Current Heart Failure Reports (Curr Heart Fail Rep )

Publisher: Springer Verlag


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Springer Verlag

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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The loss of contractile function is a hallmark of heart failure. Although increasing intracellular Ca2+ is a possible strategy for improving contraction, current inotropic agents that achieve this by raising intracellular cAMP levels, such as β-agonists and phosphodiesterase inhibitors, are generally deleterious when administered as long-term therapy due to arrhythmia and myocardial damage. Nitroxyl donors have been shown to improve cardiac function in normal and failing dogs, and in isolated cardiomyocytes they increase fractional shortening and Ca2+ transients, independently from cAMP/PKA or cGMP/PKG signaling. Instead, nitroxyl targets cysteines in the EC-coupling machinery and myofilament proteins, reversibly modifying them to enhance Ca2+ handling and myofilament Ca2+ sensitivity. Phase I–IIa trials with CXL-1020, a novel pure HNO donor, reported declines in left and right heart filling pressures and systemic vascular resistance, and increased cardiac output and stroke volume index. These findings support the concept of nitroxyl donors as attractive agents for the treatment of acute decompensated heart failure.
    Current Heart Failure Reports 09/2014; 11(3).
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    ABSTRACT: Heart failure (HF) is a major healthcare concern. Acute HF carries a high mortality and a high rehospitalisation rate. HF has a variety of detrimental effects on other organs. In recent years, the interactions between heart failure and the kidney have been the subject of significant investigations; this interaction, defined as “cardiorenal syndrome”, is relatively well characterized. We describe here another interaction between the heart and the liver, the “cardiohepatic syndrome”, in acute HF patients. Recent publications have shown that liver function test (LFT) abnormalities were associated with AHF severity. Clinical signs of systemic congestion were found to be associated with cholestasis, when signs of hypoperfusion were associated with liver cytolysis. Defining the LFT profile in AHF may play an important role in the future management of AHF patients.
    Current Heart Failure Reports 06/2014;
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    ABSTRACT: The purpose of this review is to discuss the educational challenges faced by health care professionals in the care and management of patients with heart failure (HF). Self-care is a vital component in HF management, and promotion of self-care through education is a fundamental aspect of patient-centered care and supports patients’ right to autonomy. The ultimate goal is not simply to convey knowledge, but to promote patients’ understanding and to enhance their self-care skills by assuming an active role in their care. As such, health care professionals are confronted with a number of patient-related issues as they strive to provide high-quality education. Beyond assessing patients’ individual information needs and preferences, they are tasked with addressing several obstacles that impede patients’ ability to engage in self-care. Factors such as cognitive impairment and low health literacy have a major impact on patients’ ability to understand, absorb, and recall information. Moreover, the existence of negative beliefs, which are strong determinants of patients’ attitudes towards their disease and treatment, may also influence their response to educational messages. Health care professionals must not only identify and overcome these obstacles, but they must act effectively within the limitations of their working environment and of the health care system.
    Current Heart Failure Reports 06/2014;
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    ABSTRACT: Growth differentiation factor 15 (GDF-15) is a stress-responsive cytokine expressed in the cardiovascular system. GDF-15 is emerging as a biomarker of cardiometabolic risk and disease burden. GDF-15 integrates information from cardiac and extracardiac disease pathways that are linked to the incidence, progression, and prognosis of heart failure (HF). Increased circulating levels of GDF-15 are associated with an increased risk of developing HF in apparently healthy individuals from the community. After an acute coronary syndrome, elevated levels of GDF-15 are indicative of an increased risk of developing adverse left ventricular remodeling and HF. In patients with established HF, the levels of GDF-15 and increases in GDF-15 over time are associated with adverse outcomes. The information provided by GDF-15 is independent of established risk factors and cardiac biomarkers, including BNP. More studies are needed to elucidate how the information provided by GDF-15 can be used for patient monitoring and formulating treatment decisions. Further understanding of the pathobiology of GDF-15 may lead to the discovery of new treatment targets in HF.
    Current Heart Failure Reports 09/2012; 9(4).
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    ABSTRACT: Anemia is a common comorbidity in heart failure (HF), and is associated with increased morbidity and mortality. However, it remains unclear whether anemia is merely a marker of poor prognosis or whether anemia itself confers risk. The pathogenesis of anemia in HF is multifactorial. Iron deficiency also confers risk in HF, either with or without associated anemia, and treatment of iron deficiency improves the functional status of patients with HF. An ongoing large clinical trial studying the use of darbepoetin–alfa in patients with anemia and systolic HF is expected to provide information that should improve our understanding of anemia in HF.
    Current Heart Failure Reports 09/2012; 9(4).
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    ABSTRACT: More than half of patients with heart failure (HF) have a normal ejection fraction (EF). These patients are typically elderly, are predominantly female, and have a high incidence of multiple comorbid conditions associated with development of ventricular hypertrophy and/or interstitial fibrosis. Thus, the cause of HF has been attributed to diastolic dysfunction. However, the same comorbidities may also impact myocardial systolic, ventricular, vascular, renal, and extracardiovascular properties in ways that can also contribute to symptoms of HF by way of mechanisms not related to diastolic dysfunction. Accordingly, the descriptive term HF with normal EF has been suggested as an alternative to the mechanistic term diastolic HF. In this article, we review the current understanding of nondiastolic mechanisms that may contribute to the HF with normal EF syndrome to highlight potential pathways for research that may lead to new targets for therapy.
    Current Heart Failure Reports 02/2009; 6(1):57-64.
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    ABSTRACT: Atrial fibrillation (AF) and congestive heart failure (CHF) are common cardiac conditions that frequently coexist. There is a complex interplay between the two conditions, with each increasing the morbidity and mortality associated with the other. The management of AF in patients with CHF requires special care because of the increased risk of antiarrhythmic drug therapy in the group. This report reviews current treatment options and assesses the role of the newer therapies of biventricular pacing for CHF and radiofrequency ablation for AF. It also discusses results of the AF-CHF study, which were reported in November 2007.
    Current Heart Failure Reports 02/2008; 5(1):11-15.
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    ABSTRACT: Cardiac resynchronization therapy (CRT) improves clinical outcome and survival in advanced heart failure. However, some patients do not respond clinically or show improvement in left ventricular function. Our focus has turned to why such “nonresponders” exist. Follow-up of CRT has led to several explanations, varying by individual patient, and has shown the importance of device programming in CRT in heart failure. The failing heart displays delayed contraction in the ventricle, also referred to as mechanical dyssynchrony. Simply pacing both ventricles simultaneously might not be adequate to optimize systolic function. Individually tailoring the atrioventricular (AV) timing can improve left ventricular filling and cardiac output, and adjusting the interventricular (VV) pacing delay has also been shown to improve hemodynamics. Increasing evidence regarding AV and VV optimization is emerging. This article reviews the current data on optimization, including the physiology, numerous approaches, and current issues.
    Current Heart Failure Reports 02/2008; 5(1):38-43.
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    ABSTRACT: Heart transplantation remains the gold standard treatment for "end-stage" dilated cardiomyopathy. However, its epidemiologic impact on the heart failure problem continues to be small due to limited donor organ availability and contraindications. Therefore, several "conventional" surgical procedures have been developed to reverse the vicious cycle of ventricular remodeling that accompanies systolic heart failure and to improve symptoms and survival of the patients. This review discusses indications, results, and limitations of the most common surgical methods currently used to arrest or reverse cardiac remodeling.
    Current Heart Failure Reports 01/2008; 4(4):214-20.
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    ABSTRACT: Mild hyponatremia is common in patients hospitalized for worsening heart failure, and it is a major predictor of post-discharge mortality and morbidity irrespective of left ventricular ejection fraction. Recent data also suggest that standard therapy for heart failure does not improve or normalize serum sodium concentration during hospitalization. There are conclusive data that vasopressin antagonists improve or normalize serum sodium in this patient population. However, it is not known if this improvement or normalization in serum sodium is associated with an improvement in post-discharge outcomes. Future trials with vasopressin antagonists in patients hospitalized with worsening heart failure and hyponatremia are in order.
    Current Heart Failure Reports 01/2008; 4(4):207-13.
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    ABSTRACT: As part of the recommended modern post-myocardial infarction (MI) management, including reperfusion strategies, antiplatelet therapy, and beta-blockers, we may wonder whether the impact of early inhibition of the renin-angiotensin system (RAS) is as important as it was 20 years ago. This review demonstrates that significant clinical benefit can be derived from angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) even when added to other currently recommended treatment strategies in post-MI patients. Moreover, the effects of RAS inhibition extend far beyond the early post-MI neurohormonal activation and left ventricular remodeling phases. The favorable effects of RAS inhibition on important prognostic markers such as atrial fibrillation, renal function, and diabetes have recently been unraveled. Post-MI RAS inhibition also benefits all age groups, including elderly patients.
    Current Heart Failure Reports 01/2008; 4(4):190-7.
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    ABSTRACT: The presence of heart failure or left ventricular systolic dysfunction in the setting of acute myocardial infarction is associated with poor prognosis. Aldosterone is an important downstream mediator of the renin-angiotensin-aldosterone system that promotes myocardial collagen deposition, myocardial fibrosis, apoptosis, ventricular remodeling, and endothelial dysfunction. It may play an important role in the increased morbidity and mortality and the development and progression of heart failure after acute myocardial infarction. Extending the findings from the Randomized Aldactone Evaluation Study (RALES) in patients with chronic heart failure, the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) demonstrated that the selective aldosterone blocker eplerenone offered a significant survival benefit, attenuation of progression of heart failure, and prevention of sudden cardiac death when used in addition to optimal medical therapy. The current evidence-based guidelines now suggest that aldosterone blockade should be an integral component of heart failure therapy to improve outcomes in this high-risk population.
    Current Heart Failure Reports 01/2008; 4(4):183-9.
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    ABSTRACT: The possibility of modifying cardiac metabolism by switching the fuel used by the myocardium could become increasingly important. Inhibitors of free fatty acid (FFA) oxidation could have an important role in therapeutic strategy for patients with heart failure, and shifting the energy substrate preference away from FFA metabolism and toward glucose metabolism may be an effective adjunctive treatment. Additionally, abnormalities of glucose homeostasis in patients with heart failure contribute to the progression of the primary disease. If not adequately treated, these abnormalities can contribute to the occurrence of complications, including severe left ventricular dysfunction. Apart from meticulous metabolic control of frank diabetes, special attention should be paid to insulin resistance, a distinct clinical entity. The observed combined beneficial effects of FFA inhibitors on left ventricular function and glucose metabolism represent an additional advantage of these drugs, especially when abnormalities of myocardial and glucose metabolism coexist.
    Current Heart Failure Reports 01/2008; 4(4):236-242.
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    ABSTRACT: Obesity is associated with structural and functional changes in the heart. These changes may be precursors to more overt forms of cardiac dysfunction and heart failure. However, it is not known 1) whether cardiac hypertrophy in obese individuals results directly from increased adioposity or from the effects of comorbid conditions such as hypertension, diabetes, and sleep-disordered breathing and 2) whether functional changes (eg, mild reductions in systolic and diastolic function) in obese patients progress over time to the point where they cause heart failure, unless ischemic heart disease develops. Establishing a clear link between obesity and heart failure is complicated by the fact that obesity must be present for many decades before the risk of heart failure increases substantially. At present, there are no longitudinal studies of changes in cardiac size and function in humans with obesity. This article reviews data showing structural and functional changes in the heart in obesity and the evidence that these are or are not progressive over time. At present, we believe it is uncertain whether there is a true "cardiomyopathy of obesity."
    Current Heart Failure Reports 01/2008; 4(4):221-8.
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    ABSTRACT: Primary myocardial diseases, or cardiomyopathies, affect millions of individuals worldwide. Although there are sizable environmental contributors to the etiology of these diseases, many cardiomyopathies have a high degree of heritability and, thus, genetic aspects of diagnosis and therapy warrant special consideration. The past two decades have seen enormous progress in elucidating the epidemiology, genetic architecture, and pathophysiology of these diseases. In this review, we focus on translating advances in the genetics of cardiomyopathies to clinical care. We discuss the underlying genetic and phenotypic complexity of these disorders, highlighting the implications for diagnosis, treatment, screening, and prognosis of patients and their family members.
    Current Heart Failure Reports 01/2008; 4(4):229-35.
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    ABSTRACT: Studies suggest that cardiac transfer of stem and progenitor cells can have a favorable impact on tissue perfusion and contractile performance after acute myocardial infarction (AMI). Although the mechanistic background of stem cell therapy is still intensely debated, stem cell therapy has been introduced into the clinical setting, where the first randomized, controlled trials indicate that it is feasible and safe in patients. Preliminary efficacy data indicate that stem cells have the potential to enhance myocardial perfusion and/or contractile performance in patients with AMI. The field now is rapidly moving toward intermediate-size, double-blind trials to gather more safety and efficacy data and the first insights into clinical end points. Ultimately, large outcome trials will be needed. At the same time, continued basic research is needed to elucidate the underlying mechanism of stem cell therapy.
    Current Heart Failure Reports 01/2008; 4(4):198-203.
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    ABSTRACT: Improvement of health-related quality of life (HRQL) is increasingly recognized as a priority in the management of heart failure (HF). In this review, we highlight the dramatic improvement in HRQL often observed in patients with severe HF and give particular emphasis to the nonpharmacologic therapy of cardiac resynchronization therapy, left ventricular assist devices, and cardiac rehabilitation. We juxtapose this to the less consistent improvement in HRQL seen with interventions aimed at treatment of acute HF syndromes. Conflicting data wherein HRQL improves in parallel to a detrimental or neutral effect on cardiovascular morbidity and mortality are also presented. We conclude with future directions and make the case for HF-specific instruments intended for the assessment of HRQL in hospitalized patients, longitudinal studies in which HRQL is followed over time, and continued attention to the preferences of those with severe and acute HF.
    Current Heart Failure Reports 10/2007; 4(3):170-7.
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    ABSTRACT: Erythropoietin (EPO) is a glycoprotein hormone implicated in the regulation of red blood cell production. Anemia is common in chronic heart failure (CHF) patients and associated with an inappropriately low EPO-production, suggesting a role for its recombinant human form (rhEPO) in treatment. Although safety concerns have been raised regarding treatment with rhEPO in patients with chronic kidney disease, treatment with rhEPO in patients with CHF has so far been safe and well tolerated. The effect of rhEPO on outcome in anemic CHF patients is under investigation in a phase III clinical trial. In addition to its erythropoietic effects, EPO has been detected in the cardiovascular system, fueling intense research into possible non-hematopoietic effects. EPO has been shown to exert protective effects on the heart during acute myocardial ischemia and improve cardiac function in experimental CHF. Acute protection is mediated through reduction of apoptotic cell death. Improvement of cardiac function in CHF is related to myocardial neovascularization. EPO exhibits a vast array of beneficial effects in cardiovascular disease. In addition to the correction of anemia in CHF, rhEPO might benefit patients with cardiovascular disease.
    Current Heart Failure Reports 10/2007; 4(3):127-33.
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    ABSTRACT: The adversarial relationship between the heart and the kidney in heart failure results from normal homeostatic mechanisms which become inappropriate in the setting of heart failure. The cardio-renal syndrome represents the sum total of this adversarial relation and is clinically manifest as worsening renal function limiting diuresis in spite of volume overload. Tubuloglomerular feedback is a major pathophysiologic component of this syndrome. Adenosine, acting via A1 receptors, plays a major role in tubuloglomerular feedback in the normal state and in cardio-renal syndrome. Preclinical studies and initial human studies suggest that adenosine antagonism increases diuresis and preserves glomerular filtration in the setting of decompensated heart failure. Considering the ubiquitous distribution of adenosine receptors in the body, it is crucial to tailor this therapeutic agent to avoid side effects, especially neurotoxicity. Larger studies are presently underway to understand the therapeutic potential of this novel class of agents.
    Current Heart Failure Reports 10/2007; 4(3):153-7.
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    ABSTRACT: Over the past few years, acute worsening of renal function has emerged as a powerful and independent predictor of adverse cardiac outcomes among patients hospitalized with acute heart failure exacerbation. This phenomenon has been recently termed acute cardio-renal syndrome. Acute cardio-renal syndrome is not uncommon, affecting roughly one third of acute decompensated heart failure patients. The mechanism of acute cardio-renal syndrome is poorly understood and difficult to elucidate in light of the complex and multifactorial comorbidities associated with acute heart failure syndrome. Acute cardio-renal syndrome is commonly explained by hypoperfusion of the kidney with intravascular volume depletion, hypotension and low flow state ("pre-renal syndrome"). This perception, however, is challenged by the actual hemodynamics present during acute cardio-renal syndrome characterized by hypervolemia, normal cardiac output, and elevated filling pressures of the systemic and venous circulation. This review discusses the long-standing and unnoticed evidence in support of the notion that right-sided failure with raised filling pressure of the renal vein by itself can indeed lead to acute worsening renal function with oliguria, azotemia, and reduced glomerular filtration rate.
    Current Heart Failure Reports 10/2007; 4(3):134-8.