Therapeutic algorithm for symptomatic HFrEF (Heart Failure) ESC 2016 guidelines

Therapeutic algorithm for a patient with symptomatic heart failure with reduced ejection fraction. Green indicates a class I recommendation; yellow indicates a class IIa recommendation.
ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; ARNI = angiotensin receptor neprilysin inhibitor; BNP = B-type natriuretic peptide; CRT = cardiac resynchronization therapy; HF = heart failure; HFrEF = heart failure with reduced ejection fraction; H-ISDN = hydralazine and isosorbide dinitrate; HR = heart rate; ICD = implantable cardioverter defibrillator; LBBB = left bundle branch block; LVAD = left ventricular assist device; LVEF = left ventricular ejection fraction; MR = mineralocorticoid receptor; NT-proBNP = N-terminal pro-B type natriuretic peptide; NYHA = New York Heart Association; OMT = optimal medical therapy; VF = ventricular fibrillation; VT = ventricular tachycardia.
(a) Symptomatic = NYHA Class II-IV. (b) HFrEF = LVEF ,40%. (c) If ACE inhibitor not tolerated/contra-indicated, use ARB. (d) If MR antagonist not tolerated/contra-indicated, use ARB. (e) With a hospital admission for HF within the last 6 months or with elevated natriuretic peptides (BNP . 250 pg/ml or NTproBNP . 500 pg/ml in men and 750 pg/ml in women). (f) With an elevated plasma natriuretic peptide level (BNP ≥ 150 pg/mL or plasma NT-proBNP ≥ 600 pg/mL, or if HF hospitalization within recent 12 months plasma BNP ≥ 100 pg/mL or plasma NT-proBNP ≥ 400 pg/mL). (g) In doses equivalent to enalapril 10 mg b.i.d. (h) With a hospital admission for HF within the previous year. (i) CRT is recommended if QRS ≥ 130 msec and LBBB (in sinus rhythm). (j) CRT should/may be considered if QRS ≥ 130 msec with non-LBBB (in a sinus rhythm) or for patients in AF provided a strategy to ensure bi-ventricular capture in place (individualized decision).

Goal of treatment

A) Ventricular remodeling represented on pressure-volume diagram. Systolic and diastolic properties shown by end-systolic and end-diastolic pressure-volume relations (ESPVR and EDPVR, respectively) with normal pressure-volume loop (blue). Acute decrease in contractility causes shift of ESPVR with reduced stroke volume and blood pressure (red solid line). Acute neurohormonal (NH) activation increases heart rate and constricts arteries and veins, which increases arterial, venous, and ventricular end-diastolic pressures (dashed purple line). When compensation is incomplete and neurohormonal activation persists, remodeling manifests as progressive shifts toward larger volumes of both ESPVR and the EDPVR (green).


B) Goal of many drug- and device-based treatments for heart failure is to prevent, slow, or reverse remodeling so that ESPVR and EDPVR return toward normal.

Donna Mancini, and Daniel Burkhoff Circulation. 2005;112:438-448