Best of heart failure

69 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 tole ate 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 becoming increasingly apparent that we must have patients followed up closely in outpatient cardiology clinics early dur- ing this period to prevent worsening congestion, renal func- tion, and neurohormonal maladaptations [ 82 ]. In order to determine who is at highest risk of poor out- comes during this vulnerable phase, patients can be risk- stratified based on certain prognostic indicators. Hypotension (low systolic blood pressure), ventricular dyssynchrony, ane- mia, persistently elevated BNP, and hyponatremia have all been found to carry a negative prognosis in patients with AHF [ 83 ]. An additional risk-stratifying tool in the peri- discharge period is the Kansas City Cardiomyopathy Questionnaire (KCCQ), a self-reported quality of life report for functional status evaluation. Green et al. determined that patients with stable chronic HF or low New York Heart Association (NYHA) staging consistently had higher KCCQ scores and patients with decompensated HF or higher NYHA staging had lower scores [ 84 ]. Notably, a higher KCCQ score prior to discharge was associated with a higher 30-day HF readmission rate [ 85 ]. The symptoms evaluated by KCCQ tend to be the chief complaints upon re-presentation to the hospital among HF patients. Therefore, KCCQ, as well as the aforementioned clinical signs, has significant utility in a risk prediction model to minimize rehospitalizations when signs of congestion are not present. Although evidence supporting the exact goals and duties of the early post-discharge visit are lacking, the ACC and AHA mention the goal for immediate post-discharge office center- ing on reassessment of volume status and renal function, and ensuring current medications are in line with guideline- directed medical therapy (GDMT). For prognostic purposes, repeat biomarker testing can be considered [ 86 ]. Additionally, recent research has demonstrated a prognostic rationale for monitoring troponin I levels with an elevated serum level at 1 month predicting increased clinical events at 12 months [ 87 ]. Further follow-up must focus on optimizing GDMT, assessing new targets for intervention, and managing comor- bid conditions in order to prevent further precipitants and ex- acerbations [ 88 ]. Reflection on other factors such as optimiz- ing macronutrient and micronutrient status must also be con- sidered. Patient coaching is equally crucial to ensure contin- ued follow-up and adherence to medications and diet. Cardiac rehabilitation is a three-axis program that focuses on improving cardiovascular health, preventing deterioration, and minimizing rehospitalization by counseling patients about healthy lifestyle management, exercise training, and stress reduc- tion. In the HF-ACTION (heart failure: a controlled trial investi- gating outcomes of exercise training) study, cardiac rehabilitation was found to improve health-related quality of life (self-reported using KCCQ and EQ-5D questionnaires) [ 89 ]. However, data indicates that only 10% of eligible patients receive a referral at time of hospital discharge [ 90 ]. With the advent of novel access to counseling and cardiac rehab through the internet and mobile phones [ 91 ], the barriers to incorporating these non-medical ther- apeutic measures in daily life are minimized. Ambulatory invasive hemodynamic monitoring is novel intervention for continuous assessment in the outpatient set- ting. The CardioMEMS is an implantable device hat mea- sures PCWP to provide early warning of congestion prior to progression requiring inpatient management. Abrah m e al. studied its use in NYHA class III HF patients and observed a 30% relative risk reduction at 6 months post-impl ntation [ 92 ]. Although it carries inherent risks during implantation in addition to increased cost compared to standard of care, is device may prove useful for selected patients. Lastly, patients with severe stage D or NYHA class III-IV HF must be evaluated for invasive devices such as invasive cardiac defibrillators and ventricular assist devices when clinically indi- cated whether in the inpatient or outpatient s tting. Both the ESC and ACC/AHA guidelines elucidate when th se invasive devic s are indicated, and early identification of candidates is crucial for preventing continued deterioration of cardiac function [ 8 , 32 ]. Conclusion The pathophysiology behind heart failure development and exacerbation is multifaceted and, as such, should be assessed more thoroughly. We present an algorithm utilizing a ulti- modality assessment of precipitating and aggravating factors and a guideline for improved management of acute decom- pensated heart failure. This paper highlights the importance of thorough assessment, individualized treatment plans beyond clinical congestion with underutilized therapies, inclusion of noncardiac comorbidities, and continuing management fol- lowing hospitalization. We aim to provide guidance to im- prove overall cardiac function and, therefore, minimize rehos- pitalization rates among heart failure patients. Compliance with ethical standards Conflict of interest Dr. Muthiah Vaduganathan is supported by the NHLBI T32 postdoctoral training grant (T32HL007604); Dr. Andrew P. Ambrosy is supported by the NHLBI T32 postdoctoral training grant (5T32HL069749); Dr. Sean P. Collins is supported by grants through the AHA, PCORI, NIH, AHRQ, and Novartis and is a consultant for Novartis. References 1. Gheorghiade M, Vaduganathan M, Fonarow GC, Bonow RO (2013) Rehospitalization for heart failure. Probl Perspect JACC 61(4):391 – 403 2. O ’ Connor CM, Miller AB, Blair JE et al (2010) Causes of death and rehospitalization in patients hospitalized with worsening h failure and reduced left ventricular ejection fraction: results from Efficacy of Vasopressin Antagonism in Heart Failure Outcome study with Tolvaptan (EVEREST) program. Am Heart J 159:841 – 849 604 Heart Fail Rev (2018) 23:597 – 607