2013 ACCF/AHA Guideline for the Management of Heart Failure: Executive Summary

Yancy, Clyde W.; Jessup, Mariell; Bozkurt, Biykem; Butler, Javed; Casey, Donald E.; Drazner, Mark H.; Fonarow, Gregg C.; Geraci, Stephen A.; Horwich, Tamara B.; Januzzi, James L.; Johnson, Maryl R.; Kasper, Edward K.; Levy, Wayne C.; Masoudi, Frederick A.; McBride, Patrick E.; McMurray, John J.V.; Mitchell, Judith E.; Peterson, Pamela N.; Riegel, Bárbara; Sam, Flora; Stevenson, Lynne Warner; Tang, W.H. Wilson; Tsai, Emily J.; Wilkoff, Bruce L.

doi:10.1161/cir.0b013e31829e8807

Cited by 3,013 publications

(1,263 citation statements)

References 379 publications

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“…sST2 is a part of IL‐33/ST2‐system, which regulates inflammation, autoimmunity, tissue repair and fibrosis,38, 39, 40, 41 and is an established prognostic biomarker in heart failure patients 26, 42. We demonstrated previously that both human macrovascular (aortic and coronary artery) and heart microvascular endothelial cells are a source for sST2 protein 43.…”

Section: Discussionmentioning

confidence: 97%

“…Ambulatory ECG, Holter recordings and exercise tests were performed at baseline in all patients. New York Heart Association (NYHA) classification was documented for each patient at the baseline according to ESC and AHA Heart Failure Guidelines: NYHA Class I: no limitation of physical activity; NYHA Class II: slight limitation of physical activity in which ordinary physical activity leads to fatigue, palpitation, dyspnoea, or anginal pain; the person is comfortable at rest; Class III: marked limitation of physical activity in which less‐than‐ordinary activity results in fatigue, palpitation, dyspnoea, or anginal pain; the person is comfortable at rest; Class IV: inability to carry on any physical activity without discomfort but also symptoms of heart failure or the anginal syndrome even at rest, with increased discomfort if any physical activity is undertaken 4, 26. Patients were followed up between 2003 and 2013.…”

Section: Methodsmentioning

confidence: 99%

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GDF‐15 is a better complimentary marker for risk stratification of arrhythmic death in non‐ischaemic, dilated cardiomyopathy than soluble ST2

Stojković

Kaider

Koller

et al. 2018

J Cellular Molecular Medi

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Growth differentiation factor (GDF)‐15 and soluble ST2 (sST2) are established prognostic markers in acute and chronic heart failure. Assessment of these biomarkers might improve arrhythmic risk stratification of patients with non‐ischaemic, dilated cardiomyopathy (DCM) based on left ventricular ejection fraction (LVEF). We studied the prognostic value of GDF‐15 and sST2 for prediction of arrhythmic death (AD) and all‐cause mortality in patients with DCM. We prospectively enrolled 52 patients with DCM and LVEF ≤ 50%. Primary end‐points were time to AD or resuscitated cardiac arrest (RCA), and secondary end‐point was all‐cause mortality. The median follow‐up time was 7 years. A cardiac death was observed in 20 patients, where 10 patients had an AD and 2 patients had a RCA. One patient died a non‐cardiac death. GDF‐15, but not sST2, was associated with increased risk of the AD/RCA with a hazard ratio (HR) of 2.1 (95% CI = 1.1‐4.3; P = .031). GDF‐15 remained an independent predictor of AD/RCA after adjustment for LVEF with adjusted HR of 2.2 (95% CI = 1.1‐4.5; P = .028). Both GDF‐15 and sST2 were independent predictors of all‐cause mortality (adjusted HR = 2.4; 95% CI = 1.4‐4.2; P = .003 vs HR = 1.6; 95% CI = 1.05‐2.7; P = .030). In a model including GDF‐15, sST2, LVEF and NYHA functional class, only GDF‐15 was significantly associated with the secondary end‐point (adjusted HR = 2.2; 95% CI = 1.05‐5.2; P = .038). GDF‐15 is superior to sST2 in prediction of fatal arrhythmic events and all‐cause mortality in DCM. Assessment of GDF‐15 could provide additional information on top of LVEF and help identifying patients at risk of arrhythmic death.

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Section: Discussionmentioning

confidence: 97%

Section: Methodsmentioning

confidence: 99%

GDF‐15 is a better complimentary marker for risk stratification of arrhythmic death in non‐ischaemic, dilated cardiomyopathy than soluble ST2

Stojković

Kaider

Koller

et al. 2018

J Cellular Molecular Medi

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“…Chronic inotrope infusions may be the only option for stage D HFrEF patients optimally treated with goal‐directed medical therapy and not candidates for MCS or HT. If home inotropes are chosen, a discussion must take place with the patient regarding the palliative nature and potentially harmful consequences, including increased risk of death 2. Given the long‐term favourable findings of sacubitril/valsartan and our experience with this patient, sacubitril/valsartan may be a potential cost‐effective option for inotrope‐dependent patients who are not candidates for MCS and HT.…”

Section: Discussionmentioning

confidence: 99%

“…Treatment goals in acute decompensated HF include improvement of symptoms, identification of precipitating factors, optimization of volume status, titration of oral vasodilator and short‐term intravenous inotropic and vasodilator (inodilator) therapies, and patient education 2. However, costly long‐term, continuous inodilator infusions may be required for refractory HF (stage D) patients with severe systolic dysfunction, depressed cardiac output, and end‐organ mal‐perfusion while awaiting mechanical circulatory support (MCS) or heart transplantation (HT) 2. The angiotensin receptor blocker–neprilysin inhibitor, sacubitril/valsartan, is a novel therapy that can increase levels of endogenous vasoactive peptides 3, 4.…”

Section: Introductionmentioning

confidence: 99%

Use of sacubitril/valsartan in acute decompensated heart failure: a case report

Bell

Miller

et al. 2017

ESC Heart Failure

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Refractory heart failure typically requires costly long‐term, continuous intravenous inodilator infusions while patients await mechanical circulatory support or cardiac transplantation. The combined angiotensin receptor blocker–neprilysin inhibitor, sacubitril/valsartan, is a novel therapy that can increase levels of endogenous vasoactive peptides. This therapy has been recommended as an alternative agent in patients with chronic heart failure with reduced ejection fraction and New York Heart Association class II–III symptoms. Here, we report a case of a patient with refractory stage D heart failure with reduced ejection fraction who was successfully weaned off continuous intravenous inodilator support using sacubitril/valsartan after prior failed attempts using standard therapies.

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“…The study protocol will ensure optimal medical therapy for all study participants according to current practice guidelines 3, 27, 28, 29. Therefore, patients with a left ventricular ejection fraction (LVEF) ≤40% on the initial CMR scan and evidence of HF or who have diabetes mellitus (DM) will be started on open‐label eplerenone according to current practice guidelines.…”

Section: Methodsmentioning

confidence: 99%

Mineralocorticoid Receptor Antagonist Pretreatment to MINIMISE Reperfusion Injury After ST‐Elevation Myocardial Infarction (The MINIMISE STEMI Trial): Rationale and Study Design

Bulluck

Fröhlich

Mohdnazri

et al. 2015

Clinical Cardiology

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Novel therapies capable of reducing myocardial infarct (MI) size when administered prior to reperfusion are required to prevent the onset of heart failure in ST‐segment elevation myocardial infarction (STEMI) patients treated by primary percutaneous coronary intervention (PPCI). Experimental animal studies have demonstrated that mineralocorticoid receptor antagonist (MRA) therapy administered prior to reperfusion can reduce MI size, and MRA therapy prevents adverse left ventricular (LV) remodeling in post‐MI patients with LV impairment. With these 2 benefits in mind, we hypothesize that initiating MRA therapy prior to PPCI, followed by 3 months of oral MRA therapy, will reduce MI size and prevent adverse LV remodeling in STEMI patients. The MINIMISE‐STEMI trial is a prospective, randomized, double‐blind, placebo‐controlled trial that will recruit 150 STEMI patients from four centers in the United Kingdom. Patients will be randomized to receive either an intravenous bolus of MRA therapy (potassium canrenoate 200 mg) or matching placebo prior to PPCI, followed by oral spironolactone 50 mg once daily or matching placebo for 3 months. A cardiac magnetic resonance imaging scan will be performed within 1 week of PPCI and repeated at 3 months to assess MI size and LV remodeling. Enzymatic MI size will be estimated by the 48‐hour area‐under‐the‐curve serum cardiac enzymes. The primary endpoint of the study will be MI size on the 3‐month cardiac magnetic resonance imaging scan. The MINIMISE STEMI trial will investigate whether early MRA therapy, initiated prior to reperfusion, can reduce MI size and prevent adverse post‐MI LV remodeling.

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2013 ACCF/AHA Guideline for the Management of Heart Failure: Executive Summary

Cited by 3,013 publications

References 379 publications

GDF‐15 is a better complimentary marker for risk stratification of arrhythmic death in non‐ischaemic, dilated cardiomyopathy than soluble ST2

GDF‐15 is a better complimentary marker for risk stratification of arrhythmic death in non‐ischaemic, dilated cardiomyopathy than soluble ST2

Use of sacubitril/valsartan in acute decompensated heart failure: a case report

Mineralocorticoid Receptor Antagonist Pretreatment to MINIMISE Reperfusion Injury After ST‐Elevation Myocardial Infarction (The MINIMISE STEMI Trial): Rationale and Study Design

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