What is the appropriate management for a patient with heart failure with reduced ejection fraction (HFrEF) and atrial fibrillation, with an estimated left ventricular ejection fraction of 40-45% and mild left ventricular hypertrophy?

Management of HFrEF with Atrial Fibrillation (EF 40-45%)

This patient requires comprehensive guideline-directed medical therapy (GDMT) for HFrEF including beta-blockers, ACE inhibitors/ARBs (or ARNI), mineralocorticoid receptor antagonists, and SGLT2 inhibitors, along with anticoagulation for atrial fibrillation and consideration for catheter ablation given the concurrent AF. 1

Immediate Pharmacological Management

Foundational Quadruple Therapy for HFrEF

• Beta-blockers should be initiated or optimized for all patients with LVEF <50% to improve symptoms and reduce heart failure hospitalization and premature death 2, 1

  • Beta-blockers are specifically recommended for rate control in HFrEF patients with AF, especially with high heart rates 2
  • Continue despite atrial fibrillation, as beta-blockers did not increase risk in AF patients 2

• ACE inhibitors or ARBs (if ACE inhibitor not tolerated) should be started for patients with LVEF <50% to reduce heart failure hospitalization and premature death 1

  • Consider switching to angiotensin receptor-neprilysin inhibitor (ARNI) in doses equivalent to enalapril 10 mg twice daily for additional mortality benefit 2, 3

• Mineralocorticoid receptor antagonists (MRAs) are recommended for all symptomatic patients with LVEF ≤35% despite treatment with ACE inhibitor and beta-blocker 2, 1

  • Given this patient's EF is 40-45%, MRA should still be considered if symptomatic (NYHA Class II-IV) 1
  • Monitor serum potassium (contraindicated if >5.0 mmol/L) and renal function regularly 2

• SGLT2 inhibitors should be added to decrease heart failure hospitalizations and cardiovascular mortality regardless of diabetes status 1, 3

  • This represents one of the most significant recent advances in HFrEF management 3

Diuretics for Congestion Management

• Loop diuretics are recommended to reduce signs and symptoms of congestion 2
  • Adjust dose to achieve and maintain euvolemia with the lowest achievable dose 2
  • Train patient to self-adjust diuretic dose based on monitoring symptoms/signs 2

Atrial Fibrillation-Specific Management

Anticoagulation (Mandatory)

• Oral anticoagulation is required given the combination of AF and heart failure, which together increase stroke risk 4, 5
  • Direct-acting oral anticoagulants (DOACs) like apixaban are preferred over warfarin 6
  • Apixaban 5 mg twice daily (or 2.5 mg twice daily if ≥2 of: age ≥80 years, weight ≤60 kg, creatinine ≥1.5 mg/dL) 6

Rhythm Control Strategy

Catheter ablation should be strongly considered as first-line rhythm control rather than antiarrhythmic drugs for this patient. 2, 7

Factors Favoring Catheter Ablation in This Patient:

• LVEF ≥25% (patient has 40-45%) 2
• Moderately enlarged left atrium (not severely enlarged ≥55 mm) 2
• Improved outcomes with ablation: Recent meta-analysis shows catheter ablation reduces HF hospitalization (RR 0.57), cardiovascular mortality (RR 0.46), all-cause mortality (RR 0.53), and improves LVEF by 3.8% 7
• Class IIa-B recommendation from ESC guidelines for catheter ablation in HFrEF with AF 2

When to Consider Medical Therapy Instead:

• Long-standing persistent AF with controlled ventricular rates 2
• Ischemic or valvular cardiomyopathy (note: patient has mild-moderate valvular regurgitation) 2
• LA diameter ≥55 mm 2
• LVEF <25% 2
• Major comorbidities or elderly (≥80 years) 2

Special Considerations for This Patient

Asymmetric Septal Hypertrophy

• The moderate asymmetric septal hypertrophy requires evaluation for hypertrophic cardiomyopathy vs. hypertensive heart disease 1
• This may influence choice of medications (avoid vasodilators if LVOT obstruction present) 1

Improving Ejection Fraction (35% → 40-45%)

• Continue all GDMT even with improved EF - this patient has Heart Failure with Improved EF (HFimpEF) 1
• Discontinuation of GDMT leads to relapse of heart failure and left ventricular dysfunction 1
• The threshold for continuing RAAS inhibitors is EF <50%, so this patient still qualifies 1

Valvular Regurgitation

• Mild-moderate mitral and aortic regurgitation noted [@patient data@]
• Significant improvement in tricuspid regurgitation (severe → mild) and RVSP (63-68 → 30-38 mmHg) suggests improved right heart function with therapy [@patient data@]
• Continue medical optimization; transcatheter mitral valve repair reserved for severe secondary MR 3

Aortic Root Enlargement

• Aortic root increased from 4.5 to 4.7 cm [@patient data@]
• Monitor serially; surgical intervention typically considered at ≥5.5 cm in ascending aorta [@general knowledge@]

Monitoring and Follow-up

• Reassess symptoms, functional status (NYHA class), and volume status at each visit 2
• Repeat echocardiogram in 3-6 months to assess response to optimized GDMT 1
• Monitor electrolytes (especially potassium) and renal function regularly with MRA therapy 2
• Assess heart rate control in AF (target <110 bpm initially) 5
• Consider cardiopulmonary exercise testing if advanced therapies (CRT, ICD) being considered 2

Device Therapy Considerations

• ICD evaluation if LVEF remains ≤35% after 3 months of optimal medical therapy, particularly if ischemic etiology 1
• Cardiac resynchronization therapy (CRT) if QRS ≥130 msec with LBBB pattern in sinus rhythm, or individualized decision in AF with strategy to ensure biventricular capture 2, 1
• Current AF precludes standard CRT assessment; rhythm control may facilitate future CRT candidacy 2

Common Pitfalls to Avoid

• Do not discontinue GDMT despite improved EF - this leads to relapse 1
• Do not delay SGLT2 inhibitor initiation - this is now foundational therapy regardless of diabetes status 1, 3
• Do not use rate control alone without considering rhythm control via ablation in HFrEF with AF - ablation improves mortality 7
• Do not forget anticoagulation - AF plus heart failure substantially increases stroke risk 4, 5
• Avoid NSAIDs - these worsen heart failure and interfere with RAAS inhibition [@general knowledge@]