Current Heart Failure Reports (Curr Heart Fail Rep )

Publisher: Springer Verlag

Description

  • Impact factor
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  • 5-year impact
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  • Cited half-life
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  • Website
    Current Heart Failure Reports website
  • Other titles
    Current heart failure reports (Online), Current heart failure reports
  • ISSN
    1546-9549
  • OCLC
    53129493
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors own final version only can be archived
    • Publisher's version/PDF cannot be used
    • On author's website or institutional repository
    • On funders designated website/repository after 12 months at the funders request or as a result of legal obligation
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany link to published version (The original publication is available at www.springerlink.com)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification
    ​ green

Publications in this journal

  • [show abstract] [hide abstract]
    ABSTRACT: The challenges managing advanced heart failure (AHF) are mounting, not least by the presence of multiple coexisting comorbidities, the lack of evidence of clinical benefit in many subsets of AHF, but also surrounding the uncertainty of the both short-term and long-term prognosis. Clinicians are highly variable in their interpretation of clinical data and are prone to considerable bias when it comes to treatment recommendations. This manuscript provides a critical appraisal of the uncertainties as it pertains to the natural history of AHF and management decisions. First, clinical examples are explored to illustrate common errors of judgment due to unrecognized biases. Secondly, a tool is provided that promulgates a structured approach to key data elements in an attempt to create a sound platform for decision-making.
    Current Heart Failure Reports 04/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: The National Cancer Institute estimates that approximately 13.7 million Americans with a history of cancer were alive on January 1, 2012. With the rising number of cancer survivors, there is an increased focus on how chemotherapy agents modulate the cardiovascular biology and cause chemotherapy-related heart failure in certain patients. Neuregulin-1 (NRG-1) is an important cardiac growth factor that is essential for normal myocardial development and maintenance. Certain chemotherapy agents perturb the normal NRG-1 signaling in the cardiovascular system and cause cardiac dysfunction and, in some cases, symptomatic heart failure. As researchers have learned the critical importance of NRG-1 within the cardiovascular system, more attention has been focused on the potential use of NRG-1 as biomarker and therapy for the treatment of heart failure. This review will highlight the biology of NRG-1 within the cardiovascular system, its role in chemotherapy-induced heart failure, and the translational potential of NRG-1 as treatment for heart failure.
    Current Heart Failure Reports 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Obesity is both a risk factor and a direct cause of heart failure (HF) in adults. Severe obesity produces hemodynamic alterations that predispose to changes in left ventricular morphology and function, which, over time, may lend to the development of HF (obesity cardiomyopathy). Certain neurohormonal and metabolic abnormalities as well as cardiovascular co-morbidities may facilitate this process. Substantial purposeful weight loss is capable of reversing most of the alterations in cardiac performance and morphology and may improve functional capacity and quality of life in patents with obesity cardiomyopathy.
    Current Heart Failure Reports 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Clinical reports have suggested that patients with heart diseases may be particularly vulnerable to heat injury. This review examines the effects of heat stress on cardiovascular and autonomic functions in patients with chronic heart failure (CHF). Laboratory investigations have shown that cutaneous vasodilator responses to heating are impaired in patients, whereas activation of skin sympathetic nerve activation is not attenuated in CHF as compared to controls. Attenuated cutaneous vasodilation may increase the risk of a heat related illness when CHF subjects are exposed to hyperthermic conditions.
    Current Heart Failure Reports 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Heart failure readmissions result in significant costs to the health care system and to patients' quality of life, but programs to reduce readmissions have met with mixed success. Successful strategies have included multidisciplinary hospital-based quality initiatives, disease management programs, and care transition interventions. Devices like telemonitors and indwelling catheters, however, have met with mixed success. Research is still needed to elucidate the most effective interventions for readmission reduction in the HF population.
    Current Heart Failure Reports 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Approximately 20-40 % of heart failure patients with reduced ejection fraction (EF) demonstrate substantial improvements in their EF during follow-up. A subset of these patients who had originally received implantable cardioverter defibrillators (ICD) for the primary prevention of sudden cardiac death (i.e., patients with EF < 35 %) pose a challenge to cardiologists when they present with improvements in EF to above 35 % at the time of their battery depletion. Little is known about the risk of sudden cardiac death in these patients. Is the risk high enough to warrant the replacement of the ICD generator? In the following article, we review the available data on the risk of sudden cardiac death in these patients, and aim to assist the clinician and the patient in making informed decisions about whether the ICD therapy should be continued.
    Current Heart Failure Reports 02/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Enhanced peripheral chemosensitivity (PChS) is a common finding in congestive heart failure (CHF). Although initially it may be regarded as a compensatory mechanism to maintain adequate oxygenation and tissue perfusion, importantly it also contributes to disease progression. The magnitude of PChS is related to the severity of CHF but does not depend on its etiology. Numerous methodologies have been developed to assess PChS reliably; however, only two methods based on acute hypoxia have proven to be clinically and prognostically useful. The pathophysiology behind increased PChS is complex and involves disturbances in regional blood flow, gaseous neurotransmission, redox processes, and angiotensin signaling. Augmented PChS is believed to translate into sympathetic overactivity, decreased barosensitivity, reduced exercise tolerance, more arrhythmic events, and poor outcomes. In this review, we present current knowledge regarding the pathophysiology of peripheral chemoreflex, available methods for assessment, and clinical significance of increased PChS.
    Current Heart Failure Reports 02/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Heart failure (HF) is a syndrome characterized by high morbidity and mortality, despite advances in medical and device therapy that have significantly improved survival. The outcome of HF in elderly patients results from a combination of biological, functional, psychological, and environmental factors, one of which is nutritional status. Malnutrition, as well as HF, is frequently present with aging. Early detection might lead to earlier intervention. It is our goal to review the importance of nutritional status in elderly patients with HF, as well as tools for assessing it. We also propose a simple decision algorithm for the nutritional assessment of elderly patients with HF.
    Current Heart Failure Reports 01/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Both experimental and clinical evidence accumulated over the last couple of decades has linked inflammatory activation to the initiation and progression of chronic heart failure (HF). Circulating levels of inflammatory mediators are associated with cardiac function and inform risk prediction in patients, but the effect of anti-inflammatory therapy in HF remains uncertain. Interleukin (IL)-6 type cytokines are central to the inflammatory response, and convey their signals through the ubiquitously expressed glycoprotein (gp) 130 receptor subunit. IL-6-type/gp130 signaling therefore represents an inflammatory nexus, with inherent potential for disease modification. This review focuses on the current knowledge of IL-6/gp130 signaling in relation to HF, with a particular emphasis on the role of soluble gp130 (sgp130), a signaling pathway modulator. Biological aspects of sgp130 and IL-6 signaling are discussed, as are potential novel therapeutic approaches to modulate this central inflammatory signaling pathway.
    Current Heart Failure Reports 01/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Heart failure constitutes a major public health concern in the United States and is one of the leading causes of hospitalization, readmission, and death. Due to an aging U.S. population, it is estimated that the prevalence of heart failure will increase by 25 % over the coming decades, affecting approximately 3.5 % of the population by the year 2030. The ability to discriminate patients admitted with acute heart failure syndromes who are at increased risk for poor post-hospitalization outcomes is thus critical to guide therapeutic decision making for healthcare providers. This review paper will discuss clinical, hemodynamic, as well as biochemical markers that have been demonstrated to predict post-discharge outcomes among patients hospitalized with acute heart failure.
    Current Heart Failure Reports 01/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Transthyretin amyloidosis (ATTR) is either a hereditary disease related to a mutation in the transthyretin gene that leads to neuropathy and/or cardiomyopathy or an acquired disease of the elderly that leads to restrictive cardiomyopathy. The prevalence of this disease is higher than once thought and awareness is likely to increase amongst physicians and in particular cardiologists. Until recently there have been no treatment options for this disease except to treat the heart failure with diuretics and the neuropathy symptomatically. However, there are several emerging pharmacologic therapies designed to slow or stop the progression of ATTR. This article reviews novel therapeutic drugs that work at different points in the pathogenesis of this disease attempting to change its natural history and improve outcomes.
    Current Heart Failure Reports 01/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Heart failure (HF) is a growing health problem, at least in part due to the concurrent obesity epidemic plaguing developed countries. However, once a patient develops HF, an elevated BMI appears to confer a survival benefit - a phenomenon termed the "obesity paradox." The exact explanation for this paradox has been difficult to ascertain. Numerous plausible mechanisms have been asserted, including the fact that obese patients tend to be younger and more symptomatic, leading them to seek medical attention earlier in the course of their HF. Obese patients may also have larger energy reserves that help to offset the catabolic changes seen with HF. Other hypotheses highlight the limitations of BMI as an obesity classifier. The purpose of this review is to examine the various theories for the obesity paradox in HF and discuss the implications for the clinical management of obese patients with HF.
    Current Heart Failure Reports 01/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Heart failure (HF) is a complex syndrome characterized by myocardial dysfunction, derangement of multiple organ systems and poor outcome. Out of several markers of severity, abnormalities in exercise ventilation (VE) offer relevant insights into the pathophysiology of dyspnea, lung gas exchange, and control of ventilation and are now recognized as meaningful indicators of disease severity and prognosis. Ventilation inefficiency, identified as an increased slope of VE vs carbon dioxide production (VCO2) recognizes as major determinants an increased waste ventilation due to enhanced dead space, early occurrence of lactic acidosis, and an abnormal chemoreflex and/or metaboreflex activity. In some cases of HF, especially associated with advanced hemodynamic and neural deregulation, an exercise oscillatory ventilatory (EOV) pattern may occur. According to an increasing number of studies, EOV identifies the 15-30 % of higher-risk HF patients requiring aggressive treatment and provides an even more robust prediction of outcome compared to VE/VCO2 slope. Overall, a refined prevalence definition and more comprehensive use of these markers in a clinical environment and in future interventional trials seem challenging for the years to come.
    Current Heart Failure Reports 01/2014;
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    ABSTRACT: Cardiac resynchronization therapy (CRT) improves measures of systolic function and clinical status. However, its effect on diastolic function is not well established. Commonly used parameters of diastolic function are measured from echocardiography, using pulse wave and tissue Doppler technologies, as well as timing and deformation data. Review of the existing studies that address the relationship between diastolic function and CRT shows conflicting data, but general trends can be deduced. Baseline elevated filling pressure appears to identify patients most likely to derive improvement in that particular parameter. Intrinsic relaxation does not appear to be significantly impacted by CRT. Generally, changes in diastolic properties after CRT appear to be linked to changes in systolic function. Specific therapy aimed at diastolic asynchrony is lacking, partly due to an unclear relationship between diastolic asynchrony and diastolic dysfunction, and the inability to specifically impact diastolic timing with a systolic intervention such as CRT.
    Current Heart Failure Reports 12/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Acute heart failure (AHF) is one of the most common causes of hospital admission. Despite the very high short-term morbidity and mortality and high costs associated with the condition, little progress has been made toward an understanding of the complex mechanisms of AHF, and particularly the spike in mortality after AHF admission. This manuscript addresses certain hypotheses for the pathophysiology of increased mortality after an AHF episode, specifically exploring the role of neurohormonal and inflammatory activation, congestion, and end-organ damage occurring during the first hours and days of an AHF episode. The results of the recently published RELAX-AHF (Relaxin in Acute Heart Failure) study may hold the key to understanding these intricate mechanisms. In the study, congestion and end-organ damage, which were strongly associated with increased 180-day mortality, were relieved by early administration of serelaxin, which was also associated with reduction in 180-day mortality. Hence, it is possible that early treatment of AHF, including decongestion and prevention of damage to end organs, including kidneys, heart, and liver, is critical to preventing mortality in AHF. This may require a change in our strategic approach to the management of patients admitted with AHF, setting them apart from patients with chronic heart failure (HF), and developing specific treatment strategies for AHF patients beyond simply implementing therapies proven to be effective in chronic HF.
    Current Heart Failure Reports 12/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: The renin-angiotensin system (RAS) plays a major role in the pathophysiology of cardiovascular disorders. Angiotensin II (Ang-II), the final product of this pathway, is known for its vasoconstrictive and proliferative effects. Angiotensin-converting enzyme 2 (ACE2), a newly discovered homolog of ACE, plays a key role as the central negative regulator of the RAS. It diverts the generation of vasoactive Ang-II into the vasodilatory and growth inhibiting peptide angiotensin(1-7) [Ang(1-7)], thereby providing counter-regulatory responses to neurohormonal activation. There is substantial experimental evidence evaluating the role of ACE2/Ang(1-7) in hypertension, heart failure, and atherosclerosis. In this review, we aim to focus on the conceptual facts of the ACE2-Ang(1-7) axis with regards to clinical implications and therapeutic targets in cardiovascular disorders, with emphasis on the potential therapeutic role in cardiovascular diseases.
    Current Heart Failure Reports 11/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: In up to 50 % of patients undergoing continuous flow, axial pump, left-ventricular and assist device (LVAD) placement, concomitant procedures are performed. The underlying lesions have a broad spectrum of severity, complexity, and impact on clinical outcomes. This review describes the concomitant lesions often encountered with LVAD implantation and clinical relevance of their repair.
    Current Heart Failure Reports 11/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Chronic heart failure (CHF) is a complex clinical syndrome leading to exercise intolerance due to muscular fatigue and dyspnea. Hemodynamics fail to explain the reduced exercise capacity, while a significant skeletal muscular pathology seems to constitute the main underlying mechanism for exercise intolerance in CHF patients. There have been proposed several metabolic, neurohormonal and immune system abnormalities leading to an anabolic/catabolic imbalance that plays a central role in the pathogenesis of the wasting process of skeletal muscle myopathy. The impairment of the anabolic axes is associated with the severity of symptoms and the poor outcome in CHF, whereas increased cortisol levels are predictive of exercise intolerance, ventilatory inefficiency and chronotropic incompetence, suggesting a significant contributing mechanism to the limited functional status. Exercise training and device therapy could have beneficial effects in preventing and treating muscle wasting in CHF. However, specific anabolic treatment needs more investigation to prove possible beneficial effects.
    Current Heart Failure Reports 11/2013;

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