Congestive heart failure treatment of patients with current or prior symptoms of heart failure (Stage C): Difference between revisions

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Revision as of 20:44, 14 June 2022

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.

Oral Hypoglycemic agents:^[7] two oral hypoglycemic agents, metformin and thiazolidinediones are considered to be risky in patients with HF.

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.

Antidepressants: Depression is a common finding between patients suffering from HF that is usually related to high mortality rate and bad prognosis of those patients.^[9] Limited data are available on the safety and the risks associated with the usage of antidepressants in patients with heart failure. Health care providers should be aware of major cardiovascular events (as HF, MI, Stroke, cardiovascular death ) that is associated with Tricyclic antidepressants (TCAs) and Selective serotonin reuptake inhibitors (SSRIs).

Phosphodiesterase inhibitors PDE – The PDE-3 inhibitors as^[10] Cilostazol and PDE-4 as ^[11] Anagrelide should be avoided in patients with HF, because of an increase risk of high-output heart failure and fluid retention that is associated with those drugs.^[12]

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.

Chemotherapy – Cardiotoxic chemotherapeutic agents as Cyclophosphamide, Trastuzumab, Bevacizumab and Anthracyclines, should be avoided in HF patients ^[14]

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.

Antihistamines:^[16] some second generation antihistamines as terfenadine and astemizole have been reported to cause long QT syndrome and should not be used in HF patients.

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]

Nonpharmacological Interventions (DO NOT EDIT)^[37]^[38]^[39]

Self-Care Support in HF

Class I
"1. Patients with HF should receive care from multidisciplinary teams to facilitate the implementation of GDMT, address potential barriers to self-care, reduce the risk of subsequent rehospitalization for HF, and improve survival.^[40]^[41]^[42]^[43] (Level of Evidence: A) "
"2. Patients with HF should receive education and support to facilitate HF self-care in multidisciplinary manner. ^[41]^[44]^[45]^[46]^[47]^[48] (Level of Evidence: B-R) "

Class IIa
"3. In patients with HF, vaccinating against respiratory illnesses is reasonable to reduce mortality.^[49]^[50]^[51]^[52]^[53]^[54]^[55] (Level of Evidence: B-NR) "
"4. In adults with HF, screening for depression, ^[56]^[57], social isolation,^[58]^[59]^[60]^[61], frailty, ^[62]^[63] and low health literacy ^[64]^[65] as risk factors for poor self-care is reasonable to improve management. (Level of Evidence: B-NR) "

Dietary Sodium Restriction

Class IIa
"1. For patients with stage C HF, avoiding excessive sodium intake is reasonable to reduce congestive symptoms. ^[66]^[67]^[68]^[69]^[70]^[71] (Level of Evidence: C-LD) "

Management of Stage C HF: Activity, Exercise Prescription, and Cardiac Rehabilitation

Class I
"1. For patients with HF who are able to participate, exercise training (or regular physical activity) is recommended to improve functional status, exercise performance, and QOL. ^[72]^[73]^[74]^[75]^[76]^[77]^[78]^[79]^[80] (Level of Evidence: A ) "

Class IIa
"2. In patients with HF, a cardiac rehabilitation program can be useful to improve functional capacity, exercise tolerance, and health-related QOL. ^[72]^[73]^[76]^[77]^[79] (Level of Evidence: B-NR) "

Diuretics and Decongestation Strategies in Patients with HF (DO NOT EDIT)^[37]^[38]^[39]

Class I
"1. In patients with HF who have fluid retention, diuretics are recommended to relieve congestion, improve symptoms, and prevent worsening HF. ^[23]^[81]^[82]^[83]^[24] (Level of Evidence: B-NR) "
"2. For patients with HF and congestive symptoms, addition of a thiazide (eg, metolazone) to treatment with a loop diuretic should be reserved for patients who do not respond to moderate or high-dose loop diuretics to minimize electrolyte abnormalities. ^[84] (Level of Evidence: B-NR) "

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. ^[85]^[86]^[87]^[88]^[89](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.^[90]^[91]^[34]^[92]^[93]^[94]^[33]^[95] (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. ^[96]^[97]^[98]^[99]^[100] (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. ^[85]^[86]^[87]^[88]^[89](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. ^[101]^[102]^[103]^[104]^[4]^[105]^[106](Level of Evidence: A) "
"6. In patients with chronic symptomatic HFrEF, treatment with an ARNi instead of an ACEi provides high economic value. ^[107]^[108]^[109]^[110] (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. ^[111]^[112] (Level of Evidence: B-R) "
"8. ARNi should not be administered to patients with any history of angioedema.^[113]^[114]^[115]^[116] (Level of Evidence: C-LD) "
"9. ACEi should not be administered to patients with any history of angioedema. ^[117]^[118]^[119]^[120] (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. ^[121]^[122]^[123](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. ^[101]^[124]^[125]^[126]^[127] (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. ^[128]^[129]^[130] (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.^[101]^[131]^[132]^[133] (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. ^[134]^[135] (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. ^[136]^[137] (Level of Evidence: A) "

Value Statement: Intermediate Value
"2. In patients with symptomatic chronic HFreF, SGLT2i therapy provides intermediate economic value. ^[138]^[139] (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]^[140] (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.^[141] (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. ^[142]^[143] (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. ^[144]^[145]^[146]^[147] (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. ^[148]^[149] (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. ^[150]^[151]^[152] (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.^[153]^[154] (Level of Evidence: A) "
"2. In patients with HFrEF, vitamins, nutritional supplements, and hormonal therapy are not recommended other than to correct specific deficiencies. ^[155]^[156]^[157]^[158]^[159]^[160]^[161] (Level of Evidence: B-R) "

Class III (Harm)
"3. In patients with HFrEF, non-dihydropiridine calcium channel-blocking drugs are not recommended. ^[162]^[163]^[164]^[165] (Level of Evidence: A) "
"4.In patients with HFrEF, class IC antiarrhythmic medications and dronedarone may increase the risk of mortality. ^[166]^[167]^[168] (Level of Evidence: A) "
"5.In patients with HFrEF, thiazolidinediones increase the risk of worsening HF symptoms and hospitalizations. ^[169]^[170]^[171]^[172]^[173](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. ^[174]^[175]^[176](Level of Evidence: B-R) "
"7.In patients with HFrEF, NSAIDs worsen HF symptoms and should be avoided or withdrawn whenever possible. ^[177]^[178]^[179]^[180] (Level of Evidence: B-NR) "

GDMT Dosing: Sequencing and Uptitration

Class I
"1. In patients with HFrE, titration of guideline-directed medication dosing to achieve target doses showed to be efficacious in RCTs is recommended, to reduce cardiovascular mortality and HF hospitalizations, unless not well tolerated. ^[121]^[123]^[91]^[33]^[85]^[128]^[130]^[136]^[137]^[140] (Level of Evidence: A) "

Class IIa
"2. In patients with HFrEF, titration and optimization of guideline-directed medications as frequently as every 1 to 2 weeks depending on the patient's symptoms, vital signs, and laboratory findings can be useful to optimize management. (Level of Evidence: C-EO) "

Additional Medical Therapies

Management of Stage C HF: Ivabadrine

Class IIa
"1. For patients with symptomatic (NYHA class II to III) stable chronic HFrEF (LVEF ≤ 35%) who are receiving GDMT, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of ≥70 bpm at rest, ivabradine can be beneficial to reduce HF hospitalizations and cardiovascular death. ^[181]^[182](Level of Evidence: B-R) "

Pharmacological Treatment for Stage C HFrEF: Digoxin

Class IIb
"1. In patients with symptomatic HFrEF despite GDMT (or who are unable to tolerate GDMT), digoxin might be considered to decrease hospitalizations for HF. ^[183]^[184] (Level of Evidence: B-R) "

Device and Interventional Therapies for HFrEF

ICDs and CRTs

Class I
"1. In patients with nonischemic DCM or ischemic heart disease at least 40 days post-MI with LVEF ≤ 35% and NYHA class II or III symptoms or chronic GDMT, who have reasonable expectation of meaningful survival for >1 year, ICD therapy is recommended for primary prevention of SCD to reduce total mortality. ^[185]^[186]^[187]^[188]^[189]^[190]^[191]^[192]^[193](Level of Evidence: A) "

Value Statement:High Value
"2. A transvenous ICD provides high economic value in the primary prevention of SCD particularly when the patient's risk of death caused by ventricular arrhythmia is deemed high and the risk of non-arrhythmic death (either cardiac or noncardiac) is deemed low based on the patient's burden of comorbidities and functional status. ^[194]^[195]^[196]^[197]^[198]^[199] (Level of Evidence: A) "

Class I
"3. In patients at least 40 days post-MI with LVEF ≤ 30% and NYHA class I symptoms while receiving GDMT, who have reasonable expectation of meaningful survival for > 1 year, ICD therapy is recommended for primary preve≤ntion of SCD to reduce total mortality. ^[200] (Level of Evidence: B-R) "
"4. For patients who have LVEF ≤ 35%, sinus rhythm, LBBB with a QRS duration ≥150ms, and NYHA class II, III, or ambulatory IV symtpoms on GDMT, CRT is indicated to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL.^[201]^[202]^[203]^[204]^[205]^[206] (Level of Evidence: B-R) "

Value Statement:High Value
"5. For patients who have LVEF ≤ 35%, sinus rhythm, LBBB with a QRS duration of ≥ 150ms, and NYHA class II, III, or ambulatory class IV symptoms on GDMT, CRT implementation provides high economic value. ^[207]^[208]^[209]^[210]^[211]^[212] (Level of Evidence: B-NR) "

Class IIa
"6.For patients who have LVEF ≤ 35%, sinus rhythm, a non-LBBB pattern with a QRS duration ≥ 150ms, and NYHA class II, III, or ambulatory class IV symptoms on GDMT, CRT can be useful to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. ^[201]^[202]^[203]^[204]^[205]^[206]^[213]^[214]^[215]^[216]^[217]^[218] (Level of Evidence: B-R) "
"7. In patients with high-degree or complete heart block and LVEF of 36% to 50%, CRT is reasonable to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. ^[219]^[220] (Level of Evidence: B-R) "
"8. For patients who have LVEF ≤ 35%, sinus rhythm, LBBB with a QRS duration of 120 to 149 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT, CRT can be useful to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. ^[201]^[202]^[203]^[204]^[205]^[206]^[213]^[214]^[215]^[216]^[217]^[218] (Level of Evidence: B-NR) "
"9. In patients with AF and LVEF ≤ 35% on GDMT, CRT can be useful to reduce total mortality, improve symptoms and QOL, and increase LVEF, 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. ^[201]^[202]^[203]^[204]^[205]^[206]^[213]^[214]^[215]^[216]^[217]^[218] (Level of Evidence: B-NR) "
"10. For patients on GDMT who have LVEF ≤ 35% and are undergoing placement of a new or replacement device implantation with anticipated requirement for significant (>40%) ventricular pacing, CRT can be useful to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. ^[201]^[202]^[203]^[204]^[205]^[206]^[213]^[214]^[215]^[216]^[217]^[218] (Level of Evidence: B-NR) "
"11. In patients with genetic arrhythmogenic cardiomyopathy with high-risk features of sudden death, with EF ≤ 45%, implantation of ICD is reasonable to decrease sudden death. ^[221]^[222](Level of Evidence: B-NR) "

Class IIb
"12. For patients who have LVEF ≤ 35%, sinus rhythym, a non-LBBB pattern with QRS duration of 120 to 149 ms, and NYHA class III or ambulatory class IV on GDMT, CRT may be considered to reduce total mortality, reduce hospitalizations, and improve symptoms and QOL. ^[201]^[202]^[203]^[204]^[205]^[206]^[213]^[214]^[215]^[216]^[217]^[218] (Level of Evidence: B-R) "
"13.For patients who have LVEF ≤ 30%, ischemic case of HF, sinus rhythm, LBBB with a QRS duration ≥ 150ms, and NYHA class I symptoms on GDMT, CRT may be considered to reduce hospitalizations and improve symptoms and QOL. ^[201]^[202]^[203]^[204]^[205]^[206]^[213]^[214]^[215]^[216]^[217]^[218] (Level of Evidence: B-R) "

Class III (No Benefit)
"14. In patients with QRS duration < 120 ms, CRT is not recommended. ^[221]^[222]^[223]^[224]^[225]^[226](Level of Evidence: B-R) "
"15. For patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration < 150 ms, CRT is not recommended.^[201]^[202]^[203]^[204]^[205]^[206]^[213]^[214]^[215]^[216]^[217]Closing `</ref>` missing for `<ref>` tag=== HF With Preserved Ejection Fraction Related Chapters The CHF Living Guidelines: Vote on current recommendations and suggest revisions to the guidelines External Links 2013 ACCF/AHA Guideline for the Management of Heart Failure^[38] 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 ^[39] The ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult ^[227] References ↑ Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, Jessup M, Konstam MA, Mancini DM, Michl K, Oates JA, Rahko PS, Silver MA, Stevenson LW, Yancy CW (2009). 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[pmid11907286-200] Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS; et al. (2002). "Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction". N Engl J Med. 346 (12): 877–83. doi:10.1056/NEJMoa013474. PMID 11907286. Review in: ACP J Club. 2002 Nov-Dec;137(3):81

[pmid12063368-201] 201.0 ^201.1 ^201.2 ^201.3 ^201.4 ^201.5 ^201.6 ^201.7 Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E; et al. (2002). "Cardiac resynchronization in chronic heart failure". N Engl J Med. 346 (24): 1845–53. doi:10.1056/NEJMoa013168. PMID 12063368. Review in: ACP J Club. 2002 Nov-Dec;137(3):82

[pmid15152059-202] 202.0 ^202.1 ^202.2 ^202.3 ^202.4 ^202.5 ^202.6 ^202.7 Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T; et al. (2004). "Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure". N Engl J Med. 350 (21): 2140–50. doi:10.1056/NEJMoa032423. PMID 15152059. Review in: ACP J Club. 2004 Nov-Dec;141(3):60

[pmid15753115-203] 203.0 ^203.1 ^203.2 ^203.3 ^203.4 ^203.5 ^203.6 ^203.7 Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L; et al. (2005). "The effect of cardiac resynchronization on morbidity and mortality in heart failure". N Engl J Med. 352 (15): 1539–49. doi:10.1056/NEJMoa050496. PMID 15753115. Review in: ACP J Club. 2005 Sep-Oct;143(2):29

[pmid19038680-204] 204.0 ^204.1 ^204.2 ^204.3 ^204.4 ^204.5 ^204.6 ^204.7 Linde C, Abraham WT, Gold MR, St John Sutton M, Ghio S, Daubert C; et al. (2008). "Randomized trial of cardiac resynchronization in mildly symptomatic heart failure patients and in asymptomatic patients with left ventricular dysfunction and previous heart failure symptoms". J Am Coll Cardiol. 52 (23): 1834–1843. doi:10.1016/j.jacc.2008.08.027. PMID 19038680.

[pmid24678999-205] 205.0 ^205.1 ^205.2 ^205.3 ^205.4 ^205.5 ^205.6 ^205.7 Goldenberg I, Kutyifa V, Klein HU, Cannom DS, Brown MW, Dan A; et al. (2014). "Survival with cardiac-resynchronization therapy in mild heart failure". N Engl J Med. 370 (18): 1694–701. doi:10.1056/NEJMoa1401426. PMID 24678999.

[pmid21073365-206] 206.0 ^206.1 ^206.2 ^206.3 ^206.4 ^206.5 ^206.6 ^206.7 Tang AS, Wells GA, Talajic M, Arnold MO, Sheldon R, Connolly S; et al. (2010). "Cardiac-resynchronization therapy for mild-to-moderate heart failure". N Engl J Med. 363 (25): 2385–95. doi:10.1056/NEJMoa1009540. PMID 21073365. Review in: Evid Based Med. 2011 Oct;16(5):138-9

[pmid16360064-207] Feldman AM, de Lissovoy G, Bristow MR, Saxon LA, De Marco T, Kass DA; et al. (2005). "Cost effectiveness of cardiac resynchronization therapy in the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial". J Am Coll Cardiol. 46 (12): 2311–21. doi:10.1016/j.jacc.2005.08.033. PMID 16360064.

[pmid28254126-208] Gold MR, Padhiar A, Mealing S, Sidhu MK, Tsintzos SI, Abraham WT (2017). "Economic Value and Cost-Effectiveness of Cardiac Resynchronization Therapy Among Patients With Mild Heart Failure: Projections From the REVERSE Long-Term Follow-Up". JACC Heart Fail. 5 (3): 204–212. doi:10.1016/j.jchf.2016.10.014. PMID 28254126.

[pmid16555866-209] Heerey A, Lauer M, Alsolaiman F, Czerr J, James K (2006). "Cost effectiveness of biventricular pacemakers in heart failure patients". Am J Cardiovasc Drugs. 6 (2): 129–37. doi:10.2165/00129784-200606020-00007. PMID 16555866.

[pmid15353425-210] Nichol G, Kaul P, Huszti E, Bridges JF (2004). "Cost-effectiveness of cardiac resynchronization therapy in patients with symptomatic heart failure". Ann Intern Med. 141 (5): 343–51. doi:10.7326/0003-4819-141-5-200409070-00102. PMID 15353425.

[pmid22913474-211] Noyes K, Veazie P, Hall WJ, Zhao H, Buttaccio A, Thevenet-Morrison K; et al. (2013). "Cost-effectiveness of cardiac resynchronization therapy in the MADIT-CRT trial". J Cardiovasc Electrophysiol. 24 (1): 66–74. doi:10.1111/j.1540-8167.2012.02413.x. PMC 3711178. PMID 22913474.

[pmid26301323-212] Woo CY, Strandberg EJ, Schmiegelow MD, Pitt AL, Hlatky MA, Owens DK; et al. (2015). "Cost-Effectiveness of Adding Cardiac Resynchronization Therapy to an Implantable Cardioverter-Defibrillator Among Patients With Mild Heart Failure". Ann Intern Med. 163 (6): 417–26. doi:10.7326/M14-1804. PMC 8105088 Check |pmc= value (help). PMID 26301323. Review in: Evid Based Med. 2016 Jun;21(3):88

[pmid22305845-213] 213.0 ^213.1 ^213.2 ^213.3 ^213.4 ^213.5 ^213.6 Sipahi I, Chou JC, Hyden M, Rowland DY, Simon DI, Fang JC (2012). "Effect of QRS morphology on clinical event reduction with cardiac resynchronization therapy: meta-analysis of randomized controlled trials". Am Heart J. 163 (2): 260–7.e3. doi:10.1016/j.ahj.2011.11.014. PMC 4113034. PMID 22305845.

[pmid19505883-214] 214.0 ^214.1 ^214.2 ^214.3 ^214.4 ^214.5 ^214.6 Gervais R, Leclercq C, Shankar A, Jacobs S, Eiskjaer H, Johannessen A; et al. (2009). "Surface electrocardiogram to predict outcome in candidates for cardiac resynchronization therapy: a sub-analysis of the CARE-HF trial". Eur J Heart Fail. 11 (7): 699–705. doi:10.1093/eurjhf/hfp074. PMID 19505883.

[pmid21357819-215] 215.0 ^215.1 ^215.2 ^215.3 ^215.4 ^215.5 ^215.6 Zareba W, Klein H, Cygankiewicz I, Hall WJ, McNitt S, Brown M; et al. (2011). "Effectiveness of Cardiac Resynchronization Therapy by QRS Morphology in the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT)". Circulation. 123 (10): 1061–72. doi:10.1161/CIRCULATIONAHA.110.960898. PMID 21357819.

[pmid22781424-216] 216.0 ^216.1 ^216.2 ^216.3 ^216.4 ^216.5 ^216.6 Gold MR, Thébault C, Linde C, Abraham WT, Gerritse B, Ghio S; et al. (2012). "Effect of QRS duration and morphology on cardiac resynchronization therapy outcomes in mild heart failure: results from the Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) study". Circulation. 126 (7): 822–9. doi:10.1161/CIRCULATIONAHA.112.097709. PMID 22781424.

[pmid23995437-217] 217.0 ^217.1 ^217.2 ^217.3 ^217.4 ^217.5 ^217.6 Birnie DH, Ha A, Higginson L, Sidhu K, Green M, Philippon F; et al. (2013). "Impact of QRS morphology and duration on outcomes after cardiac resynchronization therapy: Results from the Resynchronization-Defibrillation for Ambulatory Heart Failure Trial (RAFT)". Circ Heart Fail. 6 (6): 1190–8. doi:10.1161/CIRCHEARTFAILURE.113.000380. PMID 23995437.

[pmid21300176-218] 218.0 ^218.1 ^218.2 ^218.3 ^218.4 ^218.5 Nery PB, Ha AC, Keren A, Birnie DH (2011). "Cardiac resynchronization therapy in patients with left ventricular systolic dysfunction and right bundle branch block: a systematic review". Heart Rhythm. 8 (7): 1083–7. doi:10.1016/j.hrthm.2011.01.041. PMID 21300176.

[pmid23924013-219] Curtis AB (2013). "Biventricular pacing for atrioventricular block and systolic dysfunction". N Engl J Med. 369 (6): 579. doi:10.1056/NEJMc1306998. PMID 23924013.

[pmid16302897-220] Doshi RN, Daoud EG, Fellows C, Turk K, Duran A, Hamdan MH; et al. (2005). "Left ventricular-based cardiac stimulation post AV nodal ablation evaluation (the PAVE study)". J Cardiovasc Electrophysiol. 16 (11): 1160–5. doi:10.1111/j.1540-8167.2005.50062.x. PMID 16302897.

[pmid24503780-221] 221.0 ^221.1 Pugh TJ, Kelly MA, Gowrisankar S, Hynes E, Seidman MA, Baxter SM; et al. (2014). "The landscape of genetic variation in dilated cardiomyopathy as surveyed by clinical DNA sequencing". Genet Med. 16 (8): 601–8. doi:10.1038/gim.2013.204. PMID 24503780.

[pmid31514951-222] 222.0 ^222.1 Gigli M, Merlo M, Graw SL, Barbati G, Rowland TJ, Slavov DB; et al. (2019). "Genetic Risk of Arrhythmic Phenotypes in Patients With Dilated Cardiomyopathy". J Am Coll Cardiol. 74 (11): 1480–1490. doi:10.1016/j.jacc.2019.06.072. PMC 6750731 Check |pmc= value (help). PMID 31514951.

[pmid31078652-223] Towbin JA, McKenna WJ, Abrams DJ, Ackerman MJ, Calkins H, Darrieux FCC; et al. (2019). "2019 HRS expert consensus statement on evaluation, risk stratification, and management of arrhythmogenic cardiomyopathy". Heart Rhythm. 16 (11): e301–e372. doi:10.1016/j.hrthm.2019.05.007. PMID 31078652.

[pmid19723701-224] Moss AJ, Hall WJ, Cannom DS, Klein H, Brown MW, Daubert JP; et al. (2009). "Cardiac-resynchronization therapy for the prevention of heart-failure events". N Engl J Med. 361 (14): 1329–38. doi:10.1056/NEJMoa0906431. PMID 19723701.

[pmid17986493-225] Beshai JF, Grimm RA, Nagueh SF, Baker JH, Beau SL, Greenberg SM; et al. (2007). "Cardiac-resynchronization therapy in heart failure with narrow QRS complexes". N Engl J Med. 357 (24): 2461–71. doi:10.1056/NEJMoa0706695. PMID 17986493.

[pmid23998714-226] Ruschitzka F, Abraham WT, Singh JP, Bax JJ, Borer JS, Brugada J; et al. (2013). "Cardiac-resynchronization therapy in heart failure with a narrow QRS complex". N Engl J Med. 369 (15): 1395–405. doi:10.1056/NEJMoa1306687. PMID 23998714.

[pmid16160202-227] Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG et al. (2005) ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation 112 (12):e154-235. DOI:10.1161/CIRCULATIONAHA.105.167586PMID: 16160202

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@@ Line 494: / Line 494: @@
 |bgcolor="LightCoral"|<nowiki>"</nowiki>'''15.''' For patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration < 150 ms, CRT is not recommended.<ref name="pmid12063368">{{cite journal| author=Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E | display-authors=etal| title=Cardiac resynchronization in chronic heart failure. | journal=N Engl J Med | year= 2002 | volume= 346 | issue= 24 | pages= 1845-53 | pmid=12063368 | doi=10.1056/NEJMoa013168 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12063368  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=12418822 Review in: ACP J Club. 2002 Nov-Dec;137(3):82] </ref><ref name="pmid15152059">{{cite journal| author=Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T | display-authors=etal| title=Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. | journal=N Engl J Med | year= 2004 | volume= 350 | issue= 21 | pages= 2140-50 | pmid=15152059 | doi=10.1056/NEJMoa032423 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15152059  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=15518444 Review in: ACP J Club. 2004 Nov-Dec;141(3):60] </ref><ref name="pmid15753115">{{cite journal| author=Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L | display-authors=etal| title=The effect of cardiac resynchronization on morbidity and mortality in heart failure. | journal=N Engl J Med | year= 2005 | volume= 352 | issue= 15 | pages= 1539-49 | pmid=15753115 | doi=10.1056/NEJMoa050496 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15753115  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=16134903 Review in: ACP J Club. 2005 Sep-Oct;143(2):29] </ref><ref name="pmid19038680">{{cite journal| author=Linde C, Abraham WT, Gold MR, St John Sutton M, Ghio S, Daubert C | display-authors=etal| title=Randomized trial of cardiac resynchronization in mildly symptomatic heart failure patients and in asymptomatic patients with left ventricular dysfunction and previous heart failure symptoms. | journal=J Am Coll Cardiol | year= 2008 | volume= 52 | issue= 23 | pages= 1834-1843 | pmid=19038680 | doi=10.1016/j.jacc.2008.08.027 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19038680  }} </ref><ref name="pmid24678999">{{cite journal| author=Goldenberg I, Kutyifa V, Klein HU, Cannom DS, Brown MW, Dan A | display-authors=etal| title=Survival with cardiac-resynchronization therapy in mild heart failure. | journal=N Engl J Med | year= 2014 | volume= 370 | issue= 18 | pages= 1694-701 | pmid=24678999 | doi=10.1056/NEJMoa1401426 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24678999  }} </ref><ref name="pmid21073365">{{cite journal| author=Tang AS, Wells GA, Talajic M, Arnold MO, Sheldon R, Connolly S | display-authors=etal| title=Cardiac-resynchronization therapy for mild-to-moderate heart failure. | journal=N Engl J Med | year= 2010 | volume= 363 | issue= 25 | pages= 2385-95 | pmid=21073365 | doi=10.1056/NEJMoa1009540 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21073365  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=21436182 Review in: Evid Based Med. 2011 Oct;16(5):138-9] </ref><ref name="pmid22305845">{{cite journal| author=Sipahi I, Chou JC, Hyden M, Rowland DY, Simon DI, Fang JC| title=Effect of QRS morphology on clinical event reduction with cardiac resynchronization therapy: meta-analysis of randomized controlled trials. | journal=Am Heart J | year= 2012 | volume= 163 | issue= 2 | pages= 260-7.e3 | pmid=22305845 | doi=10.1016/j.ahj.2011.11.014 | pmc=4113034 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22305845  }} </ref><ref name="pmid19505883">{{cite journal| author=Gervais R, Leclercq C, Shankar A, Jacobs S, Eiskjaer H, Johannessen A | display-authors=etal| title=Surface electrocardiogram to predict outcome in candidates for cardiac resynchronization therapy: a sub-analysis of the CARE-HF trial. | journal=Eur J Heart Fail | year= 2009 | volume= 11 | issue= 7 | pages= 699-705 | pmid=19505883 | doi=10.1093/eurjhf/hfp074 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19505883  }} </ref><ref name="pmid21357819">{{cite journal| author=Zareba W, Klein H, Cygankiewicz I, Hall WJ, McNitt S, Brown M | display-authors=etal| title=Effectiveness of Cardiac Resynchronization Therapy by QRS Morphology in the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT). | journal=Circulation | year= 2011 | volume= 123 | issue= 10 | pages= 1061-72 | pmid=21357819 | doi=10.1161/CIRCULATIONAHA.110.960898 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21357819  }} </ref><ref name="pmid22781424">{{cite journal| author=Gold MR, Thébault C, Linde C, Abraham WT, Gerritse B, Ghio S | display-authors=etal| title=Effect of QRS duration and morphology on cardiac resynchronization therapy outcomes in mild heart failure: results from the Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) study. | journal=Circulation | year= 2012 | volume= 126 | issue= 7 | pages= 822-9 | pmid=22781424 | doi=10.1161/CIRCULATIONAHA.112.097709 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22781424  }} </ref><ref name="pmid23995437">{{cite journal| author=Birnie DH, Ha A, Higginson L, Sidhu K, Green M, Philippon F | display-authors=etal| title=Impact of QRS morphology and duration on outcomes after cardiac resynchronization therapy: Results from the Resynchronization-Defibrillation for Ambulatory Heart Failure Trial (RAFT). | journal=Circ Heart Fail | year= 2013 | volume= 6 | issue= 6 | pages= 1190-8 | pmid=23995437 | doi=10.1161/CIRCHEARTFAILURE.113.000380 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23995437  }} </ref><ref name="pmid21300176">{{cite journal| author=Nery PB, Ha AC, Keren A, Birnie DH| title=Cardiac resynchronization therapy in patients with left ventricular systolic dysfunction and right bundle branch block: a systematic review. | journal=Heart Rhythm | year= 2011 | volume= 8 | issue= 7 | pages= 1083-7 | pmid=21300176 | doi=10.1016/j.hrthm.2011.01.041 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21300176  }} </ref ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B-NR]])'' <nowiki>"</nowiki>
-|}
-{|class="wikitable" style="width:80%"
+For patients whose comorbidities or frailty limit survival with good functional capacity to <1 year, ICD and cardiac resynchronization therapy with defibrillation (CRT-D) are not indicated
-|-
-| colspan="1" style="text-align:center; background:LightCoral"| [[ACC AHA guidelines classification scheme#Classification of Recommendations|Class III]] (No Benefit)
-|-
-|bgcolor="LightCoral"|<nowiki>"</nowiki>'''16.''' For patients whose comorbidities or frailty limit survival with good functional capacity to <1 year, ICD and cardiac resynchronization therapy with defibrillation (CRT-D) are not indicated. <ref name="pmid9411221">{{cite journal| author=Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators| title=A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. | journal=N Engl J Med | year= 1997 | volume= 337 | issue= 22 | pages= 1576-83 | pmid=9411221 | doi=10.1056/NEJM199711273372202 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9411221  }} </ref><ref name="pmid10942742">{{cite journal| author=Kuck KH, Cappato R, Siebels J, Rüppel R| title=Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest : the Cardiac Arrest Study Hamburg (CASH). | journal=Circulation | year= 2000 | volume= 102 | issue= 7 | pages= 748-54 | pmid=10942742 | doi=10.1161/01.cir.102.7.748 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10942742  }} </ref><ref name="pmid10725290">{{cite journal| author=Connolly SJ, Gent M, Roberts RS, Dorian P, Roy D, Sheldon RS | display-authors=etal| title=Canadian implantable defibrillator study (CIDS) : a randomized trial of the implantable cardioverter defibrillator against amiodarone. | journal=Circulation | year= 2000 | volume= 101 | issue= 11 | pages= 1297-302 | pmid=10725290 | doi=10.1161/01.cir.101.11.1297 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10725290  }} </ref><ref name="pmid8960472">{{cite journal| author=Moss AJ, Hall WJ, Cannom DS, Daubert JP, Higgins SL, Klein H | display-authors=etal| title=Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. 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Multicenter Unsustained Tachycardia Trial Investigators. | journal=N Engl J Med | year= 1999 | volume= 341 | issue= 25 | pages= 1882-90 | pmid=10601507 | doi=10.1056/NEJM199912163412503 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10601507  }} </ref><ref name="pmid: 11907286">{{cite journal| author=Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS | display-authors=etal| title=Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. | journal=N Engl J Med | year= 2002 | volume= 346 | issue= 12 | pages= 877-83 | pmid=: 11907286 | doi=10.1056/NEJMoa013474 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11907286  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=12418821 Review in: ACP 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 |}