目的探讨舒张性心力衰竭（DHF）的诊断和治疗。方法对近3年住院治疗的DHF患者的临床资料进行回顾性分析。结果DHF占全部心力衰竭患者的46．2％，男女比例为1：1．47，原发病以高血压、冠心病为主。结论患者存在心力衰竭的症状和体征，心脏超声示左心室舒张功能障碍，左心室射血分数≥50％，即诊断DHF；治疗应用血管紧张素转换酶抑制剂、硝酸酯类血管扩张剂、利尿剂、钙通道阻滞剂和β受体阻滞剂以缓解DHF症状，一般不用洋地黄类强心剂，同时针对基础疾病采取治疗措施。     

心脏舒张功能临床评价的研究进展

舒张性心力衰竭（DHF）是指心室收缩功能正常，但具有充血性心力衰竭的客观症状、体征的临床综合征。目前诊断DHF多采用改良的DHF诊断标准，同时符合下述3条诊断为明确的DHF：①明确DHF证据；②客观证据说明此次心力衰竭事件发生后短期收缩功能正常（心力衰竭发生72h内EF〉50％）；③心导管检查证实存在舒张功能障碍的客观依据。只具备①和②两条，诊断可能的DHF；只有第一条存在，而EF〉50％的标准并不是在心力衰竭发生72h内获取的，则诊断疑似的DHF。另有学者认为，只要满足有充血性心力衰竭的症状、体征，且EF〉50％，不用测定舒张功能指标也可诊断DHF。     

舒张性心力衰竭临床诊治分析

舒张性心力衰竭（diastolic heart failure，DHF）是指在心室收缩功能正常的情况下，心室松弛性和顺应性减低使心室充盈量减少和充盈压升高，从而导致肺循环和体循环瘀血的一种综合征，占充血性心力衰竭总人数的30％左右。现对我院2004～2008年收治150例舒张性心力衰竭患者的临床资料进行分析，报告如下。     

舒张性心力衰竭临床诊治分析

舒张性心力衰竭(diastolic heart failure,DHF)是指在心室收缩功能正常的情况下,心室松弛性和顺应性减低,从而使心室充盈量减少以及充盈压升高,导致肺循环和体循环瘀血的一种综合征.由于DHF临床特征不典型,为了进一步探讨该病的临床特点及诊治方法,现对我院2008年6月至2010年12月收治的60例舒张性心力衰竭患者的临床资料分析如下.     

慢性舒张性心力衰竭合并COPD老年患者的临床护理措施分析

目的研究探讨慢性舒张性心力衰竭(DHF)合并慢性阻塞性肺病(COPD)老年患者的临床护理措施。方法对2009年3月至2013年4月期间来我院治疗的80例DHF合并COPD老年患者进行临床干预性护理;待护理3个月后,对患者血压、心率、肺功能等指标进行测定。结果对所有患者实施干预性护理措施后,患者的心肺功能、血压与干预前相比均有明显改善,差异具有统计学意义(P<0.05)。结论对慢性舒张性心力衰竭合并慢性阻塞性肺病老年患者实行临床干预性护理,对患者的血压、心肺功能的恢复有显著的疗效,同时也减轻了患者的痛苦,有利于患者恢复健康。     

Diastolic heart failure: recognition, diagnosis and management

A variety of community-based epidemiological studies have suggested that 30-50% of patients with heart failure symptoms appear to have preserved left ventricular (LV) systolic function when assessed by echocardiography or similar techniques suggesting 'diastolic heart failure' (DHF) as its cause. The prognosis of these patients is characterised by morbidity and mortality similar to, but less overt than, patients with systolic dysfunction. However, rates of readmission for symptom control are broadly similar in patients with DHF or in those with systolic impairment. Thus, there are many similarities in the portrayal of both systolic and DHF but equally; there are also many key differences. Certainly, while there are several successful therapies for patients with systolic heart failure, the management of patients with DHF is poorly defined. In this review, the gaps in current knowledge and practice, which is creating this therapeutic void will be addressed.     

Diastolic heart failure: recognition,diagnosis and management

A variety of community-based epidemiological studies have suggested that 30 – 50% of patients with heart failure symptoms appear to have preserved left ventricular (LV) systolic function when assessed by echocardiography or similar techniques suggesting ‘diastolic heart failure’ (DHF) as its cause. The prognosis of these patients is characterised by morbidity and mortality similar to, but less overt than, patients with systolic dysfunction. However, rates of readmission for symptom control are broadly similar in patients with DHF or in those with systolic impairment. Thus, there are many similarities in the portrayal of both systolic and DHF but equally; there are also many key differences. Certainly, while there are several successful therapies for patients with systolic heart failure, the management of patients with DHF is poorly defined. In this review, the gaps in current knowledge and practice, which is creating this therapeutic void will be addressed.     

Bisoprolol inhibits sodium current in ventricular myocytes of rats with diastolic heart failure

1. Changes in sodium currents (I(Na)) in heart failure contribute to cardiac electrophysiological alterations and, thereby, to ventricular arrhythmias. Bisoprolol has anti-arrhythmic effects, but its direct effect on I(Na) in cardiac cells remains unclear. Accordingly, in the present study we investigated the effects of bisoprolol on ventricular I(Na) in diastolic heart failure (DHF) and normal rats. 2. The DHF model was produced by abdominal aortic coarctation for 4 weeks and single ventricular myocytes were isolated by enzymatic dissociation. The electrophysiological actions of bisoprolol on I(Na) currents were investigated using a whole-cell patch-clamp technique. 3. The membrane capacitance of rats in the DHF group was significantly greater than that of the control group and the current-voltage curve was simultaneously shifted downward. Bisoprolol concentration-dependently decreased I(Na) in ventricular myocytes of both groups (at -45 mV), with IC(50) values of 19.53 +/- 0.06 and 40.78 +/- 0.03 micromol/L in the control and DHF groups, respectively. 4. In both groups, the current-voltage curves were shifted upwards, whereas activation potentials, peak currents and reversal potentials showed no significant changes. At -45 mV, the descent ratio of current densities in the DHF group was lower than that of the control group. In both groups, inactivation curves were shifted to more negative potentials, but activation curves and recovery curves were not altered. Changes in the half-inactivation voltage, V(0.5), and the slope of the inactivation curve, S, were similar for both groups. 5. In conclusion, bisoprolol concentration-dependently decreases I(Na) in ventricular myocytes of DHF and normal rats, which could be responsible, at least in part, for its anti-arrhythmic effects.     

卡维地洛对舒张性心力衰竭患者血浆脑钠肽及心功能的影响

目的评价卡维地洛对舒张性心力衰竭(DHF)患者血浆脑钠肽及心功能的影响。方法 46例DHF患者,按入院顺序随机分为卡维地洛治疗组23例,对照组23例。两组均给予常规治疗,包括血管紧张素转换酶抑制剂、钙离子拮抗剂及利尿剂,治疗组在此治疗基础上加用卡维地洛6.25mg,2次/d,逐渐增至25mg,2次/d。治疗4周后随访8周,检测两组患者血浆脑钠肽浓度及左室射血分数(LVEF)。结果 8周后随访,与对照组比较,治疗组血浆脑钠肽浓度降低显著(P<0.01),LVEF增加明显(P<0.01),未见严重不良反应。结论卡维地洛能明显降低DHF患者血浆脑钠肽浓度,改善心功能,且安全有效。     

Update in the management of diastolic heart failure

Diastolic heart failure (DHF) is characterized by the clinical presentation of heart failure in the setting of preserved left ventricular systolic function and evidence of diastolic dysfunction. It is estimated to be present in at least one-third of patients, who represent the signs and symptoms of heart failure, and is especially prevalent among the elderly population. Despite an increasing understanding of the pathophysiology of this disease and the improvement of diagnostic and prognostic assessment, the management of DHF remains to be established. Medical therapy consists of the cautious use of diuretics, and some studies suggested the beneficial role of beta-blockers and calcium antagonists. The rationale of current therapy is largely dependent on understanding the pathophysiology of DHF and observations from clinical trials that included relatively small numbers of patients. Large, multicenter, randomized, controlled studies are needed to define the role of various therapeutic agents in DHF, and whether the prognosis of the disease will be altered. The SWEDIC trial observed that carvedilol treatment in patients with DHF was associated with an improvement in diastolic indices measured by Doppler echocardiography. The CHARM-Preserved trial reported a non-significant reduction of cardiovascular death or admission for heart failure. Other studies which are underway include PEP-CHF and the Hong Kong Diastolic Heart Failure study. They will play a pivotal role in ascertaining the therapeutic efficacy of various agents and will help experts to set up treatment guidelines for this common condition.     

Pravastatin attenuates left ventricular remodeling and diastolic dysfunction in angiotensin II-induced hypertensive mice

BACKGROUND: A substantial proportion of patients with heart failure have a normal ejection fraction and diastolic dysfunction. However, there are few data available to guide the therapy of these patients. The effects of statins on cardiac remodeling are well documented in animal models and it is reported that statin therapy revealed a survival benefit in patients with diastolic heart failure (DHF). However, the exact mechanisms of statins possibly explaining the decreased cardiovascular morbidity and mortality in patients with DHF have not been elucidated. METHODS: We used 8-week-old male C57BL/6J mice, in which angiotensin II was subcutaneously infused for 4 weeks to mimic cardiac remodeling and fibrosis. They were treated with either normal saline or pravastatin in daily doses, which did not lower the serum cholesterol levels and blood pressure. RESULTS: Pravastatin improved diastolic dysfunction in angiotensin II-induced hypertensive mice, which was associated with the amelioration of left ventricular hypertrophy and remodeling. However, statin treatment showed no effect on the increased systolic blood pressure or cholesterol levels by angiotensin II infusion. The cardioprotective effects of pravastatin were closely associated with the downregulation of collagen I, transforming growth factor-beta, matrix metalloproteinases-2 and -3, atrial natriuretic factor, interleukin-6, tumor necrosis factor-alpha, ROCK1 gene expression, and the upregulation of endothelial nitric oxide synthase gene expression. CONCLUSIONS: The beneficial effects of pravastatin on DHF and structural remodeling are through cholesterol- independent mechanism of statins or "pleiotropic" effects of statins involving improving or restoring endothelial function and decreasing vascular inflammation. These findings suggest the potential involvement of ROCK1. Thus, treatment with pravastatin might be beneficial in patients with DHF.     

Left Ventricular Diastolic Dysfunction in Diabetic Patients

Patients with signs and symptoms of heart failure and a preserved left ventricular (LV) systolic function may have significant abnormalities in diastolic function. This condition is called diastolic heart failure (DHF) and is observed in about 40% of patients with chronic heart failure (CHF). Diabetes mellitus is one of the major risk factors for DHF. Diastolic dysfunction is observed in about 40% of patients with diabetes mellitus and correlates with poor glycemic control. Suggested mechanisms for diastolic dysfunction in the diabetic heart are: (i) abnormalities in high-energy phosphate metabolism; (ii) impaired calcium transport; (iii) interstitial accumulation of advanced glycosylation end products; (iv) imbalance in collagen synthesis and degradation; (v) abnormal microvascular function, (vi) activated cardiac renin-angiotensin system; (vii) decreased adiponectin levels; and (viii) alteration in the metabolism of free fatty acids and glucose. Because most large, randomized clinical trials in CHF have enrolled only patients with systolic dysfunction, the specific management of diastolic dysfunction is largely unknown. The CHARM-Preserved (Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity-Preserved) trial, the only mega trial specific for DHF (LV ejection fraction >40%), showed that the angiotensin II type 1 receptor antagonist (angiotensin receptor blocker [ARB]) candesartan cilexetil reduced hospital admissions for CHF but not cardiovascular death. Currently, the pharmacologic treatment used in systolic heart failure is also recommended in DHF and includes administration of diuretics and nitrates for pulmonary congestion, and long-term management with ACE inhibitors, ARBs, aldosterone antagonists, and beta-adrenoceptor antagonists. Poor glycemic control is associated with a high incidence of heart failure in diabetic patients, but the preferable antihyperglycemic regimen for DHF in patients with diabetes mellitus needs to be determined in further studies.     

Duration of the beneficial effects of levosimendan in decompensated heart failure as measured by echocardiographic indices and B-type natriuretic peptide

Levosimendan is effective in the treatment of decompensated heart failure. The beneficial effects of a single dose of levosimendan last much longer than those of other inotropes. However, the exact duration of the beneficial effects is unknown. We prospectively determined the duration of the cardiac effects, as measured by echocardiography, of levosimendan (LS) following a 24-hour infusion regimen in patients with decompensated heart failure (DHF). The effects of LS on plasma B-type natriuretic peptide (BNP) were also examined. Twenty patients with DHF displaying (1) deteriorating symptoms despite optimal oral therapy, (2) left ventricular ejection fractions (LVEF) < 35%, and (3) cardiac indices of < 2.5 L/m/min received 24 hours of LS infusion. Echocardiography and BNP measurements were performed pre- and postinfusion and were reassessed on days 7, 30, and 90. Left ventricular systolic function indices (cardiac output and LVEF), LV filling pressure indices, and right ventricular systolic function indices all improved following LS treatment. Most of these improvements were sustained for at least 7 days (P < 0.05) and returned to baseline by day 30 postinfusion and remained so on day 90. Plasma BNP also displayed the same pattern of transient improvements. In conclusion, LS transiently improved the cardiac function, and the effects lasted for at least 7 days after discontinuation of infusion. Most effects, except LVEF, were not significantly different from baseline on day 30.     

辛伐他汀减轻舒张功能不全大鼠心肌线粒体损伤

目的：探讨辛伐他汀对舒张功能不全心衰（DHF）大鼠心脏功能的作用及机制。方法：50只雄性SD大鼠,随机分为对照组、DHF组、辛伐他汀1mg组（S1组）、2mg组（S2组）和4mg组（S4组）。采用腹主动脉缩窄建立DHF模型,S1、S2、S4组大鼠术后灌胃分别给予辛伐他汀1、2、4mg·kg^-1·d^-1,对照纽和DHF组大鼠给予同等量生理盐水。4周末心脏B超检测心功能,颈动脉插管记录血流动力学,分光光度计检测心肌线粒体丙二醛（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）含量,电镜检测心肌线粒体超微结构。结果：DHF组大鼠左室后壁（LVPW）、室间隔（IVS）、左室心脏指数（LVM）、E／A比值增高,左室收缩压（LVSP）、左室舒张末期压（LVEDP）升高,左室松弛时间常数（Tau）延长,平均左室内压最大下降速率（LV-dp／dtmax）下降,心肌SOD和GSH-Px下降、MDA增加,电镜示心肌细胞肌丝排列不整齐、线粒体肿胀及空泡化等线粒体损伤。辛伐他汀改善DHF大鼠心功能和血流动力学指标,同时减轻线粒体结构和功能损伤,随着辛伐他汀剂量的增加,以上指标改善程度越明显。结论：辛伐他汀减轻DHF大鼠心肌细胞和线粒体损伤是辛伐他汀保护DHF大鼠心功能的重要机制。     

氯沙坦钾对高血压左心室肥厚的治疗效果

目的探讨氯沙坦钾对高血压左心室肥厚患者的治疗效果。方法以本院收治的40例高血压左心室肥厚患者为实验对象,所有患者均使用氯沙坦钾进行治疗,回顾性分析患者临床治疗前后临床症状和各项临床检查指标的变化对比情况。结果经过治疗,所有患者临床症状都有所缓解,患者临床治疗前后血压值水平,以及心脏超声检查结果与临床治疗前对比差异有统计学意义（P〈0.05）。结论本次实验结果表明,使用氯沙坦钾治疗高血压左心室肥厚,能够显著改善患者的各项临床症状,使各项指标值逐步恢复正常,能够对患者的心室肥厚问题产生逆转作用,因而具有较高的临床推广和使用价值。