Early Worsening Heart Failure in Patients Admitted for Acute Heart Failure: Time Course, Hemodynamic Predictors, and Outcome

Torre‐Amione, Guillermo; Milo-Cotter, Olga; Kaluski, Edo; Perchenet, Loı̈c; Kobrin, Isaac; Frey, Aline; Rund, Michele M.; Weatherley, Beth Davison; Cotter, Gad

doi:10.1016/j.cardfail.2009.04.001

Cited by 58 publications

(62 citation statements)

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“…In part due to the ageing of the population and more effective treatment of chronic heart failure (HF), its prevalence is expected to increase by 25% over the next 20 years 3 and the problem has expanded worldwide 4, 5. Patients hospitalized for HF have a 40–50% rate of HF exacerbation, of which 10–15% is in‐hospital worsening heart failure (WHF)6, 7, 8, 9, 10 and 30–40% is rehospitalization, within the first 6 months after discharge as well as a 10–15% mortality rate 11. Compared with ambulatory patients with stable chronic HF, patients hospitalized for AHF have a dramatic increase in their risk of death, similar or worse than that after a hospitalization for acute myocardial infarction or stroke 12.…”

Section: Introductionmentioning

confidence: 99%

Serelaxin in addition to standard therapy in acute heart failure: rationale and design of the RELAX‐AHF‐2 study

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Voors

Ponikowski

et al. 2017

European J of Heart Fail

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Patients admitted for acute heart failure (AHF) experience high rates of in‐hospital and post‐discharge morbidity and mortality despite current therapies. Serelaxin is recombinant human relaxin‐2, a hormone with vasodilatory and end‐organ protective effects believed to play a central role in the cardiovascular and renal adaptations of human pregnancy. In the phase 3 RELAX‐AHF trial, serelaxin met its primary endpoint of improving dyspnoea through day 5 in patients admitted for AHF. Compared to placebo, serelaxin also reduced worsening heart failure (WHF) by 47% through day 5 and both all‐cause and cardiovascular mortality by 37% through day 180. RELAX‐AHF‐2 ( ClinicalTrials.gov NCT01870778) is designed to confirm serelaxin's effect on these clinical outcomes. RELAX‐AHF‐2 is a multicentre, randomized, double‐blind, placebo‐controlled, event‐driven, phase 3 trial enrolling ∼6800 patients hospitalized for AHF with dyspnoea, congestion on chest radiograph, increased natriuretic peptide levels, mild‐to‐moderate renal insufficiency, and systolic blood pressure ≥125 mmHg. Patients are randomized within 16 h of presentation to 48 h intravenous infusions of serelaxin (30 µg/kg/day) or placebo, both in addition to standard of care treatments. The primary objectives are to demonstrate that serelaxin is superior to placebo in reducing: (i) 180 day cardiovascular death, and (ii) occurrence of WHF through day 5. Key secondary endpoints include 180 day all‐cause mortality, composite of 180 day combined cardiovascular mortality or heart failure/renal failure rehospitalization, and in‐hospital length of stay during index AHF. The results from RELAX‐AHF‐2 will provide data on the potential beneficial effect of serelaxin on cardiovascular mortality and WHF in selected patients with AHF.

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Section: Introductionmentioning

confidence: 99%

Serelaxin in addition to standard therapy in acute heart failure: rationale and design of the RELAX‐AHF‐2 study

Teerlink

Voors

Ponikowski

et al. 2017

European J of Heart Fail

Self Cite

105

103

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“…WHF may be more likely in the context of poor renal function on admission, being associated with low renal perfusion pressure and marked neurohormonal activation 12. Measures indicative of worse haemodynamic function on admission and 6 h later, such as decreased cardiac power output and increased mean arterial pressure, are associated with a higher rate of in‐hospital WHF by Day 7 4. Other admission characteristics predictive of in‐hospital WHF include increased respiratory rate (which may indicate pulmonary oedema), hyponatraemia, low oxygen saturation, high troponin levels, and the need for more aggressive management, such as mechanical ventilation, i.v.…”

Section: What Is the Clinical Relevance Of In‐hospital Worsening Hearmentioning

confidence: 99%

“…Studies defining in‐hospital WHF as worsening symptoms and signs of HF and a need for additional intravenous (i.v.) or mechanical therapy suggest that 10–25% of patients admitted with AHF develop WHF,11, 14 although incidence rates of up to 42% have been reported 4, 14. Conversely, results from the Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND‐HF), the largest trial of patients with AHF to date ( n = 7141), showed that only approximately 5% of patients experienced in‐hospital WHF,20 which perhaps reflects the more rigorous definition used in the study [≥1 sign, symptom, or radiological evidence of new, persistent, or worsening AHF requiring addition of a new i.v.…”

Section: Introductionmentioning

confidence: 99%

“…These studies have raised interest in the validity of in‐hospital WHF as a useful endpoint for evaluating new AHF therapies and in clinical practice 4, 11. If the concept is validated, reducing the occurrence of in‐hospital WHF might itself become a worthwhile treatment target; however, as authors, we had some scepticism as to the clinical utility of this outcome in the absence of a standard definition.…”

Section: Introductionmentioning

confidence: 99%

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In‐hospital worsening heart failure: a clinically relevant endpoint?

et al. 2017

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Outcome measures used for the clinical evaluation of patients with acute heart failure differ between studies and may neither adequately address the characteristic presenting symptoms and signs nor reflect the pathophysiological processes involved. In‐hospital worsening of heart failure (WHF) is associated with poor outcomes and thus a potential endpoint conveying clinically meaningful prognostic information.Current definitions of WHF are based on the combination of worsening symptoms and signs and the intensification of treatment during admission. Definitions vary across studies and do not fully account for baseline therapy or circumstances in which there is failure to respond to treatment. Further, there are limited data to inform healthcare professionals as to which patients are most at risk of developing in‐hospital WHF.In this opinion piece, we review the definitions for WHF used in recent and ongoing clinical trials and propose a novel definition, which captures failure to respond to treatment as well as clinical worsening (deterioration of symptoms and signs) of the patient's condition. Such a definition, applied consistently across studies, would help clarify the characteristics of patients likely to develop in‐hospital WHF, allow comparative assessments of the effectiveness of interventions, and help guide appropriate patient management in order to improve outcomes.

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“…Etwa 30% der Patienten verspüren allerdings nur eine geringe oder gar keine Verbesserung der Dyspnoe [19,29]. Bei rund 40% der ADHF-Patienten verschlechtert sich unter den therapeutischen Maßnah-men die Herzinsuffizienz während des Krankenhausaufenthalts ("worsening of heart failure"), was einen neuen Parameter für die Beurteilung moderner Herzinsuffizienztherapien darstellt [45]. Derzeit gibt es therapeutische Ansätze, die auf unterschiedlichen Ebenen angreifen: Gefäße, Stauung, Nephroprotektion und Inotropie (.…”

Section: Behandlungsstrategien Bei Akuter Herzinsuffizienzunclassified

Moderne Arzneitherapie in der kardiovaskulären Intensivmedizin

Lemm¹,

Dietz²,

Janusch³

et al. 2015

Internist

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Vasoactive drugs and inotropes are important in the hemodynamic management of patients with cardiogenic shock despite modest volume administration. Currently, the concept of cardiac relief is pursued in the treatment of acute heart failure. In this article we present the use of different drugs in the intensive care unit for acute heart failure and cardiogenic shock. In acute heart failure catecholamines are only used during the transition from heart failure to cardiogenic shock. Here, the therapeutic concept of ventricular unloading is more sought after. This can be achieved by the use of diuretics, nitrates, levosimendan (inodilatator), or in the future serelaxin. The hemodynamic management in cardiogenic shock occurs after moderate volume administration with dobutamine to increase inotropy. If no adequate perfusion pressures are achieved, norepinephrine can be administered as a vasopressor. If there is still no sufficient increase in cardiac output, the inodilatator levosimendan can be used. Levosimendan instead of phosphodiesterase inhibitors in this case is preferable. The maxim of hemodynamic management in cardiogenic shock is the transient use of inotropes and vasopressors in the lowest dose possible and only for as long as necessary. This means that one should continuously check whether the dose can be reduced. There are no mortality data demonstrating the utility of hemodynamic monitoring based on objective criteria—but it makes sense to use inotropes and vasopressors sparingly.

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Early Worsening Heart Failure in Patients Admitted for Acute Heart Failure: Time Course, Hemodynamic Predictors, and Outcome

Cited by 58 publications

References 18 publications

Serelaxin in addition to standard therapy in acute heart failure: rationale and design of the RELAX‐AHF‐2 study

Serelaxin in addition to standard therapy in acute heart failure: rationale and design of the RELAX‐AHF‐2 study

In‐hospital worsening heart failure: a clinically relevant endpoint?

Moderne Arzneitherapie in der kardiovaskulären Intensivmedizin

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