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PubMed1999

Decreased responsiveness of vascular postjunctional alpha1-, alpha2-adrenoceptors and neuropeptide Y1 receptors in rats with heart failure.

Heart failure is associated with increased sympathetic nerve activity. We hypothesized that chronic sympathetic stimulation in heart failure resulted in decreased vascular sympathetic responsiveness. A pithed rat model was employed to evaluate peripheral vascular alpha-adrenoceptor and neuropeptide Y (NPY) receptor responsiveness. Heart failure was induced in Sprague-Dawley rats by coronary artery ligation. Sham operated rats (Sham) served as controls. Two months after this surgical procedure, both heart failure (n = 30) and Sham (n = 30) rats underwent standard pithing procedure. Pressor responses to preganglionic sympathetic nerve stimulation (PNS) and activation of postjunctional alpha1- and alpha2-adrenoceptors as well as Y1 receptors were studied. In response to PNS, cardiac index was similar between heart failure and sham rats (P = n.s.). Mean arterial pressure (MAP) increased in a frequency-dependent fashion after PNS in heart failure rats as well as in control rats. All the agonists used, i.e. the alpha1-adrenoceptor agonist phenylephrine, the alpha2-adrenoceptor agonists clonidine and BHT933 as well as NPY, induced dose-dependent increases in MAP in heart failure and in sham rats. However, in rats with heart failure, the response to all the agonists studied was significantly decreased and the dose response curves were shifted to the right (P < 0.01). We conclude that in vivo vascular response to postjunctional alpha1- and alpha2-adrenoceptors as well as Y1 receptors are decreased in rats with heart failure.

Adrenergic alpha-Agonists↗

PubMed2004

The epidemiology of heart failure.

Heart failure is becoming increasingly common. More than 20 million people worldwide are estimated to have heart failure. Prevalence is rising because the population is ageing: in both men and women, the prevalence of heart failure in those aged 80-89 years is roughly 10 times the prevalence in those aged 50-59 years. Coronary artery disease is now the most common cause of heart failure. Better treatment of myocardial infarction means that more people survive with impaired myocardial function, and some of these will develop heart failure in time. Hypertension is also an important contributing factor. Valvular disease, once a major cause of heart failure, has become less prevalent. The median survival after diagnosis of heart failure was only 1.7 years for men and 3.2 years for women, according to Framingham data for the years 1948 to 1988. After five years, only 25% of men and 38% of women were still alive. Preventive and treatment measures have improved this picture somewhat: deaths from heart failure have decreased by about 12% per decade. However, heart failure continues to carry a grave prognosis.

Cardiac Output, Low↗

PubMed2004

Platelet activation in heart failure.

Heart failure is a common disease in aging western populations. Not only severe but even mild to moderate heart failure is associated with increasing risk for stroke. This can partly be attributed to concomitant atrial fibrillation, a well-known risk factor for stroke. Furthermore, the increased risk for thromboembolic events in congestive heart failure has been attributed to a hypercoagulable state including formation of intraventricular thrombi. However, more recently, enhanced platelet activation has been described in patients with heart failure in sinus rhythm. Vascular endothelial dysfunction and reduced formation of the platelet inhibitor nitric oxide appear to contribute to platelet activation in heart failure. This review article summarizes the historical knowledge of abnormal platelet function in heart failure, focuses on pathophysiological changes in heart failure which could influence platelet activation, and discusses drug regimens investigated in heart failure to reduce platelet activation either by direct anti-platelet effects or by modulating the release of platelet inhibiting substances.

Anticoagulants↗

PubMed2004

The role of implantable sensors for management of heart failure.

Heart failure is a chronic disease with significant morbidity and mortality worldwide. Drugs such as ACE-inhibitors, beta-blockers and diuretics have helped control heart failure but the incidence of hospitalizations remains high. Rigorous continuous monitoring of patients and tailored therapy based on individual clinical and hemodynamic profile has been shown to limit the symptoms of heart failure. Self-monitoring or prescribed frequent in-clinic monitoring is logistically difficult and is fraught with patient non-compliance. Consequently, implantable sensors that can monitor patient's clinical status on a continuous basis are desirable. The disadvantage with an implantable sensor is obviously that the patient has to undergo an invasive procedure, which in itself has a certain risk, although minimal, associated with it. In addition, the risk of having an implantable device has to be weighed against the benefit of monitoring the patient on a continuous basis. The risk benefit question has been answered in part by the recent success of cardiac resynchronization therapy (CRT) in treating symptoms of heart failure. A recent study has performed a meta analysis on major heart failure trials conducted to date and concluded that CRT reduces mortality and morbidity. The CRT device is a specialized pacemaker with capabilities of continuous heart monitoring and embedded therapeutic decisions. A trend of heart rates offers significant insights into the progression of heart failure and patient status. In addition, using complex algorithms, several of the heart rate variability (HRV) parameters, identified in several studies for risk stratification and prognostication, can also be calculated. Furthermore, in recent devices based on heart rate intervals, autonomic balance (critical measure of progression of heart failure) can be estimated with sophisticated algorithms. Finally, technologies that can monitor patients' activity e.g. accelerometers, can be easily incorporated into the device. Such measures may be used to evaluate the efficacy of a new therapy or simply to provide patient status. Based on advances in technology, several patient clinical features can be monitored and trended over time. The measured metrics will help form a comprehensive and objective clinical profile of the patient that the physician can act upon. Prospective studies are needed to answer the efficacy of such diagnostic measures in management of heart failure.

Biosensing Techniques↗

PubMed2006

Platelets and heart failure.

Heart failure is associated with increased risk of venous thromboembolism, stroke, and sudden death. Platelet abnormalities have been well described in heart failure but the significance of platelets in contributing to the thromboembolic complications of heart failure remains uncertain. Furthermore, the role of antiplatelet agents in heart failure remains unclear. This review will focus on platelet activation and the role of platelet dysfunction in heart failure, with particular regard to pathophysiology and outcome. The effects of heart failure therapeutics on platelet function and antiplatelet therapy in heart failure will also be discussed.

Adrenergic beta-Antagonists↗

PubMed2001

Systematic review of the impact of beta blockers on mortality and hospital admissions in heart failure.

Heart failure is a common condition that carries a high burden of mortality and morbidity. Several randomised trials have evaluated the effects of beta blockers in heart failure. This paper gives a systematic overview of published randomised trials of beta blockers in heart failure using standard methods. In all, 22 randomised controlled trials were identified with a total of 10480 patients, and an average of 11 months of treatment. The average age was 61 years and 4% were female. Most studies excluded patients with severe heart failure. Death rates in patients randomised to receive beta blockers compared to controls were 458/5657 (8.0%) and 635/4951 (12.8%) respectively, odds ratio 0.63, 95% CI 0.55-0.72, P<0.00001. Similar reductions were observed for hospital admissions for worsening heart failure (11.3 vs. 17.1%, respectively, odds ratio 0.63) and for the composite outcome of death or heart-failure hospital admission (19.4 vs. 26.9%, respectively, odds ratio 0.66). These results show that beta blockers reduce the risk of mortality or the need for heart-failure hospital admission by approximately one third. Absolute reductions of 5-6% in event rates were observed over approximately 1 year of treatment period. These important benefits should be implemented as a priority, since treatment with beta blockers is inexpensive and heart failure carries a high risk of death and disability. Further information on the effect of beta blockers in elderly patients and women would be helpful.

Adrenergic beta-Antagonists↗

PubMed2003

Acute and chronic endothelial dysfunction: implications for the development of heart failure.

Heart failure has been characterized by a reduction in cardiac contractile function resulting in reduced cardiac output. The clinical symptoms including mild tachycardia, reduced arterial pressure, increased venous or filling pressure and exercise intolerance have conceptually, to a large degree, been attributed to cardiac myocyte dysfunction. More recently, a vascular component has been recognized to contribute to heart failure. Among the most studied vascular mechanisms that might contribute to the development of heart failure has been the reduced production of nitric oxide or the reduced bioactivity of NO associated with both basic models of heart failure and disease in patients. The still evolving concept that heart failure is a cytokine activated state has, in addition, focused attention on the possibility that the cytokine driven isoform of NO synthase (NOS), iNOS, may produce sufficient quantities of NO to actually suppress cardiac myocyte function contributing to the reduced inotropic state in the failing heart. Thus, our view of the role of NO in the development of heart failure has evolved from simply a reduction in production of NO in blood vessels, to altered substrate availability (i.e. L-arginine), to increased scavenging of NO by superoxide anion, to increased production of NO from iNOS. As these concepts develop, our approach to the therapeutics of heart failure has also progressed with the recognition of the need to develop treatments directed towards addressing one or more of these etiologies. This review will focus on these aspects of the involvement of NO in the development of heart failure and some of the treatments that have developed from our understanding of the basic biology of NO to address these pathohysiologic states.

Acute Disease↗

PubMed2005

Palliative care for end-stage heart failure.

Heart failure is growing in prevalence. Despite an array of treatments targeting a complicated pathophysiology, heart failure ultimately leads to death, and thus there is a clear need to provide palliative care to persons with end-stage heart failure. Palliative care, or education and support of the patient and family and management of distressing symptoms, should be provided throughout the course of the illness. Clinicians need additional information about how to palliate symptoms in advanced heart failure. This article summarizes recent reports about prognostication and identification of patients who are likely to die soon, and the management of fatigue, dyspnea, pain, and depression in heart failure. Palliative care or supportive care of the patient and family should be incorporated into comprehensive care throughout the course of heart failure. Data about hospice care for persons with heart failure are summarized.

Heart Failure↗

PubMed1996

[Neurohormonal factors in heart failure. I].

Heart failure is a physiopathological condition, with an increasing incidence and prevalence, involving the action of a series of mechanisms known as 'compensators', which are phylogenetically ready to normalize minute volume and blood pressure. These mechanisms include the activation of a series of neurohormonal systems: the sympathetic nervous system, the aldosterone renin-angiotensin system, vasopressin arginine, endothelin, which are basically vasoconstrictors, with the counterpoint of other vasodilator systems, such as the endothelial relaxation factor, certain prostaglandins and the bradykinin-kallikrein system, which modulate global response. The authors review the physiopathology of each of these systems, as well as their significance in the diagnosis and prognostic evaluation of heart failure. We analyze the possible deleterious effects of neurohormonal activation, anatomically and at the cardiovascular function level, and try to determine if they are capable of explaining the evolution and progression of heart failure, in a truly vicious circle, up until the irreversible heart failure phase. We review the current importance of the inhibition of the aldosterone renin-angiotensin system in the prophylaxis and treatment of heart failure. Furthermore, we describe the present-day value of the inhibition of the sympathetic nervous system in some forms of heart failure. We also analyze the different pharmacological treatment for heart failure: diuretics, inotropic agents, vasodilators (in their different pharmacological types), paying particular attention to their action on neurohormonal systems and their implications in the prognosis and evolution of heart failure.

Adrenergic beta-Antagonists↗

PubMed2002

Antiarrhythmic therapy in heart failure.

Heart failure is the term used for a cardiovascular syndrome whose definition lacks uniform criteria. It is associated with a very high mortality rate. Approximately 50% of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT). In severe heart failure, death may also occur due to bradyarrhythmias. Other arrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation, and sustained or non-sustained VT. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations (such as fibrosis) may be prominent. Re-entrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. The treatment of the underlying disease process and optimal management of heart failure is of major importance. Revascularization, beta-blocker therapy, and angiotensin converting enzyme inhibitors are all essential to appropriate therapy. Treatment of arrhythmias is performed either because patients are symptomatic or to reduce the risk of sudden cardiac death. The implantable cardioverter-defibrillator (ICD) is the best available therapy to prevent sudden cardiac death from VT. Devices with back-up pacing also offer protection against bradyarrhythmias. There is evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy (e.g. amiodarone) because of atrial fibrillation or non-sustained VT that may activate the device.

Algorithms↗

PubMed2003

Energy metabolism in heart failure.

Heart failure (HF) is a syndrome resulting from the inability of the cardiac pump to meet the energy requirements of the body. Despite intensive work, the pathogenesis of the cardiac intracellular abnormalities that result from HF remains incompletely understood. Factors that lead to abnormal contraction and relaxation in the failing heart include metabolic pathway abnormalities that result in decreased energy production, energy transfer and energy utilization. Heart failure also affects the periphery. Patients suffering from heart failure always complain of early muscular fatigue and exercise intolerance. This is linked in part to intrinsic alterations of skeletal muscle, among which decreases in the mitochondrial ATP production and in the transfer of energy through the phosphotransfer kinases play an important role. Alterations in energy metabolism that affect both cardiac and skeletal muscles argue for a generalized metabolic myopathy in heart failure. Recent evidence shows that decreased expression of mitochondrial transcription factors and mitochondrial proteins are involved in mechanisms causing the energy starvation in heart failure. This review will focus on energy metabolism alterations in long-term chronic heart failure with only a few references to compensated hypertrophy when necessary. It will briefly describe the energy metabolism of normal heart and skeletal muscles and their alterations in chronic heart failure. It is beyond the scope of this review to address the metabolic switches occurring in compensated hypertrophy; readers could refer to well-documented reviews on this subject.

Animals↗

PubMed2003

The role of echocardiography in the diagnosis and management of heart failure.

Heart failure has emerged as one of the most pressing health care issues in the United States. It is estimated that 4.8 million people have chronic heart failure, and approximately 400,000 new cases are diagnosed each year. Since the incidence of heart failure increases significantly with age, its prevalence is likely to increase as the population grows older. The American Heart Association and American College of Cardiology developed clinical practice heart failure guidelines to assist physicians in the diagnosis and management of patients with heart failure, in the hopes of reducing hospitalizations and mortality. These guidelines emphasize the importance of echocardiography in the management of acute and chronic heart failure. However, the guidelines do not elaborate on all the potential applications of echocardiography for this condition. This review was undertaken to examine in detail, the role of echocardiography in the initial management and long-term follow-up of patients with heart failure.

Disease Management↗

PubMed1997

The role of nitric oxide and cytokines in heart failure.

Heart failure is a common problem associated with considerable mortality and morbidity. The mechanisms underlying the heart failure syndrome, which remain poorly understood, may involve an inflammatory process. Nitric oxide (NO) and various cytokines could play an important role in this inflammatory process. Recent evidence has emerged in both animal models and humans suggesting that both of these mediators may play an important role in heart failure. NO is synthesized by the NO synthase family of enzymes. Two of these enzymes are constitutive, endothelial NO synthase and neuronal NO synthase. The third enzyme, inducible NO synthase, is capable of producing large amounts of NO once induced by mediators such as interleukin (IL)-1, IL-2, IL-6, tumour necrosis factor (TNF)-alpha, and interferon-gamma. Endothelial NO synthase is present in the heart in the endocardium, cardiac myocytes, and cardiac conduction tissue. Inducible NO synthase is present in cardiac myocytes, endocardium, vascular smooth muscle cells, and infiltrating inflammatory cells. Evidence from both animal models and patients suggests that NO exerts a negative inotropic effect. Increased inducible NO synthase, TNF-alpha, and IL-6 have been found in patients with heart failure in several studies. In other studies, decreased endothelial NO synthase was found in patients with heart failure. TNF-alpha and IL-6 may be produced in heart failure and may induce inducible NO synthase, resulting in NO production, which acts as a negative inotrope. Endothelial NO synthase may be decreased as a result of downregulation by TNF-alpha or inducible NO synthase. The possible role of these mediators in heart failure needs further evaluation because these findings could have novel therapeutic implications.

Animals↗

PubMed2000

Exploring new treatment strategies in heart failure.

Heart failure remains a major and increasing cause of mortality and morbidity, even when the best available treatments are used. One of its key causes is neuroendocrine activation via the sympathetic nervous system and the renin-angiotensin system (RAS). Neuroendocrine blockers of the sympathetic nervous system (beta-blockers) and of the RAS (angiotensin-converting enzyme [ACE] inhibitors and angiotensin II type 1 [AT1] receptor blockers) therefore have an important potential therapeutic role in heart failure. The promising results from clinical trials with beta-blockers suggest that these drugs will become an established part of the future management of patients with mild to moderate symptomatic heart failure. Blockade of the RAS with ACE inhibitors has also been shown to be effective in reducing the risk of morbidity and mortality in patients with heart failure. Blockade of the AT1-receptor, with agents such as candesartan, produces more specific and, theoretically, more complete blockade of the major negative cardiovascular effects of angiotensin II than is possible using ACE inhibitors, whilst maintaining placebo-like tolerability. Furthermore, AT1-receptor blockade leads to increased stimulation of the angiotensin II type 2 (AT2) receptor, which, according to experimental data, may have favourable cardiovascular effects. Following encouraging results from two pilot studies, a major new international study programme - CHARM (Candesartan in Heart failure - Assessment of Reduction in Mortality and morbidity) - has been initiated to define the clinical benefits of candesartan cilexetil in a wide variety of patients with symptomatic heart failure. CHARM is the first study to accept all relevant heart failure patients who may benefit from RAS blockade, irrespective of their left ventricular function or tolerance of ACE inhibitors. The 6500 patients to be recruited will be divided among three integrated outcome studies. Two of these studies will examine the effect of candesartan cilexetil versus placebo in patients with an ejection fraction of 40% or less who are tolerant or intolerant of ACE inhibitors. The third study arm will examine the benefits of candesartan cilexetil in a previously seldom studied group: those with symptomatic heart failure, but with preserved left-ventricular systolic function. Recruitment of patients into the study has started.

Adrenergic beta-Antagonists↗

PubMed2001

Pathophysiology of chronic heart failure.

Heart failure is a changing paradigm. The hemodynamic model, which served our needs well from the 1950s through the early 1980s, has now been largely abandoned, except for the management of decompensated patients in the hospital. The pathophysiology is exceedingly complex and involves structural changes, such as loss of myofilaments, apoptosis and disorganization of the cytoskeleton, as well as disturbances in Ca(2+) homeostasis, alteration in receptor density, signal transduction, and collagen synthesis. A more contemporary working hypothesis is that heart failure is a progressive disorder of left ventricular remodeling, usually resulting from an index event, that culminates in a clinical syndrome characterized by impaired cardiac function and circulatory congestion. This change in the framework of our understanding of the pathophysiology of heart failure is predicated on the results of numerous clinical trials conducted during the past 20 years. New therapies are now evolving that are designed to inhibit neuroendocrine and cytokine activation, whereas drugs specifically designed to heighten cardiac contractility and "unload" the left ventricle have proven to be unhelpful in long-term management of patients with chronic heart failure. However, the hemodynamic model is still relevant for patients in the hospital with decompensated heart failure, where positive inotropic drugs and vasodilators are still widely used. The modern treatment of chronic heart failure is now largely based on the neurohormonal hypothesis, which states that neuroendocrine activation is important in the progression of heart failure and that inhibition of neurohormones is likely to have long-term benefit with regard to morbidity and mortality. Thus, the evolution of treatment for chronic heart failure as a result of clinical trials has provided much enlightenment for our understanding of the fundamental biology of the disorder, a reversal of the usual flow of information from basic science to clinical investigation.

Adrenergic beta-Antagonists↗

PubMed2001

Genomics and the pathophysiology of heart failure.

Heart failure is not a single disease entity, but a syndrome with various causes, including hypertension, ischemic and congenital heart disease, cardiomyopathy, and myocarditis. Because of the multiple etiologies and secondary adaptations contributing to heart failure, the study of the cellular and molecular mechanisms underlying the development and progression of this syndrome has been rather challenging. Much has been learned about the remodeling processes in heart failure, which involve complex interactions among numerous mediators in signaling and regulatory pathways. The Human Genome Project and related projects have provided a preliminary database for a genome-wide analysis of complex polygenic disorders such as heart failure. With the aid of expressed sequence tag technology and microarray applications, both known and previously uncharacterized genes involved in the induction and regression of cardiac hypertrophy and its progression to heart failure can be analyzed simultaneously. Deciphering the complexity of sequence-structure-function relationships in heart failure is a goal for the future, and will require advances in structural biology, proteomics, and computational technology. In this review, we summarize the cellular and molecular aspects of heart failure, and how recent applications of genomic technologies have been successful in achieving a more complete portrait of gene expression in this pathologic state.

Animals↗

PubMedDate not supplied

Palliation of heart failure.

Heart failure is the major cause of morbidity and mortality in the United States. Stage D heart failure has a greater mortality rate than many cancers and has equivalent symptom burden and severity. There has been a paradigm shift in our understanding of the pathophysiology of heart failure. Progressive heart failure is associated with ventricular remodeling and a maladaptive neurohumoral response. Drug classes have evolved that curtail ventricular remodeling, and blunt neurohumoral responses reduce morbidity and mortality. Despite combination drug and device therapies, the management of Stage D heart failure includes palliation. Both cardiology and palliative specialists need to learn from one another in order to palliate these highly symptomatic patients. Such collaboration will enhance care and are the basis for well-conceived research trials.

Cardiovascular Agents↗

PubMed2001

Practical aspects of using beta-adrenergic blockade in systolic heart failure.

Heart failure exacts a severe human and public health toll. In the United States, heart failure afflicts approximately 5 million patients and is responsible for or contributes to 3 million hospitalizations and 300,000 deaths yearly. Physicians can have a major impact on this disease by using effective agents for the treatment of heart failure (particularly angiotensin-converting enzyme [ACE] inhibitors and beta blockers), yet the actual clinical use of these drugs (especially the use of beta blockers by primary physicians) is disappointingly low. Many physicians appear to be reluctant to prescribe beta blockers for two reasons. First, they are concerned about the potential interference of beta blockers with important compensatory mechanisms that support the failing heart and fear that such interference may lead to clinical deterioration. Second, they fail to identify patients with heart failure (especially those with mild or moderate symptoms) or regard such patients as being too well to require additional treatment. These reasons should no longer be used as excuses to avoid the use of these drugs, given the persuasive evidence that beta blockers can improve symptoms and prolong life in patients with heart failure. Instead, physicians must recognize that long-term activation of the sympathetic nervous system primarily exerts deleterious (rather than compensatory) effects in patients with heart failure and that these actions can be antagonized effectively and safely by the appropriate use of beta-blocking drugs.

Adrenergic beta-Antagonists↗