Congestive heart failure treatment of patients with current or prior symptoms of heart failure (Stage C)

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Medical Therapy:

Summary
Acute Pharmacotherapy
Chronic Pharmacotherapy in HFpEF
Chronic Pharmacotherapy in HFrEF
Diuretics
ACE Inhibitors
Angiotensin receptor blockers
Aldosterone Antagonists
Beta Blockers
Ca Channel Blockers
Nitrates
Hydralazine
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ACC/AHA Guideline Recommendations

Initial and Serial Evaluation of the HF Patient
Hospitalized Patient
Patients With a Prior MI
Sudden Cardiac Death Prevention
Surgical/Percutaneous/Transcather Interventional Treatments of HF
Patients at high risk for developing heart failure (Stage A)
Patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms (Stage B)
Patients with current or prior symptoms of heart failure (Stage C)
Patients with refractory end-stage heart failure (Stage D)
Coordinating Care for Patients With Chronic HF
Quality Metrics/Performance Measures

Implementation of Practice Guidelines

Congestive heart failure end-of-life considerations

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Patients who have concomitant disorders
Obstructive Sleep Apnea in the Patient with CHF
NSTEMI with Heart Failure and Cardiogenic Shock

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahmoud Sakr, M.D. [2],Seyedmahdi Pahlavani, M.D. [3], Edzel Lorraine Co, D.M.D., M.D. [4]

Overview

Several measures [1] have been listed for patients in Stage A or B as previously mentioned and the Class 1 recommendations for those patients are also appropriate for patients with current or previous symptoms of HF. The effectiveness of diuretics and safety of their usage is an important aspect of the treatment that should be closely monitored along with daily measurement of weight and moderate sodium restriction. Physical activity is highly recommended, although heavy labor or sports shouldn’t be a part of it. A reduction in physical activity promotes physical deconditioning, and an increase of weight which may be associated with more strain on the failing heart.[2] Patients with chronic conditions such as HF are also recommended to be immunized with influenza and pneumococcal vaccines in order to reduce the risk of respiratory infection.

Drugs that should be Avoided or Used with Caution in Patients with HF

Pharmacological therapy should be closely monitored and several classes of drugs should be avoided in case of HF:

  • Calcium Channel blockers: There is no direct role of these drugs in the management of HF, due to negative and possible deleterious effect in patients with HF due to systolic dysfunction[3]. Vasoelective Calcium Channel blockers as amlodipine and felodipine have not been linked to adverse effect in HF treatment, but there is no evidence of efficacy for these drugs in the management of HF.[4] However, amlodipine and felodipine appear to be safe for the treatment of concomitant disease in HF patients, such as angina or hypertension.
  • Antiarrhythmic agents: Negative inotropic effect exerted by most antiarrhythmic drugs can precipitate HF in patients with reduced LV function. The reduction in LV function can also reduce the elimination of these drugs leading to further drug toxicity. Other antiarrhythmic drugs can induce some proarrhythmic effect, especially class 1 agents and class 3 agents Ibutilide and sotalol;[5] the same class 3 agents in addition to dofetilide can induce torsades to pointes.

Amiodarone is considered the safest of the antiarrhythmic drugs because of its minimal proarrhythmic effect and is generally the preferred drug for treating arrhythmias in HF patients.

  • Nonsteroidal anti-inflammatory drugs (NSAID):[6] The administration of non-selective NSAIDs in HF patients is linked with an increased risk of HF exacerbation, increased renal dysfunction, and abnormal responses to ACEIs and diuretics. COX-2 selective inhibitors have not been fully investigated, but observational studies indicate that they may be linked with an increased rate of HF exacerbation and increased mortality.

Aspirin benefits and risks are not well established in patients with HF and Vascular disease (includingCAD). The potential interaction between ACEIs and beta blockers is of great importance. Although no data has proven that aspirin causes more frequent HF exacerbations and interactions with those drugs, health care providers should be aware of the possibility of such risks, but no recommendation for or against aspirin therapy in patients with heart failure can be made before further data are available.

Metformin - one of the most common side effects of metformin is lactic acidosis, which can be fatal in patients with HF.

Thiazolidinediones -[8] the biggest risk of using Thiazolidinediones is fluid retention which may cause severe worsening of patients with HF.

PDE-5 inhibitors such as sildenafil, vardenafil, and tadalafil, are widely used in the management of erectile dysfunction in men. The use of those agents with any form of nitrate therapy is contraindicated because of severe hypotensive effect that can be life threatening.[13] In a trial where sildenafil and placebo were randomly assigned to 34 HF patients, no significant difference of symptomatic hypotension was observed, but HF patients with borderline low blood pressure and/or low volume status are in risk of severe hypotension and should avoid any PDE-5 inhibitors use.

  • Tumor Necrosis Factor alpha inhibitors TNF-alpha: New onset or worsening of pre-existing heart failure have been linked to TNF-alpha inhibitors.[15] Infliximab has been specifically contraindicated in doses over 5mg/kg in patients with heart failure.

Serum potassium should be closely monitored in HF patients, in order of preventing either hypokalemia or hyperkalemia, which could greatly affect cardiac excitability and conduction, leading to sudden cardiac death.[17] Serum potassium should be maintained between 4.0 to 5.0 mEq per liter range, because low potassium level may affect digitalis and antiarrhythmic drugs treatment, while high potassium level can prevent the use of treatments known to prolong life.[17]

Supervision of HF patients with close monitoring of treatment and diet is a very important aspect of the follow-up process in those individuals. Body weight and medications should be closely monitored, because any minor change in those parameters can have a significant effect over symptoms and hospitalization of patients with HF.[18] Patient education is a crucial aspect of the management of HF, patient and family surveillance over any new change of symptoms or body weight is important in allowing early detection of those changes and implementing new treatment strategies to reduce further complications.[19]

Pharmacological Therapy of HF

Improving symptoms, reducing mortality and slowing or reversing myocardial deterioration are the main goals of pharmacological therapy in HF patients. The therapy should be also directed at preventing arrhythmias, embolic events and other exacerbating factors. Different strategies have been implemented in the treatment of HF, but the ACC/AHA recommendations are based on a combination of 3 types of drugs: a Diuretic, an ACEI or an ARB, and a beta blocker[20]. A review of data from several trials, provide clear evidence supporting the central role of these drugs in HF patient Therapy. The Diuretics play an important role in controlling fluid retention and achieving a euvolemic state. On the other hand, ACEI and a beta blocker should be started and maintained in patients who can tolerate them because of their major effect in controlling symptoms and reducing mortality. Digoxin can be added to this regime as a fourth agent to reduce symptoms, reduce recurrent hospitalization, control great and rhythm, and enhance exercise tolerance.

Diuretics

Different classes of diuretics have been implicated in the treatment of CHF. Loop Diuretics such as furosemide, bumetanide and torsemide, act on the inhibition of sodium and chloride reabsorption in the loop of Henle, whereas thiazide diuretics, metolazone, and potassium sparing diuretics as spironolactone act on the distal portion of the renal tubule. [21]Loop diuretics increase sodium secretion up to 25 % of the filtered load of sodium, enhance free water clearance and maintain their efficacy unless severe renal impairment is present.[22]Thiazide diuretics in contrast, increase the fractional excretion of sodium to a maximum of 10% of the filtered load, decrease free water clearance and lose their efficacy in patients with impaired renal function. For such reasons, loop diuretics are much preferred, unless hypertension with mild fluid retention is present in HF patients, where thiazide diuretics may have a better antihypertensive effect in this case.

Different short-studies demonstrated the efficacy of diuretics in improving various symptoms of HF, reducing jugular venous pressure, pulmonary congestion, peripheral edema and body weight, all within days of initiation of therapy.[23] No long term studies have been conducted so far to reveal the effects of diuretic therapy on morbidity and mortality, but an improvement in cardiac function and exercise tolerance in patients with HF have been demonstrated in intermediate-term trials.[24]

Diuretics produce great symptomatic benefits,[25] much more rapidly than any other drugs for HF, they can adequately control the fluid retention of HF, relieving pulmonary edema and peripheral edema within hours or days. However, Diuretics should not be used alone in controlling Stage C HF. They should be combined with an ACEI and a beta blocker to avoid further clinical deterioration and maintain the HF symptoms under control.[24]

Appropriate dose of diuretics should used in treatment of HF,[26] because low doses will cause fluid retention, which can lead to a reduced response to ACEIs and ARBs and an increase risk of decompensation with the use of beta blockers, while excessive diuretics will lead to volume contraction which can increase the risk of hypotension and renal insufficiency with ACEIs, ARBs and beta blockers.[27]

Loop diuretics are usually the first diuretics to be used to control pulmonary and/or peripheral edema. Furosemide is the most commonly used, but some patients may respond favorably to other agents in this category (as torsemide and Bumetanide) because of superior absorption and longer time of action.[28]

The starting dosage is usually 20 to 40 mg of furosemide or its equivalent, but the exact dosing should always be monitored according to diuresis and other clinical symptoms, since the ultimate goal is to eliminate the evidence of fluid retention such as jugular venous pressure elevation and peripheral edema. Outpatients with HF are usually started with low dose until urine increases and weigh decreases by 0.5 to 1.0 kg daily. Diuretic therapy should be also combined with moderate dietary sodium restriction. Unstable or severe disease, should be controlled with intravenous diuretics( bolus or continuous infusion) and thiazide diuretics can be added for a synergistic effect.[29]

Reducing overall volume may decrease intracardiac filling pressure resulting in a lower cardiac output via the Frank-Starling relationship. This effect is usually a minor effect and does not alter the course of the therapy. On the other hand, an unexplained increase in BUN and creatinine should be closely monitored and suspected as a sign of abnormal tissue perfusion. In this case renal function and other end organ perfusion should be assessed to avoid any concomitant complications.

Angiotensin Converting Enzyme Inhibitors

Patients with moderate to severe HF or asymptomatic left ventricular dysfunction show a great improvement in survival rate with the usage of ACE inhibitors.[30] ACE inhibitors enhance the action of kinins and augment kinin-mediated prostaglandin production, so the effect of ACEIs cannot be solely explained by the suppression of Angiotensin II production. Furthermore, it has been proven that ACEIs modify cardiac remodeling more favorably than ARBs in experimental models of HF.[31] Several studies indicates that ACEIs can alleviate symptoms,[32] improve clinical status and sense of well being in patients with HF.

Another important aspect of ACEIs therapy is the reduction of mortality and hospitalization in such patients.[33] These benefits were noticed in patients with mild, moderate or even severe symptoms of HF, with or without CAD. In general ACEIs should be used together with a beta blocker and should not be used without diuretics in patients with a current or recent history of fluid retention, because of the important role of diuretics in maintaining sodium balance and preventing the development of peripheral and pulmonary edema.[24]

For the reasons mentioned above, ACEI therapy should be started in asymptomatic or symptomatic patients with HF. The beginning therapy should be a low dose ( eg, 2.5 mg of enalapril twice a day, 6.25 mg of captopril three time a day or 5 mg of lisinopril once a day). The dose should be gradually increased in one to two week if the initial therapy is tolerated and try to target a dose of 20 mg of enalapril twice a day, or 50 mg of captopril three times a day or up to 40 mg of lisinopril a day.[34] Plasma potassium and renal function should be assessed one to two weeks after starting or changing a dose and periodically thereafter. Physicians should attempt to target certain doses which have been proved to reduce the risk of cardiovascular events. If these target doses of ACEIs cannot be used or poorly tolerated than intermediate doses should be implemented. [35]

NSAIDs should be avoided since they may cause an increase in adverse effects of ACEIs in patients with HF and a decrease in the favorable effect of ACEIs therapy.[24] Some evidence suggests that aspirin may inhibit the acute hemodynamic benefits of ACEIs.[36] If the patient has a know history of coronary artery disease(CAD) then use of ASA along with ACEIs is recommended. However, but in patients with no history of CAD, there is no evidence to support the use of aspirin.

Treatment of HFrEF Stage C and D

Abbreviations: ACEI: angiotensin-converting enzyme inhibitor, ARB: angiotensin receptor-blocker, ARNI: angiotensin receptor-neprilysin inhibitor, BP: blood pressure, bpm: beats per minute, C/I: contraindication, COR: Class of Recommendation, NT-proBNP: creatinine clearance, NYHA: cardiac resynchronization therapy–device, pts: diagnosis, HF: guideline-directed management and therapy, CrCl: creatinine clearance, CRT-D: cardiac resynchronization therapy–device, Dx: diagnosis, GDMT: guideline-directed management and therapy, HF: heart failure, HFrEF: heart failure with reduced ejection fraction, ISDN/HYD: isosorbide dinitrate hydral-nitrates, K+: potassium, LBBB: left bundle-branch block, LVAD: left ventricular assist device, LVEF: left ventricular ejection fraction, MI: myocardial infarction, NSR: normal sinus rhythm, NYHA: New York Heart Association

†Hydral-Nitrates green box: The combination of ISDN/HYD with ARNI has not been robustly tested. BP response should be carefully monitored.
§Participation in investigational studies is also appropriate for stage C, NYHA class II and III HF.

2022 AHA/ACC/HFSA Heart Failure Guideline/ 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure/2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline,2013 ACC/AHA Guideline, 2009 ACC/AHA Focused Update and 2005 Guidelines for the Diagnosis and Management of Heart Failure in the Adult (DO NOT EDIT) [37][38][39]

Pharmacological Treatment for HFrEF (DO NOT EDIT)[37][38][39]

Renin-Angiotensin System Inhibition With ACEi or ARB or ARNi

Class I
"1. In patients with HFrEF and NYHA class II to III symptoms, the use of ARNi is recommended to reduce morbidity and mortality. [40][41][42][43][44](Level of Evidence: A) "
"2. In patients with previous or current symptoms of chronic HFrEF, the use of ACEi is beneficial to reduce morbidity and mortality when the use of ARNi is not feasible.[45][46][34][47][48][49][33][50] (Level of Evidence: A) "
"3. In patients with previous or current symptoms of chronic HFrEF who are intolerant to ACEi because of cough or angioedema and when the use of ARNi is not feasible, the use of ARB is recommended to reduce morbidity and mortality. [51][52][53][54][55] (Level of Evidence: A) "
"5. In patients with chronic symptomatic HFrEF NYHA class II or III who tolerate an ACEi or ARB, replacement by an ARNi is recommended to further reduce morbidity and mortality. [40][41][42][43][44](Level of Evidence: B-R) "
Class Value Statement: High Value
"4. In patients with previous or current symptoms of chronic HFrEF, in whom ARNi is not feasible, treatment with an ACEi or ARB provides high economic value. [56][57][58][59][4][60][61](Level of Evidence: A) "
"6. In patients with chronic symptomatic HFrEF, treatment with an ARNi instead of an ACEi provides high economic value. [62][63][64][65] (Level of Evidence: A) "
Class III (Harm)
"7. ARNi should not be administered concomitantly with ACEi or within 36 hours of the last dose of an ACEi. [66][67] (Level of Evidence: B-R) "
"8. ARNi should not be administered to patients with any history of angioedema.[68][69][70][71] (Level of Evidence: C-LD) "
"9. ACEi should not be administered to patients with any history of angioedema. [72][73][74][75] (Level of Evidence: C-LD) "

Beta Blockers

Class I
"1. In patients with HFrEF, with current or previous symptoms, use of 1 of the 3 beta blockers proven to reduce mortality (eg, bisoprolol, carvedilol,sustained-release metoprolol succinate) is recommended to reduce mortality and hospitalizations. [76][77][78](Level of Evidence: A) "
Class Value Statement: High Value
"2. In patients with HFrEF, with current or previous symptoms, beta blocker therapy provides high economic values. [56][79][80][81][82] (Level of Evidence: A) "

Mineralocorticoid Receptor Antagonists (MRAs)

Class I
"1. In patients with HFrEF and NYHA class II to IV symptoms, an MRA (spironolactone or epleronone) is recommended to reduce morbidity and mortality, if eGFR is >30 mL/min/1.73 m2 and serum potassium is <5.0 mEq/L. Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation and closely monitored thereafter to minimize risk of hyperkalemia and renal insufficiency. [83][84][85] (Level of Evidence: A) "
Value Statement: High Value
"2. In patients with HFrEF and NYHA II to IV symptoms, MRA therapy provides high economic value.[56][86][87][88] (Level of Evidence: A) "
Class III (Harm)
"3. In patients taking MRA whose serum potassium cannot be maintained at <5.5 mEq/L, MRA should be discontinued to avoid life-threatening hyperkalemia. [89][90] (Level of Evidence: B-NR) "

Sodium-Glucose Contransporter 2 Inhibitors

Class I
"1. In patients with symptomatic chronic HFrEF, SGLT2i are recommended to reduce hospitalization for HF and cardiovascular mortality, irrespective of the presence of type 2 diabetes. [91][92] (Level of Evidence: A) "
Value Statement: Intermediate Value
"2. In patients with symptomatic chronic HFreF, SGLT2i therapy provides intermediate economic value. [93][94] (Level of Evidence: A) "

Hydralazine and Isosorbide Dinitrate

Class I
"1. For patients self-identified as African American with NYHA class III-IV HFrEF who are receiving optimal medical therapy, the combination of hydralazine and isosorbide dinitrate is recommended to improve symptoms and reduce morbidity and mortality. [32][95] (Level of Evidence: A) "
Value Statement: High Value
"2. For patients self-identified as African American with NYHA class III to IV HFrEF who are receiving optimal medical therapy with ACEi or ARB, beta blockers, and MRA, the combination of hydralazine and isosorbide dinitrate provides high economic value.[96] (Level of Evidence: A) "
Class IIb
"3. In patients with current or previous symptomatic HFrEF who cannot be given first-line agents, such as ARNi, ACEi, or ARB, because of drug intolerance or renal insufficiency, a combination of hydralazine and isosorbide dinitrate might be considered to reduce morbidity and mortality. [97][98] (Level of Evidence: C-LD) "

Other Drug Treatment

Class IIb
"1. In patients with HF class II to IV symptoms, omega-3 polyunsaturated fatty acid (PUFA) supplementation may be reasonable to use as adjunctive therapy to reduce mortality and cardiovascular hospitalizations. [99][100][101][102] (Level of Evidence: B-R) "
"2. In patients with HF who experience hyperkalemia (serum potassium level ≥ 5.5 mEq/L) while taking a renin-angiotensin-aldosterone system inhibitor (RAASi), the effectiveness of potassium binders (patiromer, sodium zirconium cyclosilicate) to improve outcomes by facilitating continuation of RAASi therapy is uncertain. [103][104] (Level of Evidence: B-R) "
Class III (No Benefit)
"3. In patients with chronic HFrEF without a specific indication (eg, venous thromboembolism [VTE], AF, a previous thromboembolic event, or a cardioembolic source), anticoagulation is not recommended. [105][106][107] (Level of Evidence: B-R) "

Drugs of Unproven Value or That May Worsen HF

Class III (No Benefit)
"1. In patients with HFrEF, dihydropiridine calcium channel-blocking drugs are not recommended treatment for HF.[108][109] (Level of Evidence: A) "
"2. In patients with HFrEF, vitamins, nutritional supplements, and hormonal therapy are not recommended other than to correct specific deficiencies. [110][111][112][113][114][115][116] (Level of Evidence: B-R) "
Class III (Harm)
"3. In patients with HFrEF, non-dihydropiridine calcium channel-blocking drugs are not recommended. [117][118][119][120] (Level of Evidence: A) "
"4.In patients with HFrEF, class IC antiarrhythmic medications and dronedarone may increase the risk of mortality. [121][122][123] (Level of Evidence: A) "
"5.In patients with HFrEF, thiazolidinediones increase the risk of worsening HF symptoms and hospitalizations. [124][125][126][127][128](Level of Evidence: A) "
"6.In patients with type 2 diabetes and high cardiovascular risk, the dipeptidyl peptidase-4 (DPP-4) inhibitors saxagliptin and alogliptin increase the risk of HF hospitalization and should be avoided in patients with HF. [129][130][131](Level of Evidence: B-R) "
"7.In patients with HFrEF, NSAIDs worsen HF symptoms and should be avoided or withdrawn whenever possible. [132][133][134][135] (Level of Evidence: B-NR) "








Class I
"1. Measures listed as Class I recommendations for patients in stages A and B are also appropriate for patients in Stage C. (Level of Evidence: A, B and C as appropriate)"
"2. The clinical strategy of inhibition of the renin-angiotensin system with ACE inhibitors (Level of Evidence:A)[45][46][34][47][49] or ARBs (Level of Evidence: A)[51][52][53][136][40] or ARNI (Level of Evidence: B-R)[77][78][137] in conjunction with evidence based beta blockers and aldosterone antagonists in selected patients is recommended for patients with chronic HFrEF to reduce morbidity and mortality. "
"3. Patients with HFrEF and hypertension should be prescribed GDMT titrated to attain systolic blood pressure less than 130 mm Hg. (Level of Evidence: C-EO) "
"4. Diuretics and salt restriction are indicated in patients with current or prior symptoms of HFrEF who have evidence of fluid retention. (Level of Evidence: C) "
"5. The use of ACE inhibitors is beneficial for patients with prior or current symptoms of chronic HFrEF to reduce morbidity and mortality (Class I, Level of Evidence: A)[45][46][34][47][49]"
"6. Beta-blockers (using 1 of the 3 proven to reduce mortality, i.e., bisoprolol, carvedilol, and sustained release metoprolol succinate) are recommended for all stable patients with current or prior symptoms of HFrEF, unless contraindicated.[138][139][140][141][142][143][144][145][146][147][148][149] (Level of Evidence: A) "
"7. The use of ARBs to reduce morbidity and mortality is recommended in patients with prior or current symptoms of chronic HFrEF who are intolerant to ACE inhibitors because of cough or angioedema(Class I, Level of Evidence: A)[51][52][53][136][40][54][55] "
"8. 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. (Class I, Level of Evidence: B-R)[40] "
"9. Aldosterone receptor antagonists [or mineralocorticoid receptor antagonists] are recommended in patients with NYHA class II-IV and who have LVEF of 35% or less, unless contraindicated, to reduce morbidity and mortality. Patients with NYHA class II should have a history of prior cardiovascular hospitalization or elevated plasma natriuretic peptide levels to be considered for aldosterone receptor antagonists. Creatinine should be 2.5 mg/dL or less in men or 2.0 mg/dL or less in women (or estimated glomerular filtration rate >30 mL/min/1.73 m2), and potassium should be less than 5.0 mEq/L. Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation and closely followed thereafter to minimize risk of hyperkalemia and renal insufficiency.[83][85][150](Level of Evidence: A) "
"10. Aldosterone receptor antagonists are recommended to reduce morbidity and mortality following an acute MI in patients who have LVEF of 40% or less who develop symptoms of HF or who have a history of diabetes mellitus, unless contraindicated.[84](Level of Evidence: B) "
"11. Patients with chronic HF with permanent/persistent/paroxysmal AF and an additional risk factor for cardioembolic stroke (history of hypertension, diabetes mellitus, previous stroke or transient ischemic attack, or ≥75 years of age) should receive chronic anticoagulant therapy.[151][152](Level of Evidence: A) "
"12. The selection of an anticoagulant agent (warfarin, dabigatran, apixaban, or rivaroxaban) for permanent/persistent/paroxysmal AF should be individualized on the basis of risk factors, cost, tolerability, patient preference, potential for drug interactions, and other clinical characteristics, including time in the international normalized ratio therapeutic range if the patient has been taking warfarin. (Level of Evidence: C) "
"13. Drugs known to adversely affect the clinical status of patients with current or prior symptoms of HF and reduced LVEF should be avoided or withdrawn whenever possible (e.g., non steroidal anti-inflammatory drugs, most antiarrhythmic drugs, and most calcium channel blocking drugs). [153][154][155][156][157][158][159](Level of Evidence: B) "
"14. Exercise training is beneficial as an adjunctive approach to improve clinical status in ambulatory patients with current or prior symptoms of HF and reduced LVEF. [160][161][162][163](Level of Evidence: B) "
"15. An implantable cardioverter-defibrillator is recommended as secondary prevention to prolong survival in patients with current or prior symptoms of HF and reduced LVEF who have a history of cardiac arrest, ventricular fibrillation, or hemodynamically destabilizing ventricular tachycardia.[164][165][166](Level of Evidence: A) "
"16. Implantable cardioverter-defibrillator therapy is recommended for primary prevention of sudden cardiac death to reduce total mortality in patients with non-ischemic dilated cardiomyopathy or ischemic heart disease at least 40 days post-MI, a LVEF less than or equal to 35%, with NYHA functional class II or III symptoms while receiving chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for more than 1 year. [167][168][169][170][171][172][173][174](Level of Evidence: A) "
"17. Implantable cardioverter-defibrillator therapy is recommended for primary prevention of sudden cardiac death to reduce total mortality in selected patients at least 40 days post-MI with LVEF of 30% or less, and NYHA class I symptoms while receiving GDMT, who have reasonable expectation of meaningful survival for more than 1 year.[175][176][177](Level of Evidence: B) "
"18. CRT is indicated for patients who have LVEF of 35% or less, sinus rhythm, left bundle-branch block (LBBB) with a QRS duration of 150 ms or greater, and NYHA class II, III, or ambulatory IV symptoms on GDMT.. [178][179][180][181][182] [183][184][185][186][187][188][189][190][191][192][193][194] (Level of Evidence: A for NYHA class III/IV), (Level of Evidence: B for NYHA class II ) "
"19. Addition of an aldosterone antagonist is reasonable in selected patients with moderately severe to severe symptoms of HF and reduced LVEF who can be carefully monitored for preserved renal function and normal potassium concentration. Creatinine should be less than or equal to 2.5 mg/dL in men or less than or equal to 2.0 mg/dL in women and potassium should be less than 5.0 mEq/L. Under circumstances where monitoring for hyperkalemia or renal dysfunction is not anticipated to be feasible, the risks may outweigh the benefits of aldosterone antagonists. [195][196][197](Level of Evidence: B) "
"20. The combination of hydralazine and nitrates is recommended to improve outcomes for patients self-described as African-Americans, with moderate-severe symptoms on optimal therapy with ACE inhibitors, beta blockers and diuretics.[198][199][200](Level of Evidence: B) "
Class III (No Benefit)
"1. Calcium channel blocking drugs are not recommended as routine treatment for patients with HFrEF.[118][201][108] (Level of Evidence: A) "
"2. Anticoagulation is not recommended in patients with chronic HFrEF without AF, a prior thromboembolic event, or a cardioembolic source. [202][106](Level of Evidence: B) "
"3. Statins are not beneficial as adjunctive therapy when prescribed solely for the diagnosis of HF in the absence of other indications for their use. [203][204](Level of Evidence: A) "
"4. Use of nutritional supplements as treatment for HF is not indicated in patients with current or prior symptoms of HF and reduced LVEF.[205][206] (Level of Evidence: B) "
"5. Hormonal therapies other than to replete deficiencies are not recommended and may be harmful to patients with current or prior symptoms of HF and reduced LVEF. (Level of Evidence: C) "
"6. CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms.[180][181][207](Level of Evidence: B) "
"7. CRT is not indicated for patients whose comorbidities and/or frailty limit survival with good functional capacity to less than 1 year.[208](Level of Evidence: C) "
Class III (harm)
"1. Routine combined use of an ACEI, ARB, and aldosterone antagonist is potentially harmful for patients with HFrEF. (Level of Evidence: C) "
"2. ARNI should not be administered concomitantly with ACE inhibitors or within 36 hours of the last dose of an ACE inhibitor. (Level of Evidence: B-R)[66][67] "
"3. ARNI should not be administered to patients with a history of angioedema. (Level of Evidence: C-EO) "
"4. Inappropriate use of aldosterone receptor antagonists is potentially harmful because of lifethreatening hyperkalemia or renal insufficiency when serum creatinine is more than 2.5 mg/dL in men or more than 2.0 mg/dL in women (or estimated glomerular filtration rate <30 mL/min/1.73 m2), and/or potassium more than 5.0 mEq/L.[90][209] (Level of Evidence: B) "
"5. Drugs known to adversely affect the clinical status of patients with current or prior symptoms of HFrEF are potentially harmful and should be avoided or withdrawn whenever possible (e.g., most antiarrhythmic drugs, most calcium channel blocking drugs (except amlodipine), NSAIDs, or thiazolidinediones).[117][124] [210][211][212][213](Level of Evidence: A) "
"6. Long-term use of an infusion of a positive inotropic drug may be harmful and is not recommended for patients with current or prior symptoms of HF and reduced LVEF, except as palliation for patients with end-stage disease who cannot be stabilized with standard medical treatment (Stage D). (Level of Evidence: C) "
Class IIa
"1. It is reasonable to treat patients with atrial fibrillation and HF with a strategy to maintain sinus rhythm or with a strategy to control ventricular rate alone. [214][215][216][217][218](Level of Evidence: A) "
"2. Chronic anticoagulation is reasonable for patients with chronic HF who have permanent/persistent/paroxysmal AF but are without an additional risk factor for cardioembolic stroke. [219][220][221][222](Level of Evidence: B) "
"3. Maximal exercise testing with or without measurement of respiratory gas exchange is reasonable to facilitate prescription of an appropriate exercise program for patients presenting with HF. (Level of Evidence: C) "
"4. Angiotensin II receptor blockers are reasonable to use as alternatives to ACEIs as first-line therapy for patients with mild to moderate HF and reduced LVEF, especially for patients already taking ARBs for other indications.[223][224][225][226][227][228][229][230][231] (Level of Evidence: A) "
"5. Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF ≤35%) who are receiving GDEM†, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest. (Level of Evidence: B-R)[232][233][234][235] "
"6. Digitalis can be beneficial in patients with current or prior symptoms of HF and reduced LVEF to decrease hospitalizations for HF.[236][237][238][239][240][241][242] (Level of Evidence: B) "
"7. A combination of hydralazine and isosorbide dinitrate can be useful to reduce morbidity or mortality in patients with current or prior symptomatic HFrEF who cannot be given an ACE inhibitor or ARB because of drug intolerance, hypotension, or renal insufficiency, unless contraindicated.[243][244][245][246][247] (Level of Evidence: B)"
"8. CRT can be useful for patients who have LVEF of 35% or less, sinus rhythm, a non-LBBB pattern with a QRS duration of 150 ms or greater, and NYHA class III/ambulatory class IV symptoms on GDMT.[182][178][179][181](Level of Evidence: B) "
"9. CRT can be useful in patients with AF and LVEF of 35% or less on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) atrioventricular nodal ablation or pharmacological rate control will allow near 100% ventricular pacing with CRT.[248][249](Level of Evidence: C) "
"10. CRT can be useful for patients on GDMT who have LVEF of 35% or less, and are undergoing placement of a new or replacement device with anticipated requirement for significant (>40%) ventricular pacing.[250][251][252][253](Level of Evidence: C) "
"11. Omega-3 polyunsaturated fatty acid (PUFA) supplementation is reasonable to use as adjunctive therapy in patients with NYHA class II-IV symptoms and HFrEF or HFpEF, unless contraindicated, to reduce mortality and cardiovascular hospitalizations. [99][100](Level of Evidence: B) "
†GDEM=Guideline Directed Evaluation and Management (Following Class I Recommendations for Heart Failure)
Class IIb
"1. The addition of an ARB may be considered in persistently symptomatic patients with reduced LVEF who are already being treated with conventional therapy and in whom an aldosterone antagonist is not indicated or tolerated.[136][254][255][256][257][258][259] (Level of Evidence: B) "
"2. CRT may be considered for patients who have LVEF of 35% or less, sinus rhythm, a non-LBBB pattern with QRS duration of 120 to 149 ms, and NYHA class III/ambulatory class IV on GDMT.[181][207](Level of Evidence: B) "
"3. CRT may be considered for patients who have LVEF of 35% or less, sinus rhythm, a non-LBBB pattern with a QRS duration of 150 ms or greater, and NYHA class II symptoms on GDMT.[180][181] (Level of Evidence: B) "
"4. CRT may be considered for patients who have LVEF of 30% or less, ischemic etiology of HF,

sinus rhythm, LBBB with a QRS duration of 150 ms or greater, and NYHA class I symptoms on GDMT. [180] [181](Level of Evidence: C) "

Treatment of Patients with HF and preserved ejection fraction HFpEF (DO NOT EDIT) [260]

Class I

1. Systolic and diastolic blood pressure should be controlled in patients with HFpEF in accordance with published clinical practice guidelines to prevent morbidity. (Class I, Level of Evidence: B)

"2. Patients with HFpEF and persistent hypertension after management of volume overload should be prescribed GDMT titrated to attain systolic blood pressure less than 130 mm Hg.[261][262] (Level of Evidence: C-LD)"
"3. Physicians should control ventricular rate in patients with HF and normal LVEF and atrial fibrillation. (Level of Evidence: C)"
"4. Physicians should use diuretics to control pulmonary congestion and peripheral edema in patients with HF and normal LVEF. (Level of Evidence: C)"
Class III (No Benefit)
"1. Routine use of nutritional supplements is not recommended for patients with HFpEF. (Level of Evidence: C) "
Class IIa
"1. Coronary revascularization is reasonable in patients with HF and normal LVEF and coronary artery disease in whom symptomatic or demonstrable myocardial ischemia is judged to be having an adverse effect on cardiac function. (Level of Evidence: C) "
"2. Restoration and maintenance of sinus rhythm in patients with atrial fibrillation and HFpEF is reasonable to improve symptoms. (Level of Evidence: C) "
"3. The use of beta-adrenergic blocking agents, ACEIs, ARBs, or calcium antagonists in patients with HFpEF and controlled hypertension is reasonable to minimize symptoms of HF. (Level of Evidence: C) "
Class IIb
"1.The use of ARBs might be considered to decrease hospitalizations for patients with HFpEF.[262](Level of Evidence: B) "
"2. The usefulness of digitalis to minimize symptoms of HF in patients with HF and normal LVEF is not well established. (Level of Evidence: C) "

Related Chapters

External Links

References

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  39. ↑ 39.0 39.1 39.2 Jessup M, Abraham WT, Casey DE, Feldman AM, Francis GS, Ganiats TG et al. (2009) 2009 focused update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 119 (14):1977-2016.DOI:10.1161/CIRCULATIONAHA.109.192064 PMID: 19324967
  40. ↑ 40.0 40.1 40.2 40.3 40.4 McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR; et al. (2014). "Angiotensin-neprilysin inhibition versus enalapril in heart failure". N Engl J Med. 371 (11): 993–1004. doi:10.1056/NEJMoa1409077. PMID 25176015. Review in: Evid Based Med. 2015 Apr;20(2):61 Review in: Ann Intern Med. 2015 Feb 17;162(4):JC2
  41. ↑ 41.0 41.1 Wachter R, Senni M, Belohlavek J, Straburzynska-Migaj E, Witte KK, Kobalava Z; et al. (2019). "Initiation of sacubitril/valsartan in haemodynamically stabilised heart failure patients in hospital or early after discharge: primary results of the randomised TRANSITION study". Eur J Heart Fail. 21 (8): 998–1007. doi:10.1002/ejhf.1498. PMID 31134724.
  42. ↑ 42.0 42.1 Velazquez EJ, Morrow DA, DeVore AD, Duffy CI, Ambrosy AP, McCague K; et al. (2019). "Angiotensin-Neprilysin Inhibition in Acute Decompensated Heart Failure". N Engl J Med. 380 (6): 539–548. doi:10.1056/NEJMoa1812851. PMID 30415601.
  43. ↑ 43.0 43.1 Desai AS, Solomon SD, Shah AM, Claggett BL, Fang JC, Izzo J; et al. (2019). "Effect of Sacubitril-Valsartan vs Enalapril on Aortic Stiffness in Patients With Heart Failure and Reduced Ejection Fraction: A Randomized Clinical Trial". JAMA. 322 (11): 1077–1084. doi:10.1001/jama.2019.12843. PMC 6749534 Check |pmc= value (help). PMID 31475296.
  44. ↑ 44.0 44.1 Wang Y, Zhou R, Lu C, Chen Q, Xu T, Li D (2019). "Effects of the Angiotensin-Receptor Neprilysin Inhibitor on Cardiac Reverse Remodeling: Meta-Analysis". J Am Heart Assoc. 8 (13): e012272. doi:10.1161/JAHA.119.012272. PMC 6662364 Check |pmc= value (help). PMID 31240976.
  45. ↑ 45.0 45.1 45.2 CONSENSUS Trial Study Group (1987). "Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS)". N Engl J Med. 316 (23): 1429–35. doi:10.1056/NEJM198706043162301. PMID 2883575.
  46. ↑ 46.0 46.1 46.2 SOLVD Investigators. Yusuf S, Pitt B, Davis CE, Hood WB, Cohn JN (1991). "Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure". N Engl J Med. 325 (5): 293–302. doi:10.1056/NEJM199108013250501. PMID 2057034.
  47. ↑ 47.0 47.1 47.2 Pfeffer MA, Braunwald E, Moyé LA, Basta L, Brown EJ, Cuddy TE; et al. (1992). "Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators". N Engl J Med. 327 (10): 669–77. doi:10.1056/NEJM199209033271001. PMID 1386652.
  48. ↑ "Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators". Lancet. 342 (8875): 821–8. 1993. PMID 8104270.
  49. ↑ 49.0 49.1 49.2 Køber L, Torp-Pedersen C, Carlsen JE, Bagger H, Eliasen P, Lyngborg K; et al. (1995). "A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group". N Engl J Med. 333 (25): 1670–6. doi:10.1056/NEJM199512213332503. PMID 7477219.
  50. ↑ Woodard-Grice AV, Lucisano AC, Byrd JB, Stone ER, Simmons WH, Brown NJ (2010). "Sex-dependent and race-dependent association of XPNPEP2 C-2399A polymorphism with angiotensin-converting enzyme inhibitor-associated angioedema". Pharmacogenet Genomics. 20 (9): 532–6. doi:10.1097/FPC.0b013e32833d3acb. PMC 2945219. PMID 20625347.
  51. ↑ 51.0 51.1 51.2 Cohn JN, Tognoni G, Valsartan Heart Failure Trial Investigators (2001). "A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure". N Engl J Med. 345 (23): 1667–75. doi:10.1056/NEJMoa010713. PMID 11759645.
  52. ↑ 52.0 52.1 52.2 Pfeffer MA, McMurray JJ, Velazquez EJ, Rouleau JL, Køber L, Maggioni AP; et al. (2003). "Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both". N Engl J Med. 349 (20): 1893–906. doi:10.1056/NEJMoa032292. PMID 14610160. Review in: ACP J Club. 2004 Jul-Aug;141(1):3
  53. ↑ 53.0 53.1 53.2 Konstam MA, Neaton JD, Dickstein K, Drexler H, Komajda M, Martinez FA; et al. (2009). "Effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart failure (HEAAL study): a randomised, double-blind trial". Lancet. 374 (9704): 1840–8. doi:10.1016/S0140-6736(09)61913-9. PMID 19922995. Review in: Evid Based Med. 2010 Apr;15(2):51-2
  54. ↑ 54.0 54.1 Dominiak M (2008). "[Commentary to the article: ONTARGET Investigators, Yusuf S, Teo KK, Pogue J et al. Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med 2008; 358: 1547-59]". Kardiol Pol. 66 (6): 705–6, discussion 707. PMID 18700309.
  55. ↑ 55.0 55.1 Telmisartan Randomised AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease (TRANSCEND) Investigators. Yusuf S, Teo K, Anderson C, Pogue J, Dyal L; et al. (2008). "Effects of the angiotensin-receptor blocker telmisartan on cardiovascular events in high-risk patients intolerant to angiotensin-converting enzyme inhibitors: a randomised controlled trial". Lancet. 372 (9644): 1174–83. doi:10.1016/S0140-6736(08)61242-8. PMID 18757085. Review in: Ann Intern Med. 2009 Feb 17;150(4):JC2-6
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