ACC-AHA 2022 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure
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| p.27 | 1 A | Table 9. Selected Multivariable Risk Scores to Predict Development of Incident HF Risk Score Reference Year Published Framingham Heart Failure Risk Score 24 1999 Health ABC Heart Failure Score 25 2008 ARIC Risk Score 26 2012 PCP-HF 29 2019 ARIC indicates Atherosclerosis Risk in Communities; HF, heart failure; and PCP-HF, Pooled Cohort Equations to Prevent HF. or diastolic) with or without newly diagnosed HF.22 Similarly, in another small, single-center RCT, accelerated uptitration of RAAS antagonists and beta blockers reduced cardiac events in patients with diabetes and elevated NT-proBNP levels but without cardiac disease at baseline.23 | ||
| p.29 | 1 A | 5. The Framingham studies have shown a 60% increased risk of death in patients with asymptomatic low LVEF compared with those with normal LVEF, and almost half of these patients remained free of HF before their death.25 MADIT-II (Multicenter Automatic Defibrillator Implantation Trial II) showed a 31% relative risk reduction in all-cause mortality in patients with post-MI with LVEF ≤30% receiving a prophylactic ICD compared with standard of care.14 These findings provided justification for the broad adoption of ICDs for primary prevention of SCD in the post-MI setting with reduced LVEF, even in the absence of HF symptoms. 6. Although beta blockers have been shown to improve outcomes in patients with symptomatic HFrEF and in patients with reduced LVEF after MI,11 few data exist regarding the use of beta blockers in asymptomatic patients with depressed LVEF without a history of MI. There is evidence to support the role of beta blockers to prevent adverse LV remodeling in asymptomatic patients with LV systolic dysfunction, including those with nonischemic cause.43 Also, in a post hoc analysis of the SOLVD prevention trial, which included approximately 20% of participants with nonischemic HF cause, beta blockers were associated with a reduction in the risk of death and in death or hospitalization for symptomatic HF in those patients randomized to enalapril, a finding that was not seen in the placebo group.12 Given the longterm benefits of beta blockers to reduce HF hospitalizations in patients with symptomatic HFrEF,44 beta-blocker therapy is recommended to prevent symptomatic HF in patients with reduced LVEF. 7. Thiazolidinediones have been associated with fluid retention and increased rates of HF in RCTs of patients with type 2 diabetes who were predominantly free of symptomatic HF at baseline.47–49 In a smaller RCT of patients with more severely symptomatic HFrEF, pioglitazone was associated with increased rates of HF hospitalization compared with placebo.50 In patients with more mild symptoms (NYHA class I to II) but with depressed LVEF,15 rosiglitazone was associated with more fluid-related events, including worsening edema and need for increased HF medications.15 Given the evidence, thiazolidinediones should be avoided in patients with reduced LVEF. 8. Nondihydropiridine calcium channel blockers diltiazem and verapamil are myocardial depressants and generally not tolerated in HF. In previous studies of patients with HF or reduced LVEF after acute MI, diltiazem was associated with increased risk of HF,16,17 although in a smaller study of patients with nonischemic cardiomyopathy, diltiazem had no impact on mortality.45 Verapamil had no impact on survival or major cardiovascular events after acute MI.46 Although not specifically tested in asymptomatic Downloaded from http://ahajournals.org by on October 7, 2026 | ||
| p.32 | 1 A | HF indicates heart failure. A recent pilot RCT N=27) showed that providing patients with 1.5 g/d sodium meals can reduce urinary sodium and improve QOL but not improve clinical outcomes.3 Another recent pilot RCT (N=38) of 1.5 versus 2.3 g/d sodium resulted in sodium intake and improvement in BNP levels and QOL in the 1.5 g/d sodium intake arm5; the full trial is due to be completed in 2022. A third pilot RCT (N=66) of home-delivered 1.5 g/d meals showed favorable but nonsignificant trends toward improvement in clinical status and readmission rates.6 Moreover, results from RCTs have shown that reducing dietary sodium is difficult to achieve in patients with HF, even with prepared meals3 or home visits.26 | ||
| p.34 | 1 A | Torsemide 10–20 mg once 200 mg 12–16 h Thiazide diuretics Chlorthiazide 250–500 mg once or twice 1000 mg 6–12 h Chlorthalidone 12.5–25 mg once 100 mg 24–72 h Hydrochlorothiazide 25 mg once or twice 200 mg 6–12 h Indapamide 2.5 mg once 5 mg 36 h Metolazone 2.5 mg once 20 mg 12–24 h HF indicates heart failure. volume overload to decrease congestion while maintaining serum sodium. Recommendation-Specific Supportive Text | ||
| p.34 | 1 A | Downloaded from http://ahajournals.org by on October 7, 2026 1. Controlled trials with diuretics showed their effects to increase urinary sodium excretion, decrease physical signs of fluid retention, and improve symptoms, QOL, and exercise tolerance.1–5 Recent data from the nonrandomized OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) registry revealed reduced 30-day all-cause mortality and hospitalization for HF with diuretic use compared with no diuretic use after hospital discharge for HF.9 The most commonly used loop diuretic for the treatment of HF is furosemide, but some patients respond more favorably to other agents in this category (eg, bumetanide, torsemide), potentially because of their increased oral bioavailability.10–12 In outpatients with HF, diuretic therapy is commonly initiated with low doses, and the dose is increased until urine output increases and weight decreases, generally by 0.5 to 1.0 kg daily. Patients may become unresponsive to high doses of diuretic drugs if they consume large amounts of dietary sodium, are taking agents that can block the effects of diuretics (eg, NSAIDs), or have significant impairment of renal function or perfusion. 2. Diuretic resistance can be overcome in several ways, including escalation of loop diuretic dose, intravenous administration of diuretics (bolus or continuous infusion),6 or combination of different diuretic classes.13–16 The use of a thiazide or thiazide-like diuretic (eg, metolazone) in combination with a loop diuretic inhibits compensatory distal tubular sodium reabsorption, leading to enhanced | ||
| p.37 | 1 A | Downloaded from http://ahajournals.org by on October 7, 2026 Treatment with beta blockers reduces the risk of death and the combined risk of death or hospitalization in patients with HFrEF.1–3 In addition, this treatment can improve LVEF, lessen the symptoms of HF, and improve clinical status.1–3,9–11 Clinical trials have shown that beta blockers should be prescribed to all patients when HFrEF is diagnosed, including in-hospital, unless contraindicated or not tolerated.1–3,9–11 These benefits of beta blockers were observed in patients with or without CAD, and in patients with or without diabetes, older patients, as well as in women and across racial and ethnic groups but not in patients with AF.1–3,10–12 Even if symptoms do not improve, long-term treatment should be maintained to reduce the risk of major cardiovascular events. Beta blockers should be initiated at low doses, and every effort should be made to achieve the target doses of the beta blockers shown to be effective in major clinical trials, as tolerated1–3,9,10 (see Section 7.3.8, “GDMT Dosing, Sequencing and Uptitration”). Recommendation-Specific Supportive Text | ||
| p.38 | 1 A | 1. Clinical trials taken on MRA together—RALES (Randomized Aldactone Evaluation Study)1 randomized highly symptomatic patients with LVEF ≤35%; EPHESUS (Eplerenone Post–Acute Myocardial Infarction Heart Failure Efficacy and Survival Study)2 randomized patients post-MI with LVEF ≤40%; and EMPHASIS-HF (Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure)3 randomized patients with mild symptoms and LVEF ≤30%—suggest a benefit of MRA across the spectrum of HFrEF, inclusive of a wide range of etiologies and disease severities. Initiation in the ambulatory or hospital setting is appropriate.12 The starting dose of spironolactone and eplerenone is 25 mg orally daily, increased to 50 mg daily orally after a month; for eGFR 31 to 49 mL/min/1.73 m2, dosing should be reduced by half. Regular checks of serum potassium levels and renal function should be performed according to clinical status, approximately 1 week, then 4 weeks, then every 6 months after initiating or intensifying MRA, with more frequent testing for clinical instability. We elected to remove the 2013 recommendation “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” because the new recommendation covers the spectrum of symptomatic patients with HF. 2. The economic value of MRA therapy was assessed by both RCTs (RALES5 and EPHESUS6,7) and a model-based analysis.4 The model-based analysis used generic MRA costs and found therapy was high value with a cost per QALY of under $1000.4 The earlier trial-based economic analyses of MRAs from RALES and EPHESUS also found MRA therapy was high value despite using previously higher MRA costs.5–7 Downloaded from http://ahajournals.org by on October 7, 2026 | ||
| p.39 | 1 A | months).1,2 Patients enrolled had symptomatic chronic HFrEF (LVEF ≤40%, NYHA class II to IV, and elevated natriuretic peptides) and were already on GDMT. Important exclusions were eGFR <20 (EMPEROR-Reduced) or <30 mL/min/1.73 m2 (DAPA-HF), type 1 diabetes, or lower SBP <95 to 100 mm Hg. Recommendation-Specific Supportive Text 1. In the DAPA-HF and EMPEROR-Reduced trials, SGLT2i compared with placebo reduced the composite of cardiovascular death or HF hospitalization by approximately 25%.1,2,9 The benefit in reduction of HF hospitalization was greater (30%) in both trials.9 Risk of cardiovascular death was significantly lowered (18%) with dapagliflozin, as was risk of all-cause mortality (17%). Although no significant cardiovascular mortality benefit was observed with empagliflozin in a meta-analysis of DAPA-HF and EMPEROR-Reduced trials, SGLT2i therapy was associated with a reduction in all-cause mortality and cardiovascular death.9 The benefits in both trials were seen irrespective of baseline diabetes status. Furthermore, serious renal outcomes were less frequent, and the rate of decline in eGFR was slower in patients treated with SGLT2i.1,2,9 In the SOLOIST-WHF (Effect of Sotagliflozin on Cardiovascular Events in Patients With Type 2 Diabetes And Worsening Heart Failure) trial, patients with diabetes and HF hospitalization (79%: LVEF, <50%) were enrolled before discharge or within 3 days of discharge. Sotagliflozin, a dual inhibitor of sodium-glucose co-transporters 1 and 2, reduced the combined endpoint of cardiovascular death, HF hospitalization, or urgent HF visits by 33%10 but has not been approved by the US Food and Drug Administration (FDA) as of 2021. Although SGLT2i increased risk for genital infections, they were otherwise well tolerated in the trials. As the use of SGLT2i is translated into clinical practice, caution is warranted for euglycemic ketoacidosis, genital and soft tissue infections, and adjustment of diuretics, if needed, to prevent volume depletion.11 Downloaded from http://ahajournals.org by on October 7, 2026 | ||
| p.43 | 1 A | 4. In the CAST (Cardiac Arrhythmia Suppression) trial, patients with asymptomatic ventricular arrhythmias post-MI on the class IC antiarrhythmics encainide or flecainide had increased mortality.14 The applicability of CAST to patients without recent MI or to other class I antiarrhythmic drugs is uncertain, but class IC antiarrhythmic agents are generally avoided in patients with structural heart disease. In ANDROMEDA (Antiarrhythmic Trial with Dronedarone in Moderate to Severe CHF Evaluating Morbidity Decrease Study), for the class III antiarrhythmic dronedarone, patients with HFrEF who were hospitalized had increased mortality.16 In the SWORD (Survival With ORal D-sotalol) trial of the class III antiarrhythmic sotalol, patients with HF post-MI had increased mortality.15 However, SWORD was published in 1996, and whether sotalol would be harmful in the current era of GDMT and ICDs is uncertain; sotalol may be used for refractory atrial-ventricular arrhythmias with close monitoring for decompensation. Amiodarone46,47 and dofetilide48,49 are the only antiarrhythmic agents with neutral effects on mortality in clinical trials of patients with HFrEF. Class IA antiarrhythmic agents such as quinidine and class IB agents such as mexiletine have not been studied and may be indicated for the management of refractory ventricular arrhythmias in the context of the individual patient’s risk benefit calculus and in conjunction with electrophysiology consultation. 5. Thiazolidinediones increase insulin sensitivity by activating nuclear peroxisome proliferator-activated receptor gamma (PPAR-γ). Expressed in virtually all tissues, PPAR-γ also regulates sodium reabsorption in the collecting ducts of the kidney. In observational cohort studies,17 meta-analysis,18 and clinical trials,19–21 thiazolidinediones have been associated with increased incidence of fluid retention and HF events in those patients with19,21or without18,20a previous history of HF. 6. DPP-4 is a cell-surface enzyme that deactivates several peptides include glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1. DPP-4 inhibitors affect glucose regulation through multiple mechanisms, including enhancement of glucose-dependent insulin secretion, slowed gastric emptying, and reduction of postprandial glucagon and of food intake. The impact of DPP-4 inhibitors on cardiovascular outcomes in patients with diabetes and high cardiovascular risk has been assessed in multiple RCTs. Saxagliptin increased the risk of hospitalization for HF,22 as did alogliptin in a post hoc analysis Downloaded from http://ahajournals.org by on October 7, 2026 | ||
| p.47 | 1 A | Recommendation for Pharmacological Treatment for Stage C HFrEF: Soluble Guanylyl Cyclase Stimulators Referenced studies that support the recommendation are summarized in the Online Data Supplements. COR LOE Recommendation 1. In selected high-risk patients with HFrEF and recent worsening of HF already on GDMT, an oral soluble guanylate cyclase stimulator (vericiguat) may be considered to reduce HF hospitalization and cardiovascular death.1 2b B-R Synopsis In patients with progression of HFrEF despite GDMT, there may be a role for novel therapeutic agents. Oral soluble guanylyl cyclase stimulator (eg, vericiguat) directly binds and stimulates sGC and increases cGMP production. cGMP has several potentially beneficial effects in patients with HF, including vasodilation, improvement in endothelial function, as well as decrease in fibrosis and remodeling of the heart.2–7 The VICTORIA (Vericiguat Global Study in Subjects with Heart Failure with Reduced Ejection Fraction) trial randomized 5050 higher-risk patients with worsening HFrEF to vericiguat versus placebo.1 Downloaded from http://ahajournals.org by on October 7, 2026 Recommendation-Specific Supportive Text | ||
| p.64 | 1 A | Downloaded from http://ahajournals.org by on October 7, 2026 Recommendation-Specific Supportive Text 1. More prolonged use of inotropes as “bridge” therapy for those awaiting either heart transplantation or MCS may have benefit in reducing pulmonary hypertension and maintaining end-organ perfusion beyond initial stabilization of patients.1–4 2. The use of inotropes for palliation does carry with it risks for arrhythmias and catheter-related infections, although the presence of an ICD does decrease the mortality associated with arrhythmias. This risk should be shared with patients if there is planned use of inotropes in a patient without an ICD, or in whom the preference is to deactivate the ICD for palliative purposes. The rate of inappropriate shocks for sinus tachycardia is relatively low, and the concomitant use of beta blockers may help in these patients. Patients may elect to have their shocking devices deactivated, especially if they receive numerous shocks.14,15 | ||
| p.75 | 1 A | Downloaded from http://ahajournals.org by on October 7, 2026 discharge is a desired goal. Although historically this has been an in-person visit, telemedicine is being increasingly used for chronic management. A pragmatic randomized trial found that an initial telephone visit with a nurse or pharmacist to guide follow-up may reduce the need for in-person visits if they are constrained.22 Overall, the timing and method of delivery (in-person clinic versus virtual visit by video or telephone) should be individualized based on patient risk and available care delivery options. Clinical risk prediction tools may help to identify patients at highest risk of postdischarge adverse outcomes.23–25 10 COMORBIDITIES IN PATIENTS WITH HF 10.1 Management of Comorbidities in Patients With HF Recommendations for the Management of Comorbidities in Patients With HF Referenced studies that support the recommendations are summarized in the Online Data Supplements. COR LOE Recommendations Management of Anemia or Iron Deficiency 1. In patients with HFrEF and iron deficiency with or without anemia, intravenous iron replacement is reasonable to improve functional status and QOL.1–4 2a B-R 2. In patients with HF and anemia, erythropoietinstimulating agents should not be used to improve morbidity and mortality.5,6 3: Harm B-R | ||
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