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Combination of atrial fibrillation and heart failure (HFpEF and HFrEF) is strongly associated with increased mortality and morbidity.
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Atrial fibrillation can lead to or exacerbate HFrEF through tachycardia and irregularity.
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Atrial fibrillation can lead to or exacerbate HFpEF through loss of atrial systole, irregularity, and diffuse fibrosis.
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Heart failure maybe reversible or improve significantly with catheter ablation leading to the successful restoration of sinus rhythm.
Pathophysiology of Atrial Fibrillation and Heart Failure: Dangerous Interactions
Section snippets
Key points
Definitions
The 2016 European Society of Cardiology HF guidelines provide the most recent update on the diagnosis of HF.15 “Heart failure is defined as a clinical syndrome characterized by typical symptoms that may be accompanied by signs caused by structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressure at rest or during stress.”15
HFpEF is diagnosed when typical symptoms ± signs are accompanied by an LVEF greater than or equal to 50%
Atrial fibrillation causing heart failure with reduced ejection fraction
AF contributes to HFrEF in one of two possible ways: tachycardia or irregularity.5
Atrial fibrillation causing heart failure with preserved ejection fraction
AF potentiates the development and progression of HFpEF, with three key pathophysiologic processes:
- 1.
Loss of atrial systole and irregularity
- 2.
Tachycardia
- 3.
Diffuse fibrosis
Heart failure causing atrial fibrillation
There are multiple postulated mechanisms through which HF leads to AF. The effects of the failing LV may result in electrical, structural, and ionic atrial remodeling, which can facilitate and perpetuate AF.
Summary
AF and HF are modern epidemics with significant morbidity and mortality. AF can cause HFrEF and HFpEF through a range of pathophysiologic mechanisms including rapid ventricular rates, irregularity and loss of atrial systole. In turn, HF can lead to AF through elevated atrial pressure and activation of the sympathetic and renin-angiotensin systems. Reassuringly, randomized clinical trials demonstrate that the restoration of sinus rhythm with catheter ablation can arrest this dangerous
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Disclosure Statement: The authors have no conflicts of interest pertaining to this article. However, the following industry funding sources regarding activities outside the submitted work have been declared in accordance with ICMJE guidelines. P.M. Kistler has received funding from Abott for consultancy and speaking engagements. L.-H. Ling has received fellowship support from Medtronic, Biotronik, and Abott. H. Sugumar has received fellowship support from St Jude Medical and Medtronic. Additionally, these nonindustry funding sources are also disclosed: Drs H. Sugumar, S. Prabhu, L.-H. Ling, and A. Voskoboinik receive funding from Australian National Health and Medical Research Council and/or National Heart Foundation of Australia and/or Royal Australasian College of Physicians and/or Centre of Research Excellence in Cardiovascular Outcomes.