Treatment Of Acute Heart Failure Research Articles

Role of recombinant human brain natriuretic peptide combined with sodium nitroprusside in improving quality of life and cardiac function in patients with acute heart failure.

The present study aimed to investigate the role of recombinant human brain natriuretic peptide (RHBNP) combined with sodium nitroprusside (SN) in improving quality of life and cardiac function in patients with acute heart failure. A total of 96 patients with acute heart failure who were admitted to The First Affiliated Hospital of Yangtze University were included in the current study. A total of 48 patients were treated with RHBNP combined with SN (research group) and 48 patients were treated with SN alone (control group). To assess the efficacy and safety of the two treatments, the study groups were compared in terms of improvement in clinical symptoms and cardiac function indices, including pulmonary capillary wedge pressure and left ventricular ejection fraction, which was measured using a non-invasive cardiac hemodynamic detector; changes in fluid intake and 24 h urine volumes after drug use; cardiac function classification before treatment and three days after treatment; adverse drug reactions during treatment and mortality within 1 month of treatment. Following treatment, compared with the control group, the research group demonstrated significantly higher fluid intake and 24 h urine volume after drug use, improved cardiac function indices, cardiac function classification, biochemical indicators and total effective rate of treatment (all P<0.05); significantly lower total incidence of adverse reactions (P<0.05) and similar mortality within 1 month of treatment. With improvements in cardiac and other organ function, RHBNP combined with SN was found to be effective in the treatment of acute heart failure. RHBNP can effectively promote urination, reduce inflammatory responses and rapidly relieve clinical symptoms without significant adverse reactions, indicating its potential use in further clinical application.

125‐I‐Sarcosine(1), D‐Alanine(8) Angiotensin II as a Biased Radioligand for AT1 Angiotensin II Receptors

The concept of biased agonism of G protein‐coupled receptors arose from studies of the AT1 subtype of angiotensin (Ang) II receptor. A putative antagonist ligand, sarcosine1, isoleucine4, isoleucine8 Ang II (SII) showed negligible ability to activate G protein signaling pathways of the AT1 receptor, but was able to cause AT1 receptor internalization and mitogen activated protein (MAP) kinase activation at micromolar concentrations. Subsequently, a different Ang II congener; sarcosine1, D‐alanine8 Ang II was developed as a potential therapeutic (TRV‐027; TRV120027) for treatment of acute heart failure. While clinical trials did not support a therapeutic benefit of sarcosine1, D‐alanine8 Ang II for treatment of heart failure, it still promises to be a better biased agonist than SII, which acts only at micromolar concentrations. To assess the potential use of sarcosine1, D‐alanine8 Ang II as a radioligand for quantification of Ang II receptor binding, we radiolabeled sarcosine1, D‐alanine8 Ang II with 125iodine and compared its binding to that of 125I‐sarcosine1 isoleucine8 Ang II in rat liver membranes, which express high levels of AT1 receptors and negligible levels of AT2 receptors. At concentrations up to 5.6 nM, 125I‐sarcosine1, D‐alanine8 Ang II showed little evidence of saturable binding to AT1 receptors, in contrast to 125I‐sarcosine1 isoleucine8 Ang II, which showed a KD of 0.6 nM. At 5.6 nM 125I‐sarcosine1 isoleucine8 Ang II binding to AT1 receptors was 8.5 times greater than 125I‐sarcosine1, D‐alanine8 Ang II. To verify that sarcosine1, D‐alanine8 Ang II binds to liver membrane AT1 receptors, we compared the ability of sarcosine1, D‐alanine8 Ang II and Ang II to compete for 125I‐sarcosine1 isoleucine8 Ang II binding. Sarcosine1 isoleucine8 Ang II and Ang II were similar in their ability to compete for AT1 receptor binding: 6.7±0.7 nM and 15.6±0.8 nM and 84.3±1.1 and 86.7±0.3 % of total binding (IC50, n=2±SD), respectively. This suggests that iodination of tyr4 of sarcosine1, D‐alanine8 Ang II alters its ability to bind to AT1 receptors and potentially act as a biased agonist. Continuing studies will examine the ability of higher concentrations of 125/127I‐sarcosine1, D‐alanine8 Ang II to interact with Ang II receptors.Support or Funding InformationNova Southeastern University President’s Faculty Research Development Grant, Cardiovascular Neuroscience Research Fund

Spironolactone metabolite concentrations in decompensated heart failure: insights from the ATHENA-HF trial.

In Aldosterone Targeted Neurohormonal Combined with Natriuresis Therapy in Heart Failure (ATHENA-HF), high-dose spironolactone (100 mg daily) did not improve efficacy endpoints over usual care [placebo or continued low-dose spironolactone (25 mg daily) in patients already receiving spironolactone] in the treatment of acute heart failure (HF). We hypothesized that low concentrations of the long-acting active metabolites of spironolactone [canrenone and 7α-thiomethylspironolactone (7α-TMS)] in the high-dose group could have contributed to these neutral results. In patients randomized to high-dose spironolactone not previously treated with spironolactone (high-dose-naïve, n = 112), concentrations of canrenone and 7α-TMS increased at 48 and 96 h compared to baseline, and between 48 and 96 h (all P < 0.005), indicating that steady-state concentrations had not been reached by 48 h. In patients previously on low-dose, high-dose spironolactone (high-dose-previous, n = 37), concentrations of canrenone increased at 48 and 96 h compared to baseline (both P < 0.0005), with a marginal increase between 48 and 96 h (P = 0.0507). At 48 h, both high-dose groups had higher concentrations of both metabolites than the low-dose spironolactone group (P < 0.0001). Moreover, concentrations of both metabolites were higher in high-dose-previous vs. high-dose-naïve patients (P < 0.01), indicating that previous spironolactone use was significant, and that steady-state has not been reached in high-dose-naïve patients at 48 h. We found limited and inconsistent evidence of correlation between metabolite concentrations and endpoints. Lower-than-anticipated concentrations of spironolactone active metabolites were observed for at least 48 h in the high-dose spironolactone group and may have contributed to the absence of pharmacological effects of spironolactone in the ATHENA-HF trial.

Kinetensin is an Endogenous β‐arrestin‐biased Ligand of Angiotensin AT1 receptor

Kinetensin, a nonapeptide having similarities to neurotensin and angiotensin II has been isolated from human plasma more than 30 years ago, but its patho‐physiological functions and signal transduction mechanisms remain elusive. In this work, we investigated the effects of kinetensin on G protein‐coupled receptors (GPCRs), one of the largest families of the human genome and the biological target of many peptides. Using Presto‐tango system, the effects of this peptide were tested on a panel of 178 class A GPCRs. Kinetensin (10−6M) stimulated β‐arrestin activation in HTLA cells transfected with angiotensin type 1 receptor (AT1R) by 638±45% compared to basal levels (n=16). At the same concentration, kinetensin also stimulated β‐arrestin activation by histamine H1 receptor (201+22%), melatonin MT1 (187±12%) and MT2 (183±7%) receptors, MRGPRX3 (179±14%), GPR83 (186±10%) and GPR88 (190±10% n=3 in each case), but these effects were significantly smaller compared to the effects on AT1R. In contrast, kinetensin had no significant effect on β‐arrestin activation in cells transfected with other GPCRs, including receptors related to renin‐angiotensin system like AT2, MAS1 and MAS1L, or with neurotensin receptors (NTS1 and NTS2). The effects of the peptide on AT1R‐stimulated β‐arrestin activation were reproduced in HEK293T cells using nanoBRET method. These experiments demonstrated that maximal effects of kinetensin at 10−6M were 39±8% from the effects of angiotensin II (angII, 10−6M), with an EC50 of 115+21 nM (n=4). We also tested the effects of kinetensin on [Ca2+]i (a marker of G‐protein activation) in AT1R transfected HEK293T cells and we found that its effects were only a fraction of the effects of angII (14±8%, n=4). These data indicate that kinetensin is a β‐arrestin biased agonist at AT1R. Interestingly, angiotensin 1‐7 (ang1‐7), a heptapeptide with opposite actions to angII and favorable effects on the regulation of cardio‐vascular activities, demonstrated comparable effects in cells transfected with AT1R (21+7% stimulation of β‐arrestin activation and 4±8% increases in [Ca2+]i at 10−6 M, n=4). In this respect, kinetensin also resembles the effects of novel AT1R β‐arrestin biased agonist TRV027, which is currently tested in clinical trials for the treatment of acute heart failure. Overall, our results show that the nonapeptide kinetensin differentially modulates AT1R‐induced β‐arrestin and G‐protein activation, and these effects can be relevant to target this GPCR in cardio‐vascular diseases.Support or Funding InformationThis work was supported in part by grants from National Science Foundation (Nos. 1708959 &amp; 1924092) and Office of Naval Research (Nos. N00014‐18‐1‐2145 &amp; N00014‐19‐1‐2602) to YF, U.S. Department of Veterans Affairs (I01 BX004294 to CMF and EL) and National Institutes of Health (HL093178 and COBRE P30GM106392), and LSUHSC‐NO Research Enhancement Program to EL.

Sympathetic overdrive and sudden cardiac death. Beta-blocker`s capabilities with a focus on bisoprolol

The recommendations of the European Society of Cardiology for the treatment of ventricular arrhythmias and the prevention of sudden cardiac death (2015) identified more than 20 risk factors for sudden death, 3 of them due to sympathetic overdrive (sympathetic hyperactivation): increased heart rate at rest, decreased heart rate variability (standard the deviation of the RR intervals is less than 40–50 ms per day), the elongation and increase in the variance of the QT interval is more than 85–100 ms.Beta-blockers are the only drugs that affect all parts of the pathogenesis of sudden cardiac death. Therefore, they act as first-line drugs (IA) both in the aforementioned Recommendations and in the Recommendations of the European Society of Cardiology for the Diagnosis and Treatment of Acute and Chronic Heart Failure (2016) as a primary component of the combination therapy of symptomatic chronic heart failure with a reduced ejection fraction of the left ventricle.According to the results of clinical trials of chronic heart failure, beta-blockers effectively reduce the risk of sudden cardiac death. Bisoprolol is the leader among them: in the CIBIS II study, it reduced the risk of sudden death by 44 %, and in the CIBIS-III study, by 46 %.

Acute heart failure.

Acute heart failure (AHF) is a syndrome defined as the new onset (de novo heart failure (HF)) or worsening (acutely decompensated heart failure (ADHF)) of symptoms and signs of HF, mostly related to systemic congestion. In the presence of an underlying structural or functional cardiac dysfunction (whether chronic in ADHF or undiagnosed in de novo HF), one or more precipitating factors can induce AHF, although sometimes de novo HF can result directly from the onset of a new cardiac dysfunction, most frequently an acute coronary syndrome. Despite leading to similar clinical presentations, the underlying cardiac disease and precipitating factors may vary greatly and, therefore, the pathophysiology of AHF is highly heterogeneous. Left ventricular diastolic or systolic dysfunction results in increased preload and afterload, which in turn lead to pulmonary congestion. Fluid retention and redistribution result in systemic congestion, eventually causing organ dysfunction due to hypoperfusion. Current treatment of AHF is mostly symptomatic, centred on decongestive drugs, at best tailored according to the initial haemodynamic status with little regard to the underlying pathophysiological particularities. As a consequence, AHF is still associated with high mortality and hospital readmission rates. There is an unmet need for increased individualization of in-hospital management, including treatments targeting the causative factors, and continuation of treatment after hospital discharge to improve long-term outcomes.

Analysis of the Paper Entitled Traditional Chinese Medicine Use in the Treatment of Acute Heart Failure in Western Medicine Hospitals in China.

Analysis of the Paper Entitled Traditional Chinese Medicine Use in the Treatment of Acute Heart Failure in Western Medicine Hospitals in China.

Relaxin and the Cardiovascular System: from Basic Science to Clinical Practice.

The peptide hormone relaxin was originally linked to reproductive physiology, where it is believed to mediate systemic and renal hemodynamic adjustments to pregnancy. Recently, its broad range of effects in the cardiovascular system has been the focus of intensive research regarding its implications under pathological conditions and potential therapeutic potential. An understanding of the multitude of cardioprotective actions prompted the study of serelaxin, recombinant human relaxin-2, for the treatment of acute heart failure. Despite early promising results from phase II studies, recently revealed RELAX-AHF-2 outcomes were rather disappointing and the treatment for acute heart failure remains an unmet medical need. This article reviews the physiologic actions of relaxin on the cardiovascular system and its relevance in the pathophysiology of cardiovascular disease. We summarize the most updated clinical data and discuss future directions of serelaxin for the treatment of acute heart failure. This should encourage additional work to determine how can relaxin's beneficial effects be exploited for the treatment of cardiovascular disease.

Levosimendan to facilitate weaning from cardiorespiratory support in critically ill patients: current evidence and future directions.

Appropriate weaning is of crucial importance for critically ill patients requiring respiratory support. However, a remarkable proportion of them are difficult to wean. Levosimendan is a positive inotropic agent characterized by vasodilatory properties, which is used for the treatment of acute decompensated heart failure or in patients needing inotropic treatment, including cardiogenic shock, septic shock, pulmonary hypertension and right ventricular dysfunction, needed for hemodynamic support in patients with diuretic resistance, and weaning either from ventilator or from extracorporeal membrane oxygenation. This position paper will discuss the use of levosimendan in facilitating weaning from cardiorespiratory support in critically ill patients, according to available evidence and the personal experience of a group of Italian Experts.

Correction to: Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association.

Correction to: Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association.

Evaluation of kidney function throughout the heart failure trajectory-a position statement from the Heart Failure Association of the European Society of Cardiology.

Appropriate interpretation of changes in markers of kidney function is essential during the treatment of acute and chronic heart failure. Historically, kidney function was primarily assessed by serum creatinine and the calculation of estimated glomerular filtration rate. An increase in serum creatinine, also termed worsening renal function, commonly occurs in patients with heart failure, especially during acute heart failure episodes. Even though worsening renal function is associated with worse outcome on a population level, the interpretation of such changes within the appropriate clinical context helps to correctly assess risk and determine further treatment strategies. Additionally, it is becoming increasingly recognized that assessment of kidney function is more than just glomerular filtration rate alone. As such, a better evaluation of sodium and water handling by the renal tubules allows to determine the efficiency of loop diuretics (loop diuretic response and efficiency). Also, though neurohumoral blockers may induce modest deteriorations in glomerular filtration rate, their use is associated with improved long-term outcome. Therefore, a better understanding of the role of cardio-renal interactions in heart failure in symptom development, disease progression and prognosis is essential. Indeed, perhaps even misinterpretation of kidney function is a leading cause of not attaining decongestion in acute heart failure and insufficient dosing of guideline-directed medical therapy in general. This position paper of the Heart Failure Association Working Group on Cardio-Renal Dysfunction aims at improving insights into the interpretation of renal function assessment in the different heart failure states, with the goal of improving heart failure care.

Paradigm Shifts of Heart Failure Therapy: Do We Need Another Paradigm?

Heart failure (HF) is a progressive condition with intermittent acute decompensation leading to poor prognosis despite established guideline-directed therapy. A paradigm of HF therapy has been shifted over last four decades. Until the early 1970s, HF was empirically managed, then was managed with the hemodynamic concept until the early 1980s. According to the results of large randomized clinical trials, HF therapy has been shifted to the neurohormonal paradigm since the late 1980s until recently. Korean Acute Heart Failure (KorAHF) registry is a multi-center registry that recruited a total of 5625 admitted patients with acute HF from 2011 to 2014 and followed until 2019. Through KorAHF registry, we could obtain invaluable information or messages in various fields such as epidemiology, clinical characteristics, and treatment of acute HF in Korea and also had opportunities to fill the gap between guideline-directed care and real-world practice. Considering significant unmet needs in HF therapy even at this moment, we do need another paradigm shift for HF therapy, such as molecular and regenerative paradigm using gene, stem cells, mechanical support as well as novel pharmacological agents.

Nitric Oxide Resistance, Induced in the Myocardium by Diabetes, Is Circumvented by the Nitric Oxide Redox Sibling, Nitroxyl.

Aim: Impairment of tissue responsiveness to exogenous and endogenous nitric oxide (NO•), known as NO• resistance, occurs in many cardiovascular disease states, prominently in diabetes and especially in the presence of marked hyperglycemia. In this study, we sought to determine in moderate and severe diabetes (i) whether NO• resistance also occurs in the myocardium, and (ii) whether the NO• redox sibling nitroxyl (HNO) circumvents this. Results: The spectrum of acute NO• effects (induced by diethylamine-NONOate), including vasodilation, and enhanced myocardial contraction and relaxation were impaired by moderately diabetic rats ([blood glucose] ∼20 mM). In contrast, acute HNO effects (induced by isopropylamine-NONOate) were preserved even in more severe diabetes ([blood glucose] >28 mM). Intriguingly, the positive inotropic effects of HNO were significantly enhanced in diabetic rat hearts. Further, progressive attenuation of soluble guanylyl cyclase (sGC) contribution to myocardial NO• responses occurred with increasing severity of diabetes. Nevertheless, activation of sGC by HNO remained intact in the myocardium. Innovation: Diabetes is associated with marked attenuation of vascular and myocardial effects of NO and NO donors, and this NO• resistance is circumvented by HNO, suggesting potential therapeutic utility for HNO donors in cardiovascular emergencies in diabetics. Conclusion: These results provide the first evidence that NO• resistance occurs in diabetic hearts, and that HNO largely circumvents this problem. Further, the positive inotropic and lusitropic effects of HNO are enhanced in a severely diabetic myocardium, a finding that warrants further mechanistic interrogation. The results support a potential role for therapeutic HNO administration in acute treatment of ischemia and/or heart failure in diabetics.

The Role of Serial NT-ProBNP Level in Prognosis and Follow-Up Treatment of Acute Heart Failure after Coronary Artery Bypass Graft Surgery.

BACKGROUND:After coronary artery bypass graft (CABG) surgery, heart failure is still major problem. The valuable marker for it is needed.AIM:Evaluating the role of serial NT-proBNP level in prognosis and follow-up treatment of acute heart failure after CABG surgery.METHODS:The prospective, analytic study evaluated 107 patients undergoing CABG surgery at Ho Chi Minh Heart Institute from October 2012 to June 2014. Collecting data was done at pre- and post-operative days with measuring NT-proBNP levels on the day before operation, 2 hours after surgery, every next 24 h until the 5th day, and in case of acute heart failure occurred after surgery.RESULTS:On the first postoperative day (POD1), the NT-proBNP level demonstrated significant value for AHF with the cut-off point = 817.8 pg/mL and AUC = 0.806. On the second and third postoperative day, the AUC value of NT- was 0.753 and 0.751. It was statistically significant in acute heart failure group almost at POD 1 and POD 2 when analyzed by the doses of dobutamine, noradrenaline, and adrenaline (both low doses and normal doses).CONCLUSION:Serial measurement of NT-proBNP level provides useful prognostic and follow-up treatment information in acute heart failure after CABG surgery.

A multicenter, randomized, double-blind, controlled study to evaluate the efficacy and safety of dantrolene on ventricular arrhythmia as well as mortality and morbidity in patients with chronic heart failure (SHO-IN trial): rationale and design

BackgroundLeakage of Ca2+ from the sarcoplasmic reticulum (SR) is a critical contributing factor to heart failure pathophysiology. Therefore, reducing SR Ca2+ leaks may provide significant additive benefits when used in combination with conventional therapies. Dantrolene, a drug routinely used to treat malignant hyperthermia, also stabilizes the cardiac isoform of the release channel (RyR2), thus decreasing SR Ca2+ leaks. The purpose of this study is to evaluate the effect of chronic administration of dantrolene on heart failure and lethal arrhythmia in patients with chronic heart failure and reduced ejection fraction in a multicenter, randomized, double-blind, controlled study. MethodsPatients with chronic heart failure who had functional status of New York Heart Association class II and III and a left ventricular ejection fraction <40% were treated according to the Japanese Circulation Society, the European Society of Cardiology, and the American Heart Association/the American College of Cardiology guidelines for diagnosis and treatment of acute and chronic heart failure. Patients were randomized and divided into two groups in a double-blind fashion: dantrolene group and placebo group (target sample size: 300 cases). These drugs were administered for 96 weeks. The primary endpoint is cardiovascular death, first hospitalization for exacerbation of heart failure, or lethal arrhythmia [ventricular tachycardia (VT) storm, sustained VT, ventricular fibrillation] for 2 years after starting administration of dantrolene 1 cap (25mg) three times daily (if not tolerable, two times daily) or matching placebo. ResultsThis paper presents the rationale and trial design of the study. Recruitment for the study started on 8 December 2017. ConclusionsThe results of this trial will clarify the efficacy and safety of dantrolene for ventricular arrhythmia, as well as mortality and morbidity in patients with chronic heart failure and reduced ejection fraction during guideline-directed medical treatment.

Comments on “Traditional Chinese Medicine Use in the Treatment of Acute Heart Failure in Western Medicine Hospitals in China: Analysis from the China PEACE Retrospective Heart Failure Study”

Comments on “Traditional Chinese Medicine Use in the Treatment of Acute Heart Failure in Western Medicine Hospitals in China: Analysis from the China PEACE Retrospective Heart Failure Study”

Optimizing The Management of Obese HFpEF Phenotype: Can We Mind Both The Heart and The Kidney?

The adverse prognostic implications of significant renal dysfunction during treatment of acute decompensated heart failure (HF) in patients with obese HF and preserved ejection fraction (HFpEF) provide strong rationale for development of therapeutic strategies that enhance decongestion while preserving renal function in this cohort. The combination of preload sensitivity, intrinsic renal dysfunction related to obesity, glomerular hyperfiltration, reversible renal hypoperfusion (poor renal arterial perfusion and renal venous congestion), and decreased systemic vascular resistance in obesity may predispose patients to renal hemodynamic compromise during diuresis. Thus, serum creatinine increase should not be evaluated in isolation but rather considered in the context of the entire clinical picture in patients with obese HFpEF.

Bioanalytical Assessment of Plasma Concentrations of Angiotensin-Converting Enzyme II Inhibitors and Angiotensin Receptor Blockers: A Pilot Study Among Patients Hospitalized With Acute Heart Failure.

Although angiotensin-converting enzyme II inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) improve chronic heart failure (HF) outcomes, their potential harms and benefits in acute HF (AHF) is less clear. We explored the relationship between ACEI or ARB plasma concentrations among patients with AHF with in-hospital change in estimated glomerular filtration rate (eGFR). From August 2016-June 2017, patients with AHF prescribed an outpatient ACEI or ARB were enrolled before AHF treatment. All patients were given twice their home dose of diuretic intravenously and received clinical care at the discretion of the medical team. Of 61 patients in the parent study, saved plasma from 34 who were prescribed an outpatient ACEI or ARB was included in this substudy. Liquid chromatography-tandem mass spectrometry was performed to assess ACEI or ARB plasma concentrations before AHF treatment. Change in eGFR was computed using the Chronic Kidney Disease Epidemiology Collaboration equation, which adjusts for age, sex, and race; diuretic dose and enrollment eGFR were used to adjust for HF severity. Multiple linear regression adjusting for enrollment eGFR and diuretic dose was performed to examine the relationship between drug concentration (undetectable/low vs. in/above-range) and in-hospital change in eGFR. Of 34 patients with AHF, median age was 63 years (interquartile range, 58-78 years), 19 (55.9%) were women, median eGFR at enrollment was 55.6 mL/min (interquartile range, 35.2-75.3 mL/min), and for 11 (32.4%), no ACEI or ARB was detectable in plasma. Medication concentrations in- or above-reference range were associated with in-hospital decrease in eGFR of 8.3 mL/min (95% confidence interval, 15.3-1.3 mL/min decrease), after adjusting for enrollment eGFR and diuretic treatment. Bioanalytical assessment of medication levels may be useful to guide in-hospital ACEI and ARB therapy for patients with AHF.

Rationale, experimental data, and emerging clinical evidence on early and preventive use of levosimendan in patients with ventricular dysfunction.

Acute ventricular dysfunction (AVD) is a complex condition with substantial morbidity and mortality, still featuring unique therapeutic challenges. Levosimendan is a calcium sensitizer and ATP-dependent potassium channel opener that was developed as an inodilating drug for the treatment of acute heart failure and cardiogenic shock. Differently from other more widely used inotropic agents, levosimendan has some exclusive characteristics, in terms of mechanisms of action, pharmacodynamic profile, and haemodynamic effects. This may have important clinical implications. In particular, in patients with AVD or in patients with pre-existing severe ventricular impairment undergoing planned myocardial stress, the administration of levosimendan before the onset of overt symptoms or before cardiovascular therapeutic procedures may have the potential to bridge the patient through the critical phase. In this review, we will focus on the rationale, the existing experimental data, and the emerging clinical experience supporting an early, even preventive use of levosimendan in severe ventricular dysfunction, beyond its recognized indications.

Impact of hyperoxia on patients hospitalized in an intensive care unit for acute heart failure

Oxygen therapy remains a cornerstone of treatment for acute heart failure in patients with pulmonary congestion. While avoiding hypoxaemia has long been a goal of critical care practitioners, less attention has been paid to the potential hazard related to excessive hyperoxia. To evaluate the impact of early hyperoxia exposure among critically ill patients hospitalized in an intensive care unit for acute heart failure. In this preliminary study conducted in a Parisian intensive care unit, we assessed patients with acute heart failure admitted with pulmonary congestion and treated with oxygen therapy from 1 January 2015 to 31 December 2016. The hyperoxia group was defined by having at least one partial pressure of oxygen measurement>100mmHg on the first day following admission to the intensive care unit. The primary endpoint was 30-day all-cause mortality. Secondary endpoints were 30-day unplanned hospital admissions, occurrence of infections and intensive care unit and hospital lengths of stay. Seventy-five patients were included. Forty-three patients (57.3%) presented hyperoxia, whereas 32patients (42.7%) did not (control group). The baseline clinical characteristics did not differ between the two groups. The primary endpoint was not statistically different between the two groups (14.0% in the hyperoxia group vs 18.8% in the control group; P=0.85). The secondary endpoints were also not significantly different between the two groups. In the multivariable analysis, hyperoxia was not associated with increased 30-day mortality (odds ratio 0.77, 95% confidence interval 0.24-2.41). In patients referred to an intensive care unit for acute heart failure, we did not find any difference in outcomes according to the presence of hyperoxia.