舒张性心衰和收缩性心衰临床比较(英文)

目的:回顾性分析心衰患者的资料,了解舒张性心衰和收缩性心衰临床特点、费用、疗效等的异同,提高对二者的认识。方法:选择福建医科大学附属协和医院心内科住院的807例心衰患者,根据左室射血分数(LVEF)水平分为两组:LVEF>45%者为舒张性心衰(DHF)组,LVEF≤45%者为收缩性心衰(SHF)组,然后每个组根据NYHA心功能分级分为Ⅱ、Ⅲ、Ⅳ3组。比较两组的临床资料。结果:结构比:DHF和SHF分别占81.3%及18.7%。心功能:相对DHF组,SHF组的NYHAⅢ、Ⅳ级(23.5%,9.6%比47.7%,21.9%),E/A显著增大[(0.74±0.31)比(1.26±0.56)]。临床特点:DHF组女性比例较SHF组显著增大;心脏增大,心律失常比例显著增大,冠心病、肺炎、慢性肾功能不全的比例显著上升,高血压病比例、入院收缩压水平则显著较低,以上P均<0.001;SHF组平均住院时间明显延长[(12.9±8.1)d比(14.5±11.6)d,P<0.05],住院费用[12323(8530～33815)元比19554(9186～49927)元,P<0.05]、住院期间死亡率(0.5%比3.3%,P<0.01)显著较高。结论:舒张性心衰在心衰中占的比例很大,收缩性心衰的心衰更重,心脏损害更重,住院天数更长,住院费用更多、住院期间死亡率更高。     

Ventriculovascular coupling in systolic and diastolic heart failure

Pressure-volume analysis has provided critical insight into ventricular mechanics, and it has elucidated the underlying mechanisms of heart failure (HF). Renewed interest in ventriculovascular coupling, the interaction of the left ventricle and the arterial system, has developed from recent investigations focusing on the importance of heart rate control in systolic HF, blood pressure lability in the elderly, and acute pulmonary edema in patients with HF and a normal ejection fraction. These data suggest that abnormal ventriculovascular coupling may be an additional pathophysiological mechanism underlying the development of HF with a normal ejection fraction and may provide a target for novel therapies.     

Ventriculovascular coupling in systolic and diastolic heart failure

Pressure-volume analysis has provided critical insight into ventricular mechanics, and it has elucidated the underlying mechanisms of heart failure (HF). Renewed interest in ventriculovascular coupling, the interaction of the left ventricle and the arterial system, has developed from recent investigations focusing on the importance of heart rate control in systolic HF, blood pressure lability in the elderly, and acute pulmonary edema in patients with HF and a normal ejection fraction. These data suggest that abnormal ventriculovascular coupling may be an additional pathophysiologic mechanism underlying the development of HF with a normal ejection fraction and may provide a target for novel therapies.     

Effects of exercise training on diastolic and systolic dysfunction in patients with chronic heart failure

BACKGROUNDChronic heart failure (CHF) is a complex syndrome characterized by a progressive reduction of the left ventricular (LV) contractility, low exercise tolerance, and increased mortality and morbidity. Diastolic dysfunction (DD) of the LV, is a keystone in the pathophysiology of CHF and plays a major role in the progression of most cardiac diseases. Also, it is well estimated that exercise training induces several beneficial effects on patients with CHF. AIMTo evaluate the impact of a cardiac rehabilitation program on the DD and LV ejection fraction (EF) in patients with CHF.METHODSThirty-two stable patients with CHF (age: 56 ± 10 years, EF: 32% ± 8%, 88% men) participated in an exercise rehabilitation program. They were randomly assigned to aerobic exercise (AER) or combined aerobic and strength training (COM), based on age and peak oxygen uptake, as stratified randomization criteria. Before and after the program, they underwent a symptom-limited maximal cardiopulmonary exercise testing (CPET) and serial echocardiography evaluation to evaluate peak oxygen uptake (VO_2peak), peak workload (W_peak), DD grade, right ventricular systolic pressure (RVSP), and EF.RESULTSThe whole cohort improved VO_2peak, and W_peak, as well as DD grade (P < 0.05). Overall, 9 patients (28.1%) improved DD grade, while 23 (71.9%) remained at the same DD grade; this was a significant difference, considering DD grade at baseline (P < 0.05). In addition, the whole cohort improved RVSP and EF (P < 0.05). Not any between-group differences were observed in the variables assessed (P > 0.05).CONCLUSIONExercise rehabilitation improves indices of diastolic and systolic dysfunction. Exercise protocol was not observed to affect outcomes. These results need to be further investigated in larger samples.     

Mechanisms of diastolic dysfunction in heart failure

Abnormalities of diastole are common to most forms of congestive heart failure (HF). Diastolic function is broadly defined as the ability of the heart to fill adequately and at normal pressure to charge the ventricular pump for each subsequent contraction. It is determined by both active and passive processes occurring at the level of the myocyte, extracellular matrix, and left ventricular chamber. Forces extrinsic to the myocardium-such as the influence of right heart filling, pericardial and extracardiac constraints, and cardiac preload and afterload also contribute. Nearly half of patients with HF have apparently preserved systolic function, and this has focused attention on diastolic dysfunction as a dominant contributor to symptoms, sparking interest for understanding and treating diastolic abnormalities. This review focuses on the mechanisms determining normal and pathologic cardiac relaxation and distensibility and highlights how these abnormalities may be therapeutically targeted to improve diastolic function in human HF.     

Congestive heart failure arising from diastolic dysfunction in the presence of normal left-ventricular systolic function

Congestive heart failure due to diastolic dysfunction is a common clinical entity, particularly in the elderly. As outlined, such patients fall into a larger group of all patients with CHF symptoms and normal systolic function. When finding "normal" systolic function, the clinician should embark upon a carefully outlined diagnostic work-up geared toward eliminating confounding or treatable contributing causes of dyspnea or typical CHF symptoms. The prognosis for CHF patients with primarily diastolic dysfunction is not as poor as for those with LV systolic dysfunction, although the prevalence, associated morbidity, and costs are great. In contrast to the large number of successful clinical trials that have guided treatment of LV systolic failure, an extremely limited number of trials have specifically addressed themselves to diastolic dysfunction. Marked symptomatic relief can often be provided with careful attention to tailored therapy, although little is known with regard to outcome. Refinements in noninvasive imaging methods and hemodynamic indices of diastolic function may lead to improved patient care.     

Diastolic dysfunction and diastolic heart failure: Mechanisms and epidemiology

Studies have demonstrated that diastolic dysfunction is frequently present in asymptomatic community-based individuals, especially in the elderly with hypertension, coronary artery disease, and diabetes. The presence of diastolic dysfunction is a predictor for the development of heart failure (HF) and confers a higher risk of mortality. These findings have raised the question of whether treating preclinical diastolic dysfunction will be helpful in preventing or delaying the onset of clinical HF and mortality, as has been proven with treatment of asymptomatic left ventricular systolic dysfunction. In addition, in some individuals, diastolic dysfunction in the presence of a normal ejection fraction is associated with exercise intolerance as well as symptomatic clinical HF, referred to as diastolic HF. Patients with diastolic HF, who are more often elderly women, have a significant mortality and morbidity burden compared with agematched controls. Studies that further our understanding of mechanisms underlying diastolic dysfunction and diastolic HF will provide potential new targets for development of effective therapies for these conditions.     

Role of ACE2 in diastolic and systolic heart failure

A novel angiotensin-converting enzyme (ACE) homolog, named ACE2, is a monocarboxypeptidase which metabolizes several peptides. ACE2 degrades Angiotensin (Ang) II, a peptide with vasoconstrictive/proliferative effects, to generate Ang-(1-7), which acting through its receptor Mas exerts vasodilatory/anti-proliferative actions. In addition, as ACE2 is a multifunctional enzyme and its actions on other vasoactive peptides can also contribute to its vasoactive effects including the apelin-13 and apelin-17 peptides. The discovery of ACE2 corroborates the establishment of two counter-regulatory arms within the renin-angiotensin system. The first one is formed by the classical pathway involving the ACE-Ang II-AT₁ receptor axis and the second arm is constituted by the ACE2-Ang 1-7/Mas receptor axis. Loss of ACE2 enhances the adverse pathological remodeling susceptibility to pressure-overload and myocardial infarction. ACE2 is also a negative regulator of Ang II-induced myocardial hypertrophy, fibrosis, and diastolic dysfunction. The ACE2-Ang 1-7/Mas axis may represent new possibilities for developing novel therapeutic strategies for the treatment of hypertension and cardiovascular diseases. In this review, we will summarize the biochemical and pathophysiological aspects of ACE2 with a focus on its role in diastolic and systolic heart failure.     

Cardiopulmonary exercise variables in diastolic versus systolic heart failure

The response to cardiopulmonary exercise (CPX) in patients with heart failure (HF) with normal left ventricular (LV) ejection fractions (EFs) is not well characterized. To determine if CPX testing could distinguish between patients with HF with normal EFs (>50%; i.e., diastolic HF) and those with decreased EFs (> or =50%; i.e., systolic HF), CPX responses were compared between 185 patients with systolic HF (79% men, mean age 62.6 +/- 10.9 years) and 43 with diastolic HF (54% men, mean age 67.4 +/- 9.8 years) enrolled in a phase II multicenter clinical trial. All patients were evaluated with echocardiography and a standardized CPX test as part of the trial. CPX variables, including oxygen uptake at peak exercise (peak VO(2)) and the slope of the ventilation/carbon dioxide production ratio (VE/VCO(2)), were determined and analyzed by core laboratory personnel. Echocardiographic measurements included the LV EF, the E/A ratio, filling time, cavity volumes, right ventricular function, and mitral regurgitation. Patients in the diastolic HF group tended to be older (p <0.08), with more women (p <0.006) and with greater body mass indexes (p <0.02), than those in the systolic HF group. There was no significant difference in the use of beta blockers or the incidence of coronary artery disease. Patients with diastolic HF had decreased E/A ratios (0.9 +/- 0.4 vs 1.4 +/- 1.1, p <0.02, diastolic HF vs systolic HF) and increased filling times (30.4 +/- 3.2 vs 26.5 +/- 4.7 ms, p <0.01, diastolic HF vs systolic HF). No significant differences in peak VO(2) (14.4 +/- 1.9 vs 15.6 +/- 3.2 ml/kg/min, p = 0.06, diastolic HF vs systolic HF) were observed. The VE/VCO(2) ratios for the 2 groups were abnormal and comparable (32 2 +/- 7.5 vs 34.0 +/- 8.3, p = 0.3, diastolic HF vs systolic HF). In conclusion, the CPX response in patients with diastolic HF and systolic HF is markedly abnormal and indistinguishable with regard to peak VO(2) and ventilation despite marked differences in the LV EF.     

Congestive heart failure in patients with normal left ventricular systolic function: a manifestation of diastolic dysfunction.

Diastolic dysfunction is a relatively common problem that may be mild and asymptomatic or may present with congestive heart failure and severe disabling symptoms. It is frequently due to coronary artery disease or left ventricular hypertrophy and it is especially common in the older population. The pathophysiology is related to increased left ventricular passive stiffness and impaired or slowed myocardial relaxation. Patients with diastolic dysfunction are best treated with calcium channel blocking agents or beta-blocking agents (drugs that are generally avoided in patients with significant systolic dysfunction). Most treatment is based on symptomatic relief, and therefore periods of cautious trial and error are the rule. Congestive symptoms are treated with agents that reduce pulmonary venous pressure; in general positive inotropic agents and arterial vasodilators are not useful in heart failure that is due to diastolic dysfunction.     

Health-related quality of life of outpatients with systolic and isolated diastolic dysfunction

Background The impact of isolated diastolic dysfunction (IDD) and systolic dysfunction (SD) on health-related quality of life (HRQOL) is unknown. Methods and Results To evaluate HRQOL in patients with IDD and SD under treatment, information on outpatients aged 60-84 years was extracted from the records of 4,500 consecutive individuals who underwent echocardiographic examination at Sado General Hospital. The medical records of these patients were reviewed and a questionnaire, including the Medical Outcome Study Short Form 36, was mailed to 71 IDD and 99 SD patients; answers were obtained from 66 and 91 patients, respectively. The HRQOL of patients with cardiac dysfunction was impaired even when echocardiographic parameters improved with treatment. Patients with IDD showed an impairment of HRQOL similar to those with SD. Compared with males, female patients had a larger and more significant reduction in the physical and mental components of the HRQOL score. These scores correlated positively with exercise capacity in patients with IDD or SD. Conclusions Impaired HRQOL, in both its mental and physical components, is a serious problem for IDD and SD patients under treatment. Because exercise intolerance may underlie the reduced HRQOL, improving exercise capacity could be an important target for managing outpatients with heart failure. (Circ J 2008; 72: 1436 - 1442).     

Congestive heart failure in chronic kidney disease: disease-specific mechanisms of systolic and diastolic heart failure and management

There is a high burden of cardiac disease in the CKD population. Severe LVH, dilated cardiomyopathy, and coronary artery disease occur frequently and result in the manifestations of CHF,which is probably more important with respect to prognosis than symptomatic. Multiple risk factors for CVD include traditional risk factors and those unique to the CKD population. Furthermore, the distinctive aspects of CKD patients sometimes warrant special consideration in making management decisions. Nonetheless, interventions such as controlling hypertension, specific pharmacologic options, lifestyle modification, anemia management, and early nephrology referral are recommended when appropriate.     

Progression of preserved systolic function heart failure to systolic dysfunction -- a natural history study

OBJECTIVES: To assess the natural history of left ventricular (LV) structure and function in sequential heart failure admissions with preserved systolic function. BACKGROUND: Heart failure (HF) with preserved LV systolic function accounts for between 20% and 30% of typical HF populations. Few data are available concerning the natural history of structural and functional changes in the LV in this patient population. METHODS: We consented sequential admissions from the community with confirmed heart failure to participate in this study. Doppler-echocardiography was used to assess Ejection Fraction (EF), LV structure, regional wall motion and parameters of diastolic function including E:A ratio, E-wave deceleration time (DtE) and isovolumic relaxation time (IVRT). Follow-up echocardiography was carried out at three months (mean 103+/-13 days) from discharge. RESULTS: Of 210 sequential admissions with primary heart failure 56 had preserved systolic function (LVEF> or =45%). Follow-up data at three months were available in 38 patients (mean age 72 years) with preserved LV systolic function. Of the group, 9 had been admitted within three months of discharge, 5 for recurrent HF. Eight patients (21%) exhibited significant decline in LV systolic function at follow-up, all with LVEF<45%. Three exhibited regional wall-motion abnormalities with the remainder showing dilatation and global reduction in function. None of these eight had presented to hospital for any cause other than routine outpatient department (OPD) visits during the 3 months. CONCLUSION: Patients with preserved systolic function HF, a significant number may progress to systolic dysfunction with or without clinical events.