Dataset Information

Selenium and outcome in heart failure.

ABSTRACT: AIMS:Severe deficiency of the essential trace element selenium can cause myocardial dysfunction although the mechanism at cellular level is uncertain. Whether, in clinical practice, moderate selenium deficiency is associated with worse symptoms and outcome in patients with heart failure is unknown. METHODS AND RESULTS:BIOSTAT-CHF is a multinational, prospective, observational cohort study that enrolled patients with worsening heart failure. Serum concentrations of selenium were measured by inductively coupled plasma mass spectrometry. Primary endpoint was a composite of all-cause mortality and hospitalization for heart failure; secondary endpoint was all-cause mortality. To investigate potential mechanisms by which selenium deficiency might affect prognosis, human cardiomyocytes were cultured in absence of selenium, and mitochondrial function and oxidative stress were assessed. Serum selenium concentration (deficiency) was <70??g/L in 485 (20.4%) patients, who were older, more often women, had worse New York Heart Association class, more severe signs and symptoms of heart failure and poorer exercise capacity (6-min walking test) and quality of life (Kansas City Cardiomyopathy Questionnaire). Selenium deficiency was associated with higher rates of the primary endpoint [hazard ratio (HR) 1.23; 95% confidence interval (CI) 1.06-1.42] and all-cause mortality (HR 1.52; 95% CI 1.26-1.86). In cultured human cardiomyocytes, selenium deprivation impaired mitochondrial function and oxidative phosphorylation, and increased intracellular reactive oxygen species levels. CONCLUSIONS:Selenium deficiency in heart failure patients is independently associated with impaired exercise tolerance and a 50% higher mortality rate, and impaired mitochondrial function in vitro, in human cardiomyocytes. Clinical trials are needed to investigate the effect of selenium supplements in patients with heart failure, especially if they have low plasma concentrations of selenium.

SUBMITTER: Bomer N

PROVIDER: S-EPMC7540257 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Selenium and outcome in heart failure.

Bomer Nils N Grote Beverborg Niels N Hoes Martijn F MF Streng Koen W KW Vermeer Mathilde M Dokter Martin M MM IJmker Jan J Anker Stefan D SD Cleland John G F JGF Hillege Hans L HL Lang Chim C CC Ng Leong L LL Samani Nilesh J NJ Tromp Jasper J van Veldhuisen Dirk J DJ Touw Daan J DJ Voors Adriaan A AA van der Meer Peter P

European journal of heart failure 20191206 8

<h4>Aims</h4>Severe deficiency of the essential trace element selenium can cause myocardial dysfunction although the mechanism at cellular level is uncertain. Whether, in clinical practice, moderate selenium deficiency is associated with worse symptoms and outcome in patients with heart failure is unknown.<h4>Methods and results</h4>BIOSTAT-CHF is a multinational, prospective, observational cohort study that enrolled patients with worsening heart failure. Serum concentrations of selenium were me ...[more]

PMID: 31808274

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Project description:AimThe severity of cardiac impairment in acute heart failure (AHF) predicts outcome, but challenges remain to identify prognostically important non-invasive parameters of cardiac function. Left ventricular ejection fraction (LVEF) is relevant, but only in those with reduced LV systolic function. We aimed to assess the standard and advanced parameters of left and right ventricular (RV) function from echocardiography in predicting long-term outcomes in AHF.MethodsA total of 418 consecutive AHF patients presenting over 12 months were prospectively recruited and underwent bedside echocardiography within 24 h of recruitment. We retrospectively assessed 8 RV and 5 LV echo parameters of the cardiac systolic function to predict 2-year mortality, using both guideline-directed and study-specific cutoffs, based on the maximum Youden indices via ROC analysis. For the RV, these were the tricuspid annular plane systolic excursion, RV fractional area change, tissue Doppler imaging (TDI) peak tricuspid annular systolic wave velocity, both peak- and end-systolic RV free wall global longitudinal strain (RV GLS) and strain rate (mean RV GLSR), RV ejection fraction (RVEF) derived from a 2D ellipsoid model and the ratio of the TAPSE to systolic pulmonary artery pressure (SPAP). For the LV, these were the LVEF, mitral regurgitant ΔP/Δt (MR dP/dt), the lateral mitral annular TDI peak systolic wave velocity, LV GLS, and the LV GLSR.ResultsA total of 7/8 parameters of RV systolic function were predictive of 2-year outcome, with study cutoffs like international guidelines. A cutoff of < -1.8 s-1 mean RV GLSR was associated with worse outcome compared to > -1.8 s-1 [HR 2.13 95% CI 1.33-3.40 (p = 0.002)]. TAPSE:SPAP of > 0.027 cm/mmHg (vs. < 0.027 cm/mmHg) predicted worse outcome [HR 2.12 95% CI 1.53-2.92 (p < 0.001)]. A 3-way comparison of 2-year mortality by LVEF from the European Society of Cardiology (ESC) guideline criteria of LVEF > 50, 41-49, and < 40% was not prognostic [38.6% vs. 30.9 vs. 43.9% (p = 0.10)]. Of the 5 parameters of LV systolic function, only an MR dP/dt cutoff of < 570 mmHg was predictive of adverse outcome [HR 1.63 95% CI 1.01-2.62 (p = 0.047)].ConclusionWith cutoffs broadly like the ESC guidelines, we identified RV dysfunction to be associated with adverse prognosis, whereas LVEF could not identify patients at risk.

Project description:AimsInformation on the prevalence, outcome and factors associated with heart failure in patients with adult congenital heart disease (CHD) (ACHD-HF) is lacking. We aimed at assessing the prevalence and outcome of ACHD-HF, the variables associated with ACHD-HF, and the differences between major anatomical/pathophysiological ACHD subgroups.Methods and resultsWe included 3905 patients (age 35.4 ± 13.2 years) under active follow-up in our institution (last visit >2010). Outcome of ACHD-HF cases was compared with sex- and age-matched cases. Univariable and multivariable binary logistic regression with ACHD-HF diagnosis as a dependent variable was performed. Overall prevalence of ACHD-HF was 6.4% (mean age 49.5 ± 16.7 years), but was higher in patients with cyanotic CHD (41%), Fontan circulation (30%), and a systemic right ventricle (25%). All-cause mortality was higher in ACHD-HF cases when compared with controls (mortality rate ratio 4.67 (2.36-9.27); P = 0.0001). In multivariable logistic regression analysis, age at latest follow-up [per 10 years; odds ratio (OR) 1.52; 95% confidence interval (CI) 1.31-1.77], infective endocarditis (OR 4.11; 95%CI 1.80-9.38), history of atrial arrhythmia (OR 3.52; 95%CI 2.17-5.74), pacemaker implantation (OR 2.66; 95% CI 1.50-4.72), end-organ dysfunction (OR 2.41; 95% CI 1.03-5.63), New York Heart Association class (OR 9.28; 95% CI 6.04-14.25), heart rate (per 10 bpm; OR 1.27; 95% CI 1.08-1.50), ventricular dysfunction (OR 3.62; 95% CI 2.54-5.17), and pulmonary hypertension severity (OR 1.66; 95% CI 1.21-2.30) were independently related to the presence of ACHD-HF. Some variables (age, atrial arrhythmia, pacemaker, New York Heart Association, and ventricular dysfunction) were related to ACHD-HF in all anatomical/physiological subgroups, whereas others were not.ConclusionsACHD-HF is prevalent especially in complex CHD and is associated with poor prognosis. Our data provide insight in the factors related to ACHD-HF including differences between specific anatomical and physiological subgroups.

Project description:AimsPulmonary congestion (PC) expressed by residual lung ultrasound B-lines (LUS-BL) could exist in some discharged heart failure (HF) patients, which is a known determinant of poor outcomes. Detection efficacy for PC is suboptimal with widely used imaging modalities, like X-ray or echocardiography, while lung ultrasound (LUS) can sufficiently detect PC by visualizing LUS-BL. In this trial, we sought to evaluate the impact LUS-BL-guided intensive HF management post-discharge on outcome of HF patients discharged with residual LUS-BL up to 1 year after discharge. IMP-OUTCOME is a prospective, single-centre, single-blinded, randomized cohort study, which is designed to investigate if LUS-BL-guided intensive HF management post-discharge in patients with residual LUS-BL could improve the clinical outcome up to 1 year after discharge or not.Methods and resultsAfter receiving the standardized treatment of HF according to current guidelines, 318 patients with ≥3 LUS-BL assessed by LUS within 48 h before discharge will be randomly divided into the conventional HF management group and the LUS-BL-guided intensive HF management group at 1:1 ratio. Patient-related basic clinical data including sex, age, blood chemistry, imaging examination, and drug utilization will be obtained and analysed. LUS-BL will be assessed at 2 month interval post-discharge in both groups, but LUS-BL results will be enveloped in the conventional HF management group, and diuretics will be adjusted based on symptom and physical examination results with or without knowing the LUS-BL results. Echocardiography examination will be performed for all patients at 12 month post-discharge. The primary endpoint is consisted of the composite of readmission for worsening HF and all-cause death during follow up as indicated. The secondary endpoints consisted of the change in the New York Heart Association classification, Duke Activity Status Index, N terminal pro brain natriuretic peptide value, malignant arrhythmia event and 6 min walk distance at each designed follow up, echocardiography-derived left ventricular ejection fraction, and number of LUS-BL at 12 month post-discharge. Safety profile will be recorded and managed accordingly for all patients.ConclusionsThis trial will explore the impact of LUS-BL-guided intensive HF management on the outcome of discharged HF patients with residual LUS-BL up to 1 year after discharge in the era of sodium-glucose cotransporter-2 inhibitors and angiotensin receptor blocker-neprilysin inhibitor.Trial registrationClinicalTrials.gov: NCT05035459.

Dataset Information

Selenium and outcome in heart failure.

Publications

Selenium and outcome in heart failure.

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