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Diastolic heart failure is predominantly a disease of the elderly: at the age of 70 years, almost half of all patients with heart failure have diastolic heart failure. Hypertension and obesity are common underlying disorders in patients with diastolic heart failure. Patients with diastolic heart failure have an equal, or only slightly better, prognosis in terms of mortality compared to patients with systolic heart failure. Echocardiography can distinguish diastolic heart failure from systolic heart failure. Patients with heart failure and a normal ejection fraction almost certainly have a diastolic dysfunction. There is a lack of reliable data about the optimal medicinal treatment strategy for patients with diastolic heart failure. Angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, and (non-dihydropyridine) calcium antagonists have therapeutic potential. Digoxin may be contraindicated.
Diastolic heart failure is defined clinically when signs and symptoms of heart failure are present in the presence of preserved left ventricular systolic function (ejection fraction >45%). The incidence and prevalence of primary diastolic heart failure increases with age and it may be as high as 50% in the elderly. Age, female gender, hypertension, coronary artery disease, diabetes, and increased body mass index are risk factors for diastolic heart failure. Hemodynamic consequences such as increased pulmonary venous pressure, post-capillary pulmonary hypertension, and secondary right heart failure as well as decreased cardiac output are similar to those of systolic left ventricular failure, although the nature of primary left ventricular dysfunction is different. Diagnosis of primary diastolic heart failure depends on the presence of preserved left ventricular ejection fraction. Assessment of diastolic dysfunction is preferable but not mandatory. It is to be noted that increased levels of B-type natriuretic peptide does not distinguish between diastolic and systolic heart failure. Echocardiographic studies are recommended to exclude hypertrophic cardiomyopathy, infiltrative heart disease, primary valvular heart disease, and constrictive pericarditis. Myocardial stress imaging is frequently required to exclude ischemic heart disease. The prognosis of diastolic heart failure is variable; it is related to age, severity of heart failure, and associated comorbid diseases such as coronary artery disease. The prognosis of severe diastolic heart failure is similar to that of systolic heart failure. However, cautious use of diuretics and/or nitrates may cause hypotension and low output state. Heart rate control is essential to improving ventricular filling. Pharmacologic agents such as angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers are used in selected patients to decrease left ventricular hypertrophy. To decrease myocardial fibrosis, aldosterone antagonists have a potential therapeutic role. However, prospective controlled studies will be required to establish their efficacy in primary diastolic heart failure.
BACKGROUND: Heart failure consists of two phenotypes: systolic heart failure and diastolic heart failure (DHF). A growing body of evidence demonstrated benefits of beta-blocker, angiotensin-converting enzyme inhibitor, and angiotensin II receptor blocker in systolic heart failure; however, evidence leading to therapeutic strategy of DHF is lacking. METHODS AND RESULTS: The Japanese Diastolic Heart Failure Study (J-DHF) is a multicenter, prospective, randomized trial designed to assess effects of beta-blocker in patients with DHF. A total of 800 patients (400 patients in each group) will be enrolled. The primary outcome is a composite of cardiovascular death and unplanned admission to hospital for congestive heart failure. Other outcomes include all-cause mortality, worsening of the symptoms of heart failure, or a need for modification of the treatment for heart failure. Serial assessment of echocardiographic and neurohumoral parameters and cost analysis of the treatment regimen will be conducted. The follow-up period is a minimum of 2 years. CONCLUSION: This study will provide important evidences for the treatment of DHF.
Diastolic heart failure, in the absence of LV systolic dysfunction, is a common clinical condition that can be demonstrated in as many as one third of patients with congestive heart failure. Diastolic dysfunction caused by abnormalities in LV filling can be a result of many pathologic conditions, including hypertrophy, infiltrative cardiomyopathies, or myocardial ischemia. The major physiologic determinants of LV filling can be divided into cellular mechanisms, hemodynamic characteristics, and hormonal influences. Cellular mechanisms for impaired LV inactivation are determined by the handling of calcium within the myocyte during excitation-contraction-relaxation coupling. The hemodynamic characteristics of LV diastolic filling are determined by loading conditions, the time constant of isovolumic relaxation, heart rate, ventricular nonuniformity, pericardial restraint, myocardial elasticity, chamber compliance, and coronary blood flow. The sympathetic nervous system and the renin-angiotensin system are important modulators of diastolic filling, directly or indirectly. The diagnosis of heart failure is confirmed by a combination of clinical tests including invasive and noninvasive techniques, each of which has advantages and disadvantages. Treatment of medical conditions in which diastolic heart failure is a prominent component include pharmacotherapy with calcium channel antagonists, beta-adrenergic blocking agents, diuretic agents, and angiotensin-converting-enzyme inhibitors. Certain conditions associated with diastolic filling abnormalities such as pericardial disease or severe ischemic heart disease may be best managed by surgical or percutaneous intervention. Future research will include further delineation of the cellular mechanisms of active myocardial relaxation and clinical investigation into treatment directed at improving outcome.
Diastolic heart failure accounts for up to 40% of patients with congestive heart failure (CHF), and is associated with a better prognosis as compared to patients with systolic dysfunction. Nevertheless, patients with diastolic dysfunction have a significantly higher mortality as compared to the normal population. Reduced heart rate variability (HRV), a marker of autonomic dysfunction, is associated with increased mortality in patients with systolic heart failure. We therefore sought to determine to what extent HRV is altered in a population of patients with diastolic heart failure. Twenty-four hour ambulatory (Holter) recordings were performed in 19 consecutive patients with diastolic heart failure, in 9 patients with systolic heart failure, as well as in 9 healthy volunteers (normal controls). Time and frequency domain HRV variables were obtained for all three groups of patients. Both Time and Frequency domain variables were found to be reduced in both heart failure groups compared to normal controls. When compared with each other, patients with diastolic function had relatively higher values of HRV variables, compared to those with systolic dysfunction (SDNN, Total power, ULF power, all P <or= 0.05). Patients with diastolic dysfunction have reduced HRV, suggesting a disturbed sympathetic-parasympathetic balance. Nevertheless, values for HRV are not as profoundly reduced as in patients with systolic dysfunction. The relative preservation of sympathetic-parasympathetic balance may explain the better prognosis in this patient population.
Diastolic heart failure (heart failure with preserved systolic function) causes 30% to 50% of all cases of heart failure, and its prognosis is almost as ominous as that of systolic heart failure. Currently, it is diagnosed when clinical criteria for heart failure are present and left ventricular ejection fraction is preserved (higher than 40% to 50%). However, determinations of brain natriuretic peptides may play an important role in the future. Because we have no evidence from clinical trials, with the exception of the slight benefit obtained with candesartan in reducing hospitalizations in the CHARM Study, treatment of diastolic heart failure is based on the identification and treatment of the causal factor (hypertension, coronary heart disease), control of heart rate, and relief of fluid congestion. Thus, combined therapy with low-dose diuretics, antihypertensive drugs for bradycardia (beta blockers, calcium antagonists) and angiotensin antagonists seems now to be the best therapeutic strategy.
Diastolic heart failure is characterized by the presence of heart failure with preserved left ventricular ejection fraction (LVEF): documentation of diastolic dysfunction, usually by Doppler echocardiography, is strongly recommended. Heart failure with preserved LVEF is a heterogeneous and common condition, especially in the elderly, among whom represents up to 50% of all heart failure patients. Mortality is generally lower than in patients with heart failure and low LVEF, and depends on etiology, patient conditions, and comorbidities. Anyway, morbidity is very high. So far, treatment of diastolic heart failure is empirical, and is aimed to maintain cardiac output, reduce filling pressure, control heart rate and rhythm, and antagonize disease progression with diuretics, inhibitors of the renin-angiotensin-aldosterone system, nitrates, and digoxin.
Diastolic heart failure (DHF) was produced in 6-day-old piglets by intravenous administration of Doxorubicin, and ANKRD1 protein and mRNA levels were determined in atrial (A) and ventricular (V) chambers of failing vs control hearts. In controls, ANKRD1 showed a left-right (L-R) asymmetric distribution with protein levels 2-fold higher in the LA as compared to the RA, and 8-fold higher in the LV than the RV. In failing hearts, ANKRD1 levels were augmented about 2-fold in each ventricle but equally reduced in both atria as compared to controls. ANKRD1 downregulation in atria is discussed as a process associated with advanced DHF.
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.
Diastolic heart failure is a distinct clinical entity increasingly seen in older patients and requires special awareness to make the diagnosis. Although no single laboratory test is identified for making a confident diagnosis of diastolic dysfunction as the pathogenetic mechanism for heart failure, a constellation of echocardiographic and radionuclear findings are helpful in most cases. Invasive assessment of LV diastole is laborious, requiring high-fidelity pressures and accurate measures of volumes, and these are rarely needed to diagnose the condition. It appears that prognosis is significantly better for those with normal systolic function, when compared with congestive heart failure caused by impaired systolic pump function. Finally, the therapeutic approaches are substantially different for the two groups. It must be emphasized that even patients with predominant myocardial systolic dysfunction have some combined diastolic dysfunction as well. This latter group is difficult to treat. However, improvement in systolic pump function, when markedly impaired, must take precedence in management strategies.
Diastolic heart failure (DHF) has become a social burden; however, evidences leading to its therapeutic strategy are lacking. This study investigated effects of addition of angiotensin II type 1 receptor blocker (ARB) to angiotensin-converting enzyme inhibitor (ACEI) at advanced stage of DHF in hypertensive rats. Dahl salt-sensitive rats fed 8% NaCl diet from age 7 weeks served as DHF model, and those fed a normal chow served as control. The DHF model rats were arbitrarily assigned to 3 treatment regimens at age 17 weeks: ACEI (temocapril 0.4 mg/kg per day), combination of ACEI (temocapril 0.2 mg/kg per day) with ARB (olmesartan 0.3 mg/kg per day), or placebo. At age 17 weeks, this model represents progressive ventricular hypertrophy and fibrosis, relaxation abnormality, and myocardial stiffening. Data were collected at age 20 weeks. As compared with the monotherapy with ACEI, the addition of ARB induced more prominent suppression of ventricular hypertrophy and fibrosis, leading to suppression of myocardial stiffening, improvement of relaxation, and inhibition of hemodynamic deterioration. Such benefits were associated with greater decreases in reactive oxygen species (ROS) generation, macrophage infiltration, and gene expression of transforming growth factor (TGF)-beta(1) and interleukin (IL)-1beta, but not with changes in gene expression of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-alpha. Thus, ARB added to ACEI provides more benefits as compared with ACEI alone in DHF when initiated at an advanced stage. The additive effects are likely provided through more prominent suppression of ROS generation and inflammatory changes without effects on expression of MCP-1 and TNF-alpha.
Diastolic heart disease is common and appears to be the primary abnormality in a substantial proportion of all patients with CHF. The epidemiology and natural history of the condition appears different to that of systolic heart failure, resulting in significant morbidity although contributing little to overall mortality. Clinical assessment alone is inadequate to distinguish systolic from diastolic failure, and echocardiography is an essential investigation in the management of these patients. From a therapeutic standpoint an alternative approach to treatment is likely to be indicated, and the results of recent major trials in systolic heart failure cannot necessarily be extrapolated to this group of patients.
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Diastolic dysfunction and the clinical syndrome of diastolic heart failure have become well recognized as contributors to the overall burden of congestive heart failure. This increasing awareness has led to several recent investigations into the impact of diastolic abnormalities on morbidity and mortality. This article reviews the current state of knowledge regarding the prognosis of patient populations with diastolic dysfunction and diastolic heart failure.
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Diastolic heart failure occurs when signs and symptoms of heart failure are present but left ventricular systolic function is preserved (i.e., ejection fraction greater than 45 percent). The incidence of diastolic heart failure increases with age; therefore, 50 percent of older patients with heart failure may have isolated diastolic dysfunction. With early diagnosis and proper management the prognosis of diastolic dysfunction is more favorable than that of systolic dysfunction. Distinguishing diastolic from systolic heart failure is essential because the optimal therapy for one may aggravate the other. Although diastolic heart failure is clinically and radiographically indistinguishable from systolic heart failure, normal ejection fraction and abnormal diastolic function in the presence of symptoms and signs of heart failure confirm diastolic heart failure. The pharmacologic therapies of choice for diastolic heart failure are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, and beta blockers.