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Patients with concomitant atrial fibrillation (AF) and heart failure (HF) face worse symptoms, poorer prognoses, and different treatment responses than those with either condition alone.
Patients with concomitant atrial fibrillation (AF) and heart failure (HF) face worse symptoms, poorer prognoses, and different treatment responses than those with either condition alone.
AF prevalence will double in the next 20 years due to increased patient longevity and longer survival after myocardial infarction. Of note, AF triples the risk of incident HF.
With these facts in mind, there is a critical need to find the most optimal treatment for these increasingly prevalent comorbid conditions.
Medications acting on the renin-angiotensin-aldosterone system (RAAS), such as angiotensin-converting-enzyme (ACE) inhibitors, prevent AF in HF patients. When AF and HF are comorbid, however, clinicians often struggle to find the best medications.
An article published ahead-of-print in the European Heart Journal explores evidence-based treatment in comorbid AF and HF.
These experts recommend the CAN-TREAT HFrEF+AF algorithm for newly diagnosed patients with comorbid HF with reduced ejection fraction (HFrEF) and AF.
This algorithm details a cascade of treatments:
· Cardioversion if hemodynamically compromised
· Anticoagulation unless absolutely contraindicated
· Fluid balance normalization with diuretics to control signs and symptoms of HF
· Target initial heart rate is less than 110 beats per minute with stricter control if symptoms persist
· RAAS medications (eg, ACE-inhibitors, angiotensin II receptor blockers, and aldosterone antagonists)
· Early rhythm control (eg, amiodarone, cardioversion, and ablation)
· Advanced heart failure therapies (eg, resynchronization, defibrillator, and/or mechanical support)
· Treatment of other cardiovascular disease (eg, hypertension and ischemia)
Anticoagulation is necessary in AF patients because they are at great risk of thrombotic stroke. Novel oral anticoagulants are superior to vitamin K antagonists due to their decreased hemorrhagic stroke risk.
ACE-inhibitors have not been studied in comorbid AF and HF, but the CHARM trial found candesartan to be effective in this population.
Beta-blockers and aldosterone antagonists have been found to provide no additional benefit in HF patients with AF.
The AF-CHF trial found rhythm control had no effect on survival driven by poor rhythm control rates.
Digoxin has little to no evidence of efficacy in AF, and non-dihydropyridine calcium channel blockers have evidence of harm.
This review is a good reference for all clinicians who see patients with comorbid AF and HF.
The authors called for further research in patients with AF and HF, especially concerning rate control, optimal methods of rhythm control, and prevention. Further, they called for a focus on primary prevention of AF.