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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congestive heart failure (CHF) is a major public health problem that results in tremendous economic burden. Diastolic heart failure (DHF) forms an important subset with increasing incidence and prevalence. There are widely variable estimates of the prevalence, ranging from 13% to 74% of all CHF presentations, and this is predominantly a result of a lack of uniform criteria for establishing a diagnosis. New developments in management of DHF have lagged behind those for systolic heart failure (SHF), for which numerous new therapeutic and device strategies have been instituted. The renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathophysiology of both SHF as well as DHF. The beneficial role of ACE inhibitors as well as aldosterone antagonists in SHF has been well established. Because of its unique role of the RAAS in establishing fibrosis at a molecular level, RAAS blockade provides an opportunity to expand the therapeutic options for DHF. Thus far, in patients with primary DHF only the angiotensin receptor type 1 antagonist candesartan has been reported to decrease morbidity and probably mortality. Large, ongoing randomized trials including TOPCAT (Trial of Aldosterone Antagonist Therapy in Adults with Preserved Ejection Fraction Congestive Heart) and the I-PRESERVE (Irbesartan in Heart Failure with Preserved Systolic Function) are currently underway to establish the role of aldosterone antagonists in patients with DHF.
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PMID:Role of the renin-angiotensin-aldosterone system in diastolic heart failure: potential for pharmacologic intervention. 1719 27

Diastolic heart failure affects approximately 40%-50% of patients presenting with signs and symptoms of heart failure. The aim of this study was to investigate the relationship between brain natriuretic peptide (BNP) levels and functional capacity in patients admitted with dyspnea and diagnosed with isolated diastolic dysfunction. Fifty-four patients (mean age, 57.4 +/- 8.5 years) with class-2 dyspnea with isolated diastolic dysfunction were enrolled. Serum levels of BNP were measured, and peak oxygen consumption (peak VO(2)), anaerobic threshold (AT), and metabolic equivalent (MET) values were determined with a cardiopulmonary exercise test (CPET). There was a negative correlation between BNP levels and exercise duration (P < 0.05, r = -0.304), AT (P < 0.05, r = -0.380), and number of MET (P < 0.05, r = -0.322) determined by CPET. When patients were divided into 2 groups according to BNP levels; BNP < or = 50 pg/mL (n = 40) versus BNP > 50 pg/mL (n = 14) and analyzed, those with BNP levels > 50 pg/mL had lower peak VO(2) (P = 0.05) and anaerobic threshold (P = 0.01) compared with patients with BNP < or = 50 pg/mL. The results suggest that BNP levels provide an indication about the functional capacity determined by CPET in patients admitted with dyspnea and isolated diastolic dysfunction.
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PMID:Brain natriuretic peptide levels and cardiac functional capacity in patients with dyspnea and isolated diastolic dysfunction. 1737 83

Diastolic heart failure (DHF) currently accounts for more than 50% of all heart failure patients. DHF is also referred to as heart failure with normal left ventricular (LV) ejection fraction (HFNEF) to indicate that HFNEF could be a precursor of heart failure with reduced LVEF. Because of improved cardiac imaging and because of widespread clinical use of plasma levels of natriuretic peptides, diagnostic criteria for HFNEF needed to be updated. The diagnosis of HFNEF requires the following conditions to be satisfied: (i) signs or symptoms of heart failure; (ii) normal or mildly abnormal systolic LV function; (iii) evidence of diastolic LV dysfunction. Normal or mildly abnormal systolic LV function implies both an LVEF > 50% and an LV end-diastolic volume index (LVEDVI) <97 mL/m(2). Diagnostic evidence of diastolic LV dysfunction can be obtained invasively (LV end-diastolic pressure >16 mmHg or mean pulmonary capillary wedge pressure >12 mmHg) or non-invasively by tissue Doppler (TD) (E/E' > 15). If TD yields an E/E' ratio suggestive of diastolic LV dysfunction (15 > E/E' > 8), additional non-invasive investigations are required for diagnostic evidence of diastolic LV dysfunction. These can consist of blood flow Doppler of mitral valve or pulmonary veins, echo measures of LV mass index or left atrial volume index, electrocardiographic evidence of atrial fibrillation, or plasma levels of natriuretic peptides. If plasma levels of natriuretic peptides are elevated, diagnostic evidence of diastolic LV dysfunction also requires additional non-invasive investigations such as TD, blood flow Doppler of mitral valve or pulmonary veins, echo measures of LV mass index or left atrial volume index, or electrocardiographic evidence of atrial fibrillation. A similar strategy with focus on a high negative predictive value of successive investigations is proposed for the exclusion of HFNEF in patients with breathlessness and no signs of congestion. The updated strategies for the diagnosis and exclusion of HFNEF are useful not only for individual patient management but also for patient recruitment in future clinical trials exploring therapies for HFNEF.
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PMID:How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. 1789 Jul 29

Diastolic heart failure is an underestimated pathology with a high risk of acute decompensation during the perioperative period. This article reviews the epidemiology, risk factors, pathophysiology, and treatment of diastolic heart failure. Although frequently underestimated, diastolic heart failure is a common pathology. Diastolic heart failure involves heart failure with preserved left ventricular (LV) function, and LV diastolic dysfunction may account for acute heart failure occurring in critical care situations. Hypertensive crisis, sepsis, and myocardial ischaemia are frequently associated with acute diastolic heart failure. Symptomatic treatment focuses on the reduction in pulmonary congestion and the improvement in LV filling. Specific treatment is actually lacking, but encouraging data are emerging concerning the use of renin-angiotensin-aldosterone axis blockers, nitric oxide donors, or, very recently, new agents specifically targeting actin-myosin cross-bridges.
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PMID:Diastolic heart failure in anaesthesia and critical care. 1746 92

In cardiovascular diseases e.g. heart failure and coronary artery disease gender differences are evident in etiology, pathophysiology, clinical presentation, prognosis and response to treatment. Diabetes and hypertension are the major risk factors in women. Mechanisms leading to apparent diabetes or its clinical pre-stage are different in women and men and according to this result in different therapeutic implications. Diastolic heart failure is more frequent in women and effects and side effects of important groups of active pharmaceutical substances are, at least to some extent, different. Atrial fibrillation and ventricular arrhythmia differ in frequency of occurrence; drug induced tachycardia with QT interval prolongation is particularly frequent in women. Underlying pathomechanisms responsible for gender differences in pharmacotherapy are on the one hand differences in pharmacokinetic mechanisms. Particularly drugs which are metabolised via cytochrome P 450 CYP 3A pathway show different kinetics in women and men. In addition, important differences are evident in pharmocodynamics caused by effects of sex steroid hormones or products of X-chromosomal genes. The evidence of estrogen and testosterone receptors in cardiomyocytes and the vascular system, interaction of sex steroid hormones with cellular pathways and the role of X-chromosomal genes are the focus of basic research. Interactions of sex steroid hormone receptors with other nuclear receptors e.g. PPARs ("peroxisome proliferator-activated receptors") are another important underlying mechanism. The knowledge of different pharmacokinetic mechanisms has to be taken into consideration in pharmacotherapy of cardiovascular diseases, for example by adjustment of drug dosages in women, necessary in different groups of pharmaceutical substances or in the long run, gender differences in effects and side effects of drugs. In drug development both aspects have to be considered. There is more than one good reason to intensify basic and clinical research and research on health care on gender differences in cardiovascular diseases.
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PMID:[Implications of gender-specific aspects in the therapy of cardiovascular diseases]. 1787 7

The renin-angiotensin-aldosterone system (RAAS) is critical in regulating systemic blood pressure, water and electrolyte balance, and pituitary gland hormones. These physiologies appear to be primarily mediated by the angiotensin II/AT(1) receptor subtype system. Overstimulation of this system can predispose cardiovascular disease (CVD) characterized by excessive vasoconstriction, fibrosis, and cardiac remodeling. If untreated, the patient typically displays a continuum of pathophysiologic conditions progressing from atherosclerosis to left ventricle hypertrophy (LVH), coronary thrombosis, myocardial infarcts, with heart failure as an endpoint. Intervention with antihypertensive therapy is necessary to inhibit this progression. RAAS blocking drugs appear to be the most effective approach. Diastolic heart failure patients benefit from treatment with angiotensin converting enzyme (ACE) inhibitors and angiotensin AT(1) receptor blockers (ARBs). Elderly CVD patients evidence age-related changes in body composition that alter the distribution and half-life of medications, thus presenting special challenges to treatment. The presence of comorbidities such as diabetes, renal dysfunction, liver insufficiency further complicates any therapeutic strategy. In addition, noncompliance because of cognitive impairment, depression, confusion due to the complexity of dose regimens, and lack of an appropriate social support system can disrupt positive outcome. The present review discusses the roles of an overactive RAAS and sympathetic nervous system as primary contributors to CVD. In addition, treatment strategies are discussed, focusing on middle aged and elderly hypertensive and heart failure patients.
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PMID:Pathways involved in the transition from hypertension to hypertrophy to heart failure. Treatment strategies. 1798 82

Diastolic heart failure (DHF) is now firmly established as a significant contributor to the heart failure syndrome. However, compared to the better studied systolic dysfunction heart failure relatively little is known about this form of the syndrome. Epidemiological data have demonstrated that it is particularly important in the elderly likely reflecting the combination of several changes occurring in the myocardium occurring with advancing years, including progressive fibrosis and stiffening of the myocardium, the impact of hypertension over the years and the increased likelihood of ischaemic heart disease. This review will focus on the relevant aetiological factors in DHF, possible pathophysiological mechanisms and outline new and evolving therapeutic strategies for this problem.
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PMID:Diastolic heart failure in the elderly: underlying mechanisms and clinical relevance. 1816 Jan 54

Diastolic heart failure (DHF) is a major cardiovascular disorder with poor prognosis; however, its molecular mechanism still remains to be fully elucidated. We have previously demonstrated the important roles of Rho-kinase pathway in the molecular mechanisms of cardiovascular fibrosis/hypertrophy and oxidative stress, but not examined in the development of heart failure. Therefore, we examined in this study whether Rho-kinase pathway is also involved in the pathogenesis of DHF in Dahl salt-sensitive rats, an established animal model of DHF. They were maintained with or without fasudil, a Rho-kinase inhibitor (30 or 100 mg/kg/day, PO) for 10 weeks. Untreated DHF group exhibited overt heart failure associated with diastolic dysfunction but with preserved systolic function, characterized by increased myocardial stiffness, cardiomyocyte hypertrophy, and enhanced cardiac fibrosis and superoxide production. Fasudil treatment significantly ameliorated those DHF-related myocardial changes. Western blot analysis showed that cardiac Rho-kinase activity was significantly increased in the untreated DHF group and was dose-dependently inhibited by fasudil. Importantly, there was a significant correlation between the extent of myocardial stiffness and that of cardiac Rho-kinase activity. These results indicate that Rho-kinase pathway plays an important role in the pathogenesis of DHF and thus could be an important therapeutic target for the disorder.
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PMID:Long-term inhibition of Rho-kinase ameliorates diastolic heart failure in hypertensive rats. 1835 98

Diastolic heart failure (DHF), characterized by depressed myocardial relaxation performance and poor ventricular filling, is a distinct form of heart failure accounting for nearly half of the heart failure patients with otherwise normal systolic performance. Defective intracellular calcium (Ca2+) cycling is an important mechanism underlying impaired relaxation in DHF. Recently, genetic manipulation of Ca2+ handling proteins in cardiac myocytes has been explored for its potential therapeutic application in DHF. Specifically, ectopic expression of the skeletal muscle Ca2+ binding protein parvalbumin (Parv) has been shown to accelerate myocardial relaxation in vitro and in vivo. Parv acts as a unique "delayed" Ca2+ buffer during diastole by promoting Ca2+ transient decay and sequestration and corrects diastolic dysfunction in an energy-independent manner. This brief review summarizes the rationale and development of Parv gene transfer approaches for DHF, and in particular, discusses the divergent effects of Parv isoforms on cardiac myocyte Ca2+ handling and contractile function with the long-range goal of alleviating diastolic dysfunction in DHF.
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PMID:Parvalbumin isoforms for enhancing cardiac diastolic function. 1845 29

Diastolic heart failure is characterized by the symptoms and signs of heart failure, a preserved ejection fraction and abnormal left ventricular (LV) diastolic function caused by a decreased LV compliance and relaxation. The signs and symptoms of diastolic heart failure are indistinguishable from those of heart failure related to systolic dysfunction; therefore, the diagnosis of diastolic heart failure is often one of exclusion. The majority of patients with heart failure and preserved ejection fraction have a history of hypertension. Hypertension induces a compensatory thickening of the ventricular wall in an attempt to normalize wall stress, which results in LV concentric hypertrophy, which in turn decreases LV compliance and LV diastolic filling. There is an abnormal accumulation of fibrillar collagen accompanying the hypertension-induced LV hypertrophy, which is also associated with decreased compliance and LV diastolic dysfunction. There are no specific guidelines for treating diastolic heart failure, but pharmacological treatment should be directed at normalizing blood pressure, promoting regression of LV hypertrophy, preventing tachycardia and treating symptoms of congestion. Preventive strategies directed toward an early and aggressive blood pressure control are likely to offer the greatest promise for reducing the incidence of diastolic heart failure.
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PMID:Diastolic dysfunction: a link between hypertension and heart failure. 1880 1


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