Best of heart failure

65 3. Solomon SD, Dobson J, Pocock S, S Granger CB, Yusuf S, Swedberg K, Y Pfeffer MA, for the Candesartan in Hea Reduction in Mortality and morbidity (2007) Influence of nonfatal hospitaliz subsequent mortality in patients wit Circulation 116(13):1482 – 1487 4. Ramirez A, Abelmann WH (1974) C NEJM 290(9):499 – 501 5. Peacock WF, Braunwald E, Abraham Christenson R, Collins S, Diercks D, Kellerman A, Gheorghiade M, Kirk D, BM, O'Connor C, Pang P, Shah M, Sopk A, Teerlink J (2010) National Heart, L working group on emergency departme heart failure: research challenges and op 343 – 351 6. Hamo CE, Butler J, Gheorghiade M, bumpy road to drug development for Heart J Supp 18(Supplement G):G19 – G 7. Gheorghiade M, Braunwald E (2011) A assessment and management of acute JAMA 305:1702 – 1703 8. Ponikowski P, Voors AA, Anker SD et al the diagnosis and treatment of acute and task force for the diagnosis and treatment failure of the European Society of Car with the special contribution of the Hea the ESC. Eur Heart J 37(27):2129 – 2200 9. Cleland JG, Pennel D, Ray S, Murray G, Coats A, Lahiri A (1999) The Carvedil Ischemia Trial: Marker of Success (CHRI 1:191 – 196 10. Cleland JG, Pennell DJ, Ray SG, Co Murray GD, Mule JD, Vered Z, Lahiri reversible ischaemia trial: marker of suc half of the CHRISTMAS (Carvedilol Ischaemia Trial: Maker of Success Myocardial viability as a determinant o sponse to carvedilol in patients with he trial): randomised controlled trial. Lancet 11. Greene SJ, Vaduganathan M, Gheorghia road to recovery: therapeutic and clinical functional viable myocardium in heart fai fraction. Eur J Heart Fail 19(7):870 – 872 12. Adamsom PB, Magalski A, Braunschwei right ventricular hemodynamics in heart measurements derived form an implanta Am Coll Cardiol 41:565 – 571 13. Zile MR, Bennett TD, St John Sutton from chronic compensated to acute dec pathophysiological insights obtained fro of intracardiac pressures. Circulation 118 14. Stevenson LW, Perloff JK (1989) The lim signs for estimating hemodynamics in ch 261:884 – 888 15. Gheorghiade M, Follath F, Ponikowski Cleland JG, Dickstein K, Drazner MH, Jondeau G, Sendon JL, Mebazaa A, Met PS, Seferovic P, Stevenson LW, van Anker SD, Rhodes A, McMurray J, Society of Cardiology, European So Medicine (2010) Assessing and grading failure. Eur J Heart Fail 12(5):423 – 433 16. Ambrosy AP, Khan H, Udelson JE, Ment SJ, Vaduganathan M, Subacuis HP, Ko Heart Fail Rev (2018) 23:597 – 607 recommended to be in reach the target 97/10 should not be given c to risk for angioedema, stopped for 36 h bef patients with eGFR < impairment, the starti daily and ARNI is not hepatic impairment [ 3 With the results of t ommendations have b HF Guidelines. First, ACE inhibitors or an strategy of RAS inhibit or ARB or ARNI. T strategy of i hibition of evidence: A), or A (level of evidence: B – beta-blockers and aldo is ecommended for p morbidity and mortalit In the 2017 Focuse with chronic symptom tolerate an ACE inhibit recommended to furth 36 •• ]. In those patie switched to ARNI fro to note that ARNI sho with ACE inhibitors or inhibitor due to angio should not be administ edem [ 1 •• ]. In the stu inhibition, blacks and angioedema [ 35 ]. It is be educated about rec ma and to lert health scription of ACE inhi In a phase II trial i served ejection fractio reater extent than di tolerat d [ 39 ]. The eff compensated HF, in a IV symptoms, or in p time and is bei g te te Ivabradine Ivabradine is a specifi chann l. If io ch n el in spontaneously activ node, the AV node, an is a mixed Na/K curre at voltages in the dia 39 Page 4 of 9 These objective tools represent a patient-centered metric to compare congestion from admission to discharge to ensure symptomatic improvement. Orthostatic vital signs In individuals with normal cardiac function and intravascular volume levels, the typical reflex response to positional changes from sitting to standing in- cludes mild reduction in blood pressure and increase in heart rate [ 19 ]. However, in decompensated patients with intravas- cular congestion, these positional changes can have paradox- ical effects. Based on the Frank – Starling curve, sarcomeres in congested HF patients are initially overstretched but shrink within ideal range with decreased venous return and resultant decreased preload, causing an improved contractility [ 20 ]. Therefore, orthostasis may result in increased cardiac output and improved blood pressures which could indicate intravas- cular congestion requiring further diuresis. This tool has lim- itations in utility among patients with hypertrophic cardiomy- opathy, aortic stenosis, or atrial fibrillation. The Valsalva maneuver In an individual with normal intravas- cular volume levels, there is a multi-phase response to sustained Valsalva maneuver. Immediately after initiating Valsalva, the increased intrathoracic pressure causes a brief spike in blood pressure followed by decreased venous return and increased systemic vascular resistance causing a drop in blood pressure below baseline. After the strain is released, the reduced intrathoracic pressure causes a further drop in blood pressure followed by increased venous return and decreased vascular resistance (and, therefore, decreased afterload) which allows for a rebound blood pressure elevation [ 21 ]. Conversely, in patients with congestion, the release of strain results in a persistently elevated blood pressure due to increased LV dia- stolic pressure and persistently elevated central pressures [ 22 ]. This maneuver has proven to have high correlation with invasively measured ventricular filling pressures demonstrating its utility in monitoring intravascular volume status [ 23 ]. The 6-min walk test (6MWT) is a simple tool to elicit symptoms of congestion that may not be present at rest. The ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) trial found that the 6MWT was one of the most reliable predictors of mortality after hospitalization for worsene HF, alongside PCWP measurements [ 24 ]. The 6MWT can be used both in IV therapies Oral therapies 7 Multi-modality Assessment Re-assess: Congestion, NPs SBP,HR Organ injury/dysfunction Candidacy: CRT/ICD Valvular surgery CABG/PCI LVAD/HTX Fig. 3 Congestion timeline with associated therapeutic recommendations. The spectrum of hemodynamic and clinical congestion requires a thoughtful therapeutic timeline. Hemodynamic congestion typically is initiated in the outpatient setting and progresses to clinical congestion possibly requiring admission for management. IV therapies and a thorough multi-modality assessment should be performed as outlined above. Realize that hemodynamic congestion with persistent elevation of LVEDP may be present despite improvement of symptoms. Using the highlighted techniques and tools can further improve hemodynamic congestion before discharge. Post-discharge reassessment is crucial to achieve true euvolemia and prevent re-congestion. In tiation of advanced therapies must be considered on a ase by c se basis. IV, intravenous; NPs, natriuretic peptides; SBP, systolic blood pressure; HR, heart rte; CRT, cardiac resynchronization therapy; ICD, invasive cardiac defibrillator; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention; LVAD, left ventricular assist device; HTX, he rt transplant 600 Heart Fail Rev (2018) 23:597 – 607 lation. s , of strain results in a ly elevated blood pressure due to increased ia- u in monitoring intravascular volume status [ 23 ]. Pulmonary Artery Catheterization Effectiveness) trial found s Oral therapi SBP,HR asses of LVEDP may be present despite improvement of symptoms. Using ligh ca c t