Titlebook: Heart Failure; Johann Bauersachs,Javed Butler,Peter Sandner Book 2017 Springer International Publishing AG 2017 Heart failure.Reduced ejec

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Clinical Trial Design, Endpoints, and Regulatory Requirements,capacity. Therefore its clinical development program must demonstrate clinically relevant improvement in a robust clinical end point and adequate safety to justify regulatory approval and clinical use. Mortality and hospitalisations are now combined with new composite end points in order to improve

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Biomarkers of Heart Failure with Preserved and Reduced Ejection Fraction,t also as a guide to evaluate the response to treatment in the individual patient and as an entry criterion and/or a surrogate marker of efficacy in clinical trials testing novel drugs. In this chapter, we review the role of established biomarkers for heart failure management, according to the main

Comprise

Heart Failure Guidelines on Pharmacotherapy, Despite the latest advances in device and pharmacological therapeutics, it still carries a huge burden, partially reflected in the annual healthcare cost of approximately $30 billion (2012) and the 5 year mortality rate of 50%. In this article, we review the medications, proven to significantly red

ASSET

Sacubitril/Valsartan (LCZ696) in Heart Failure,rEF) by treatments that target the renin–angiotensin–aldosterone system (RAAS). It has also long been thought that enhancement of the activity of natriuretic peptides (NPs) could potentially benefit patients with HFrEF, but multiple attempts to realize this benefit had failed over the years – until

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Ivabradine,rect effect on contractility or on the vessels. It was tested in a large outcome clinical trial in stable chronic heart failure (CHF) with low ejection fraction, in sinus rhythm, on a contemporary background therapy including betablockers (SHIFT: Systolic Heart Failure Treatment with the If inhibito

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Partial Adenosine A1 Agonist in Heart Failure,central physiological role of adenosine is to preclude tissue injury and promote repair in response to stress. In the heart, adenosine acts as a cytoprotective modulator, linking cardiac function to metabolic demand predominantly via activation of adenosine A1 receptors (A1Rs), which leads to inhibi

Obstacle

New and Emerging Therapies and Targets: Beta-3 Agonists,evelopment of heart failure. This has been the basis for the development of beta-blocking therapies, targeting mainly beta1-2 adrenoreceptors (B1-2AR). The third isotype, B3AR, was more recently identified in cardiac myocytes and endothelial cells from human (and many other animal species), where it

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Novel sGC Stimulators and sGC Activators for the Treatment of Heart Failure,ced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF). The nitric oxide (NO) pathway is a key regulator in the cardiovascular system and modulates vascular tone and myocardial performance. Disruption of the NO-cyclic guanosine monophosphate (cGMP) signaling axis and impaired cGM

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Cardiac Phosphodiesterases and Their Modulation for Treating Heart Disease,nophosphate (cAMP) and cyclic guanosine 3′,5′- monophosphate (cGMP). Their dysregulation, altered intracellular targeting, and blunted responsiveness to stimulating pathways all contribute to pathological remodeling, muscle dysfunction, reduced cell survival and metabolism, and other abnormalities.

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Steroidal and Novel Non-steroidal Mineralocorticoid Receptor Antagonists in Heart Failure and Cardind disease. Pathophysiological MR activation contributes to a plethora of deleterious molecular mechanisms in the development of cardiorenal diseases like chronic kidney disease (CKD) and heart failure (HF). Accordingly, the available steroidal MR antagonists (MRAs) spironolactone (first generation