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Sacubitril-valsartan should not be given concomitantly it ACE in ibitors due to risk for ngioedema, and ACE inhibitor treatment should be stopped for 36 h before starting treatment with ARNI. For patients with eGFR < 30 mL/min/1.73 m 2 or moderate hepatic impairment, the starting dosage of ARNI is 24/26 mg twice daily and ARNI is n t recommended for patients with severe hepatic impairment [ 38 ]. With the results of the PARADIGM trial, several new rec- ommendations have been added to the 2017 Focused Update HF Guidelines. First, for patients who are not treated with ACE inhibitors or angiotensin receptor blockers, the initial strategy of RAS inhibition can include either an ACE inhibitor or ARB or ARNI. The guidelines specify that the clinical strategy of inhibition of the RAS with ACE inhibitors (level of evidence: A), or ARBs (level of evidence: A), or ARNI (level of evidence: B – R) in conjunction with evidence-based beta-blockers and aldosterone antagonists in selected patients is recommended fo atients with chronic HFrEF to r duce morbidity and mortality [ 1 •• ]. In the 2017 Focused Update of HF Guidelines, in patients with chronic symptomatic HFrEF NYHA class II or III who tolerate an ACE inhibitor or ARB, replacement by an ARNI is recommended to further reduce morbidity and mortality [ 1 •• , 36 •• ]. In those patients who are being considered to be switched to ARNI from ACE inhibitors, it is very important to note that ARNI should not be administered concomitant y with ACE inhibitors or within 36 h of the last dose of an ACE inhibitor due to angioedema risk [ 1 •• , 35 ]. Similarly, ARNI should not be administered to patients with a history of angio- edema [ 1 •• ]. In the studies with combined neprilysin an ACE inhibition, blacks and smokers were particularly at risk for angioedema [ 35 ]. It is helpful for patients receiving ARNI to be educated about recognition of the symptoms of angioede- ma and to ale t health care providers against concomitant pre- scription of ACE inhibitors with ARNI. In a phase II trial in patients with heart failure with pre- served ejection fraction, LCZ696 reduced NT-proBNP to a greater extent than did val artan at 12 weeks and was well tolerated [ 39 ]. The efficacy and safety of ARNI in acute de- compensated HF, in advanced HF patients with NYHA class IV symptoms, or in patients with HF-PEF is unclear at this time and is being tested in large-scale trials. Ivabradine Ivabradine is a specific and selective inhibitor of the If ion channel. If ion channel (the fu ny current) is highly expressed in spontaneously active cardiac regions, such as the sinoatrial node, the AV node, and the Purkinje fibers. The funny current is a mixed Na/K current that activates upon hyperpolarization at voltages in the diastolic range, and controls the rate of spontaneous activity of sinoatrial myocytes, hence the cardiac rate [ 40 ]. In the Systolic HF treatment with the If inhibitor Ivabradine Trial (SHIFT), among HFrEF with normal sinus rhythm and a baseline heart rate ≥ 70 bpm despite treatment with beta-blockers, ivabradine treatment was associated with reduction in combined end point of cardiovascular death or HF hospitalization when compared against placebo [ 41 •• ]. Interestingly, though the trial inte ded to recruit patients on target or maximally tolerat d doses of β -blockers, 26% of patients were on full-dose β -blockers. The treatment effect reflected a reduction only in the risk of hospitalization for worsening HF; there was no benefit observed for the mortality compone t of the primary end point [ 41 •• ]. Patients enrolled included a small number with paroxysmal atrial fibrillation (< 40% of the time) but otherwise in sinus rhythm and a small number experiencing ventricular pacing but with a predomi- nant sinus rhythm [ 41 •• ]. Ivabradine patie ts had higher rates of symptomatic bradycardia, atrial fibrillation, and visual side effects (phosphenes) compared to placebo [ 41 •• ]. According to the FDA drug label, ivabradine is approved to reduce hospi- talization risk for worsening HF in pati nts with stable, symp- tomatic chronic HF with LVEF ≤ 35% in sinus rhythm with resting HR of ≥ 70 bpm or higher and on maximally tolerated doses of beta-blockers and is contraindicated for patients with acute decompensated HF, BP < 90/50 mmHg, patients with sick sinus syndrome, sinoatrial, or t ird-degree AV block [ 42 ]. In the 2017 Focused Update of HF Guidelines, iv bradine is identified as a treatment that can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II and III) stable chronic HFrEF (LVEF ≤ 35%) who are receiv- ing guideline-directed medical treatment, including a beta- blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of ≥ 70 bpm at rest (class IIa recom- mendation, with level of evidence: B – R). It should be noted that the recommendation does not entail a stateme nt regarding mortality benefit. Contrary to the ESC Guidelines [ 43 ], in the 2017 AHA/ACC Focused Update of HF Guidelines, there is no recommendation for ivabradine in beta-blocker intolerant patients [ 1 •• ]. SHIFT trial w s not designed to examin the efficacy of ivabr dine in patients intolerant to bet -blockers. Efficacy and benefit of ivabradine in beta-blocker intolerant patients need to be tested in future trials. The current treatment strategies for management of patients with HF and reduced EF are summarized in Figs. 1 and 2 . Update on the Treatment of HFpEF Unfortunately there are no treatment strategies with proven benefit to reduce mortality in patients with HF with preserved EF. Current treatment strategies target treatment of the underly- ing etiology for HF-pEF and comorbidities. Thus, most of the recommendations that were present in 2013 AHA/ACC HF 39 Page 4 of 9 Curr Cardiol Rep (2018) 20: 39 Ruschitzka F, Maggioni AP, Filippatos G (2017) Epidemiol gy and one-year outc mes in patients with chronic heart failure and pre- s rved, mid-range nd reduced ejection fraction: an a aly is of the ESC Heart Failure Long-Term Registry. Eur J Heart Fail 19:1574 – 1585. https://d i.org/10.1002/ejhf.813 65. 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