Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEART FAILURE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed2000

The importance of beta blockers in the treatment of heart failure.

Heart failure, the only cardiovascular disease with an increasing incidence, is associated with significant mortality and poses a considerable economic burden. Traditionally, beta blockers have been considered to be contraindicated in patients with heart failure. Recently, however, several large randomized, controlled mortality trials have been stopped early because of significant improvement in mortality rates in patients with heart failure who were given beta blockers in addition to angiotensin-converting enzyme inhibitors, diuretics and, sometimes, digoxin. Beta blockers should now be considered standard therapy in patients with New York Heart Association class II or class III heart failure who are hemodynamically stable, who do not have dyspnea at rest and who have no other contraindications to the use of these agents.

Adrenergic beta-Antagonists↗
PubMed1994

[Current management of heart failure].

Heart failure has emerged as a major cardiovascular public health syndrome with increasing incidence, reduced quality life, risk of progression, and high mortality. It's therapy still continues to pose a major clinical problem. The main goals of therapy are: improving the quality life and prolonging the survival. For many years digitalis and diuretics have been the cornerstones of pharmacologic treatment recently completed with vasodilators. Regarding the results of experimental and clinical investigations efforts to refine therapy have focused on choosing a combination of drugs particularly those that effectively inhibit the renin-angiotensin-aldosterone (RAA) system. The ACE inhibitors proved to be effective in managing heart failure of all degrees of severity including left ventricular dysfunction and end-stage of syndrome and in prolonging survival in patients. Spironolactone which inhibits the activity of aldosterone may exert an independent and additive effect to that of ACE inhibitors. The standard therapy of heart failure became: digitalis, diuretics--including spironolactone--and ACE inhibitors. In end-stage of heart failure refractory to therapy the only choice is heart transplantation.

Adult↗
PubMedDate not supplied

[Cardiac natriuretic peptides in heart failure].

Heart failure is a clinical syndrome characterized by abnormalities of cardiac, skeletal muscle, and renal function, stimulation of the sympathetic nervous system, and a complex pattern of neurohormonal changes. Early diagnosis and treatment of heart failure are important factors in reducing morbidity and mortality associated with the disease. During the past several years many studies have demonstrated that natriuretic peptides are the biochemical markers of choice for diagnosing and risk stratification of patients with chronic heart failure. The value of natriuretic peptides has already been recognized by their inclusion in the recent European guidelines for the diagnosis of chronic heart failure. The natriuretic peptides family is comprised of four peptides, each with common 17 amino acid ring structure. The tissue-specific distribution and regulation of each peptide are different. At present, there is no consensus on the most reliable method for natriuretic peptides assay, although non-competitive immunoassay may be more suitable for clinical routine than competitive assay.

Atrial Natriuretic Factor↗
PubMed2000

Oxidative stress in congestive heart failure.

Heart failure is considered to be a complex clinical syndrome, with alterations in the multiple neurohumoral systems and subcellular cardiac sites that correlate with abnormal cardiac function. Strong evidence for the role of oxidative stress in the pathogenesis of heart failure has been provided by studies on experimental animals as well as humans. This concept is gaining more acceptance due to the fact that during heart failure, changes in different neurohormones, cytokines, nitric oxide, and activated inflammatory cells are closely linked to oxidative stress at the cellular and molecular levels. The present article provides a simple description of oxygen free radicals as well as the antioxidant defense system. Evidence for the role of oxidative stress in the pathogenesis of heart failure is reviewed in a concise manner.

Animals↗
PubMed1998

[Significance of neuroendocrine parameters in heart failure].

Heart failure is defined as a malfunction of the cardiac muscle. The ongoing interaction between pump failure and the vasculature, however, results in symptoms due to malperfusion of the pulmonary and systemic circuit. As a consequence, biologic systems of pressure and volume control are activated. In the neurohumoral heart failure model the sympathetic nervous system, the renin system and endothelin all develop their own pathologic contribution to the disease process. Thereby the role of endothelin seems to be special since its production is particularly increased in advanced disease. Like angiotensin, endothelin has major proliferative properties to promote adverse vascular and myocardial growth. The finding of increasing neurohumoral activation as heart failure progresses and the role of plasma levels of neurohormones as predictors of mortality has rearranged the primary goal of therapy to suppress these deleterious neurohumoral systems as completely as possible. Though angiotensin converting enzyme inhibitors are currently first line therapy of heart failure, uncertainties remain concerning their mechanisms of action and - associated to that - optimal dosing.

Angiotensin II↗
PubMed2004

[Current knowledge on diastolic heart failure].

Heart failure (HF) is still one of the most common causes of hospitalisation. Originally it was understood as systolic function impairment, but it is prooved that 40 to 50 percent of patients with clinical symptoms of HF have normal systolic function. These data lead to diagnosis of diastolic heart failure (DHF). The diastoly of the left ventricle consists of four stages: isovolumetric relaxation, early mitral inflow, slow mitral inflow and left atrium contraction. Authors have presented definition, epidemiology and basic pathophysiology of DHF. The categories of myocardial and non-myocardial pathogenic mechanisms have also been described. The clinical symptoms that allow to distinguish diastolic from systolic heart failure (SHF) have been pointed. The most common disorders that affect diastolic function like hypertension, coronary artery disease and diabetes have been described. Recent guidelines on therapy in diastolic heart failure have been also presented.

Diagnosis, Differential↗
PubMed1999

Genetic aspects of heart failure.

Heart failure is a major health problem and is associated with a high mortality and morbidity. Recently, the role of the genetic background in the onset and the development of the disease has been evidenced in both heart failure with and without systolic dysfunction and in familial and non-familial forms of this condition. Preliminary studies suggest that the I/D polymorphism of the Angiotensin Converting Enzyme gene influence the development of left ventricular hypertrophy, a major determinant of heart failure. Familial hypertrophic cardiomyopathy (FHC) is a highly heterogenous autosomal dominant disease. Seven genes have been identified which all encode proteins of the sarcomere or proteins involved in the regulation of contraction. More than one hundred mutations have been evidenced. Modifier genes such as the I/D polymorphism seem to play a role in the expression of the disease. Susceptibility genes have been searched for in sporadic forms of dilated cardiomyopathy and conflicting results have been published with regard to the I/D polymorphism. Finally, familial forms of dilated cardiomyopathy (FDC) are frequent. Various modes of inheritance and phenotypes have been reported and this condition appears genetically highly heterogenous. It has been postulated that the molecular defect involved in FDC is an abnormality in the transmission of contractile force. The analysis of genetic factors that predispose to heart failure looks promising: it should allow better understanding of the underlying mechanisms that promote the progression of the disease, to identify subjects at risk of the disease who would benefit from early medical management and promote the development of pharmacogenetics.

Cardiomyopathy, Hypertrophic↗
PubMed2003

Nonsteroidal anti-inflammatory drugs and heart failure.

Heart failure constitutes an increasing public health problem because of the growing incidence and prevalence, poor prognosis and high hospital (re)admission rates. Myocardial infarction is the underlying cause in the majority of patients, followed by hypertension, valvular heart disease and idiopathic cardiomyopathy. Nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit the enzymes cyclo-oxygenase (COX) 1 and 2, have been associated with the occurrence of symptoms of heart failure in several case reports and quantitative studies, mainly in patients with a history of cardiovascular disease or left ventricular impairment. NSAIDs may impair renal function in patients with a decreased effective circulating volume by inhibiting prostaglandin synthesis. Consequently, water and sodium retention, and decreases in renal blood flow and glomerular filtration rate may occur, affecting the unstable cardiovascular homeostasis in these patients. In patients with pre-existing heart failure, this may lead to cardiac decompensation. Putative renal-sparing NSAIDs, such as COX-2 selective inhibitors have similar effects on renal function as the traditional NSAIDs, and can likewise be expected to increase the risk of heart failure in susceptible patients. NSAIDs are frequently prescribed to elderly patients, who are particularly at risk for the renal adverse effects. If treatment with NSAIDs in high risk patients cannot be avoided, intensive monitoring and patient education is important.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

Effects of warfarin on markers of hypercoagulability in patients with heart failure.

Heart failure is associated with a hypercoagulable state. A single-center, randomized, double-blind, placebo-controlled trial was performed to test the hypothesis that warfarin will modify a hypercoagulable state in heart failure. This study included 76 patients with heart failure. At baseline, patients had evidence for a hypercoagulable state with elevated plasma levels of thrombin/antithrombin III (TAT) complexes (3.4 +/- 2.0 ng/ml), prothrombin fragment F1 + 2 (1.5 +/- 0.9 nmol/L), and D-dimers (630 +/- 401 ng/ml). Warfarin therapy (international normalized ratio [INR] 2.7 +/- 1.3) significantly decreased plasma levels of TAT complexes (p < 0.002), F1 + 2 (p < 0.001), and D-dimers (p < 0.001) when compared with baseline values at 1, 2, and 3 months of therapy. In contrast, patients receiving placebo had persistent elevation of TAT complexes (p = not significant [NS]), F1 + 2 (p = NS), and D-dimers (p = NS) during follow-up at 1, 2, and 3 months. The two treatment groups followed different trends over time for all three markers (p < 0.001). The effect of low-intensity warfarin (INR 1.3 +/- 0.08) versus moderate-intensity warfarin (INR 2.3 +/- 1.1 ) on markers of hypercoagulability was evaluated in 14 patients. When compared with baseline, low-intensity warfarin administration decreased plasma levels of TAT complexes (p = NS), F1 + 2 (p = 0.05), and D-dimers (p = 0.04). In these patients F1 + 2 was further reduced with moderate-intensity warfarin (p < 0.001). Our findings suggest that a hypercoagulable state in heart failure can be modified by warfarin therapy.

Adult↗
PubMed2003

Heart transplantation an answer for end-stage heart failure.

Heart transplantation remains the best treatment option for end-stage heart failure. For patients who are not candidates for transplantation, better medical management and surgical options in heart failure can improve both the length and quality of a patient's life. Continuing research on xenotransplantation and the total artificial heart may decrease the need for human transplantation in years to come and may allow others with severe heart failure to have a chance at living longer.

Contraindications↗
PubMed2004

The adrenergic pathway and heart failure.

Heart failure represents the endpoint to many triggering cardiovascular pathologies. However, there are molecular and biochemical features that remain common to the failing heart, despite the varying etiologies. Principal among these is heightened activation of the sympathetic nervous system and associated enhancement of adrenergic signaling pathways via the catecholamines, norepinephrine and epinephrine. During heart failure, several hallmark alterations in the adrenergic system contribute to loss of cardiac function. To specifically study these changes in a physiologically relevant setting, we and others have utilized advances in genetically engineered mouse technology. This chapter will discuss the many transgenic and knockout mouse models that have been developed to study the adrenergic system in the normal and failing heart. These models include genetically manipulated alterations of adrenergic receptors, linked heterotrimeric G proteins, and the regulatory G protein-coupled receptor kinases (GRKs). Among the more-interesting information gained from these models is the finding that inhibition of a particular GRK - GRK2 or beta adrenergic receptor kinase 1 (betaARK1) - is a potential novel therapeutic strategy to improve function in the setting of heart failure. Furthermore, we will discuss recent transgenic research that proposes an important role for hypertension in the development of heart failure. Overall, genetically engineered mouse models pertaining to this critical myocardial signaling system have provided novel insight into heart function under normal conditions and during states of dysfunction and failure.

Animals↗
PubMed2001

Surgical alternatives for heart failure.

Heart failure is one of the leading causes of hospitalization in the United States. Congestive heart failure is a chronic, progressive disease and its central element is remodeling of the cardiac chamber associated with ventricular dilation. Secondary mitral regurgitation is a complication of end-stage cardiomyopathy and is associated with poor prognosis. Historically, these patients were not considered operative candidates because of their high morbidity and mortality. Heart transplantation is now considered standard treatment for select patients with end-stage heart disease; however, it is applicable only to a small number of patients. In an effort to address this problem, newer and alternative surgical approaches are evolving, including mitral valve annuloplasty, the Batista procedure, and other left ventricular shape changing technologies. Using these operative techniques to alter the shape of the left ventricle, in combination with optimal medical management for heart failure, improves survival, and patients may avoid or postpone transplantation.

Cardiac Surgical Procedures↗
PubMed2003

A randomized controlled trial of adaptive ventilation for Cheyne-Stokes breathing in heart failure.

Heart failure is associated with Cheyne-Stokes breathing, which fragments patients' sleep. Correction of respiratory disturbance may reduce sleep fragmentation and excessive daytime sleepiness. This randomized prospective parallel trial assesses whether nocturnal-assist servoventilation improves daytime sleepiness compared with the control. A total of 30 subjects (29 male) with Cheyne-Stokes breathing (mean apnea-hypopnea index 19.8 [SD 2.6] and stable symptomatic chronic heart failure (New York Heart Association Class II-IV) were treated with 1 month's therapeutic (n = 15) or subtherapeutic adaptive servoventilation. Daytime sleepiness (Osler test) was measured before and after the trial with change in measured sleepiness the primary endpoint. Secondary endpoints included brain natriuretic peptide levels and catecholamine excretion. Active treatment reduced excessive daytime sleepiness; the mean Osler change was +7.9 minutes (SEM 2.9), when compared with the control, the change was -1.0 minutes (SEM, 1.7), and the difference was 8.9 minutes (95% confidence interval, 1.9-15.9 minutes; p = 0.014, unpaired t test). Significant falls occurred in plasma brain natriuretic peptide and urinary metadrenaline excretion. We conclude that adaptive servoventilation produces an improvement in excessive daytime sleepiness in patients with Cheyne-Stokes breathing and chronic heart failure. This study suggests improvements in neurohormonal activation with this treatment.

Aged↗
PubMed2000

Surgical therapies for heart failure.

Heart transplantation remains the best hope for patients with end-stage heart failure unresponsive to conventional therapy, but the number of transplant candidates continues to exceed the number of available donor hearts. Despite major advances in the medical management of heart failure, researchers continue to explore alternative surgical therapies designed to augment cardiac function. Many of these surgical therapies are still in the experimental or clinical trial phases. Surgical approaches include coronary revascularization, mitral valve repair or replacement, cardiomyoplasty, left ventricular volume reduction surgery, and bridging to recovery with the use of ventricular assist devices. Although cardiac surgeons have gained considerable experience in the treatment of patients with heart failure, many improvements and innovations lie ahead.

Cardiomyoplasty↗
PubMed2002

[Alveolar-capillary dysfunction in heart failure].

Heart failure increases the resistance to gas transfer across the alveolar-capillary interface. In different experimental conditions of vascular capillary injury, peculiar anatomical and functional abnormalities of the alveolar unit have been reported and consist of a disruption of its anatomical configuration and of a loss of fluid-flux regulation and gas exchange efficiency (i.e. "stress failure" of the alveolar-capillary membrane). In heart failure, the pathophysiological relevance of these changes has been only recently appreciated. Alveolar-capillary membrane conductance and capillary blood volume are subcomponents of lung diffusion capacity. A reduction of the former with an increase of the latter and consequent impairment of gas exchange are typical of heart failure syndrome. Alveolar-capillary membrane conductance abnormalities have been shown to be a sensitive index of the underlying lung tissue damage, bring an independent prognostic information and play a significant role in the pathogenesis of exercise limitation and ventilatory abnormalities. This review examines the current knowledge on this topic.

Adult↗
PubMed2001

Are we ready for pharmacogenomics in heart failure?

Heart failure is a major health problem and is associated with a high mortality and morbidity. Recently, the role of the genetic background in the onset and development of the disease has been evidenced in both heart failure with and without systolic dysfunction, and in familial and non-familial forms of this condition. Familial forms of dilated cardiomyopathy are more frequent than previously thought. Various modes of inheritance and phenotypes have been reported and this condition appears genetically highly heterogenous. Five genes (dystrophin, cardiac actin, desmin, lamin A/C and delta-sarcoglycan), and additional loci, have been identified in families in which dilated cardiomyopathy is isolated or associated with other cardiac or non-cardiac symptoms. It has been postulated that the molecular defect involved could lead to abnormal interactions between cytoskeletal proteins, responsible either for defect in force transmission or for membrane disruption. More recently, the identification of mutations in genes encoding sarcomeric proteins has led to a second hypothesis in which the disease might also result from a force generation defect. In non-monogenic dilated cardiomyopathy, susceptibility genes (role in the development of the disease) and modifier genes (role in the evolution/prognosis of the disease) have so far been identified. Some data suggest that the efficacy of angiotensin converting enzyme inhibitors, and side-effects, might be related to some genetic polymorphisms, such as the I/D polymorphism of the angiotensin converting enzyme gene. Although preliminary, these data are promising and might be the first step towards application of phamacogenetics in heart failure. This is of paramount importance as the medical treatment of heart failure is characterized by the need for polypharmacy. One of the major challenges of the next millenium, therefore, will be to identify genetic factors which might help define responders to major treatment classes, including angiotensin converting enzyme inhibitors, beta-adrenoreceptor antagonists, angiotensin AT1 receptor antagonists, spironolactone, vasopeptidase inhibitors and endothelin receptor antagonists.

Animals↗
PubMed1996

[Treatment of heart failure].

Heart failure is a disease which involves not only the heart but the entire circulatory system. Progression is directly related to interactions between myocardial disorders and neurohormonal and circulatory phenomena. Advances in treatment have resulted more from the development of vasodilator drugs with neurohormonal effects than from drugs with a direct effect on the myocardium. Diuretics are essential due to their rapid functional effect and the reduction in pressure on the ventricle wall. The effectiveness of digitalics is recognized not only in patients with atrial fibrillation, but also in those in sinus rhythm with ischemic heart disease. Conversion enzyme inhibitors are useful in all stages of heart failure, improving both quality of life and life expectancy as well as limiting myocardial and vascular remodeling and retarding progression of ventricular dysfunction. As current progress in the treatment of heart failure has not greatly reduced mortality, prevention is the major challenge facing all physicians. Treatment of asymptomatic ventricular function is one rational approach.

Angiotensin-Converting Enzyme Inhibitors↗